Re: Digest Number 1059

March 2, 2000

I found this list through a posting on a tick list. My awakening to tick

born diseases started in 1997 when one of my greyhounds was dx with

babesia. I didn't know how to spell it or have a clue about what it came

from. I read everything I could find on tick diseases. The dog was given

Imizol in 2 injections and he seems to be doing well. He is very large

for a greyhound 112 lb. and used to try to take my arm or hand to take

me to the kitchen for dog treats. I was bruising and skin breaking

easily because I had been on prednison for arthritis for 4 yr. I started

to question if I could catch this or if my other 2 dogs could catch

anything from toys etc that they shared.(the other 2 have tested neg.) I

asked my rheumatologist if I could catch babesia and she said people

don't catch that. She said I did check you for lyme disease a few yr ago

and you are OK. I found a new rheumatologist and asked her the same

question. She said that if I had a tick disease it would show up on a

liver profile and I had no signs. I explained to her that I am 58 yr old

and have been on antinflamotory medication non stop since I was 30 yr

old and woke up one morning while we were camping at the Jersey shore

for a wk. and felt like I was going to die. My head hurt and I was so

stiff I could hardly walk. Everything hurt, it was like having the flu.

I have never had a bulls eye rash but I had some nasty looking bites

that I blamed on flies. I started to feel better just taking aspirin.

Then after that I have always been treated for arthritis and one time

for PMR. I was in kidney failure about 19 yr ago and the nephrologist

never knew why. I have had arthroscopic surg on both knees and numerous

joint injectios. I am told it is osteoarthritis a wear and tear disease.

I have it in my knuckles and I don't walk on them. I have always had

dogs and shown dogs. I once had a Kuvasz who ran off and came home

covered with ticks. I drank all the beer in the frig and called my

husband to come home from work. We had to get the house fumigated. I no

longer have the husband but I still have my fear of ticks. I do believe

my Dr thinks I am crazy for questioning tick diseases. I have been in

tick areas freq in my life. I spent 3 yr as an Army nurse and saw my

first tick during basic training in Texas. I have since traveled a great

deal in and out of the states. I am exhausted and tired of spending a

lifetime feeling not quite right most of the time and finally feeling

good about complaining right now. I have an apt with my family Dr in a

few wk. I have never discussed my concerns about tick diseases with

him(that I am finally wondering about). What tests if any can I ask him

about? I live in Pa. near town and also wonder if there are any

lyme literate Dr. in my area. I do work but it takes most of my strenght

to just keep going. Any advise is welcome.

April 16, 2001

' ' wrote:

====

- =======================================================

-

October 31, 2001

To whomever is supposed to be moderating (Dave or Dan):

It may just be me, but whenever I open my daily digest of listserv e-mail,

there has been information or 'ads' wanting dwarfs on this " Talk or Walk "

show. I put up with it for a while, but now I want to know if they are going

to be stopped and if so, when?

Thanks,

October 31, 2001

Dave says:

> should clarify that when I say " they fight " , I mean that they " do

> battle against the antagonists " , not " they argue amongst themselves " .

Yes, but on this listserv they do that, too. And very well, I might add. :-)

October 31, 2001

So what's up with all this interviewing? I this for

real or a joke

anyone

> know. First television now interviews. Seem they all

have the same

area

> code.

.....that's because they're all from the same TV

Show....

Gretchen

http://www.geocities.com/elfsnot20

=====

" So Bin Laden thinks we are scared from the north to the south and east to

west. This from a man who is hiding in a cave. " - Anonymous; Atlanta Journal

Constitution, The Vent Section.

" We could learn a lot from crayons: some are sharp,

some are pretty, some are dull, some have weird names,

and all are different colors...but they all have to

learn to live in the same box. " - donated by Kathy McAllan ~~

__________________________________________________

November 18, 2001

In a message dated 11/18/01 8:09:02 AM Eastern Standard Time, writes:

Message: 14

Date: Sun, 18 Nov 2001 05:19:43 -0500

From: "Barbara Herskovitz" <bherk@...>

Subject: Is Your Workplace Making You Sick?

Thursday November 15 06:22 PM EST

Is Your Workplace Making You Sick?

Allergies are a growing health concern, especially in the workplace, where

more and more people are exposed to an increasing number of chemicals.

A study presented at The International Asthma and Allergy Conference

Thursday documents more than 250 agents responsible for work-related

allergies.

NewsCenter 5's Unruh said that Mike Moscow's been doing extra duty

since his secretary developed an allergy to something in the office.

Replacing the carpet didn't help. "My secretary moved down the hall to

another office, and I stayed here, and she was there, and we communicated by

phone, which was not the best way to do business," Moscow said.

Moscow enlisted the help of air-quality expert Jeff May.

"I take samples of the particles that are in the air, and then I look at

them under a microscope, and that gives me a picture really of what's in the

air," May said.

It turns out that the air in workplaces everywhere is causing increasing

allergy and asthma cases -- an estimated 5 percent of all adult asthma,

according to a study released Thursday at the International Asthma and

Allergy Conference. The most common offenders are dust and spider mites,

latex, ammonia, chlorine, detergent, and mold.

"There's mold growing in places where people don't know it. It grows in

carpets and it grows inside the heating and cooling system," May said.

The study found that latex causes a lot of workplace allergies. Many

restaurant and health care industries have stopped using latex gloves.

"Now we use powder-free gloves, because the powder in the gloves--it gets

into the air. It gets all over," May said.

In Moscow's building, the problem is dust from construction years ago. The

solution is one that could improve a lot of working environments.

"What we're going to try and do is pump some very fresh, clean air into the

office so air will leak out and not come in," Moscow said.

Thanks for posting the article. Do you have the URL or web link?

Anne HNRLA-MCS a discussion for those who have both MCS and NRLA

HNRLA-MCS

November 5, 2002

Call the school ,and get the number too the bus company then report the bus

driver. Yes, I would wait at the stop ,and confront her maybe if more parents

did that the bus drivers might start caring about the kids instead of just

the money!

November 10, 2002

Hi ,

Thank you so much for posting these articles on Lupus!!! They are so

helpful!!! The article Message: 7 was one of the best articles I have read,

as it was so clear and articulate.

Thank you again for all you do!!

----------------------------------------------------------------------------

------

6. Fw: Magnesium deficiency in systematic lupus erythematosus.

From: " Heer " <idagirl@...>

7. Fw: Systemic lupus erythematosus and lupus-like syndromes.

5/13/95

From: " Heer " <idagirl@...>

Subj: MG levels

Date: 11/8/2002 8:05:25 AM Eastern Standard Time

From, kathynye@...

Title: Magnesium deficiency in systematic lupus erythematosus.

Subject(s): MAGNESIUM deficiency diseases; SYSTEMIC lupus

erythematosus -- Diagnosis

Source: Journal of Nutritional & Environmental Medicine, Jun97, Vol. 7

Issue 2, p107, 5p, 1 chart

Author(s): Romano, J.

Abstract: Discusses the effects of reduced erythrocyte magnesium

(Mg) deficiency in patients with systematic lupus erythematosus (SLE).

Common symptom of the disorder; How to determine if SLE patients are

also prone to hypomagnesemia; Results of the study.

AN: 9711141130

ISSN: 1359-0847

Full Text Word Count: 2470

Database: Academic Search Elite

Section: ORIGINAL RESEARCH

MAGNESIUM DEFICIENCY IN SYSTEMIC LUPUS ERYTHEMATOSUS

Reduced erythrocyte magnesium (Mg) levels have been reported in

fibromyalgia syndrome (FS), chronic fatigue syndrome (CFS), myofascial

pain syndrome (MPS) and eosinophilia myalgia syndrome (EMS). These

disorders have chronic pain as a common symptom. Chronic pain also

affects some patients with systemic lupus erythematosus (SLE). To

determine if SLE patients are also prone to hypomagnesemia, red blood

cell (RBC) and plasma Mg levels were measured in all SLE patients seen

in a general rheumatology practice in a 3-year period. There were 25

such patients with a mean age of 47 years. Thirteen SLE patients had FS

and 12 did not have either FS or MPS. The mean RBC Mg level for the SLE

patients was 4.60 mg dl-1, statistically significantly lower than that

of the reference controls and 12 osteoarthritis controls. It did not

matter whether the SLE patients had ES or MPS. This finding has

implications for diagnosis and treatment.

Keywords: magnesium, myalgias, lupus, pain.

INTRODUCTION

Reduced erythrocyte magnesium (Mg) levels have been reported in

fibromyalgia syndrome (FS) [ 1], chronic fatigue syndrome (CFS) [ 2],

myofascial pain syndrome (MPS) [ 3] and eosinophilia myalgia syndrome

(EMS) [ 4]. These four disorders have chronic pain and/or fatigue as a

common denominator. Furthermore, it has been proposed that low Mg levels

predispose patients to myalgias [ 5] and that low muscle Mg levels

correspond to a low pain threshold [ 6]. Systemic lupus erythematosus

(SLE) is also a condition that can be characterized by chronic pain in

some patients. Lupus patients have often been described as having

myalgias, arthralgias and pain resulting from inflammation of such

structures as the lung pleura and/or pericardium [ 7-9]. If patients

experience pain because of a flare of this systemic inflammatory

connective tissue disease the treatment would typically be medications

such as glucocorticosteroids or even immunosuppressants [ 10, 11].

However, if low Mg is causing or contributing to increased pain in SLE

patients without any concomitant increase in inflammatory activity, the

use of these medications would not be expected to ease the pain and

could perhaps be counterproductive because of side-effects. With this in

mind the Mg levels were checked in SLE patients in a general

rheumatology practice.

PATIENTS AND METHODS

Patients

During the period September 1992 to May 1995 inclusive, 25 SLE patients

were evaluated and treated in a general rheumatology practice. All the

patients fulfilled 1982 American College of Rheumatology (ACR) criteria

for SLE [ 12]. There were four males and 21 females with a mean age of

47 years (range 18-64 years). Thirteen SLE patients (one male and 12

females) fulfilled the ACR criteria for FS [ 13]. The remaining 12

patients (three males and nine females) had neither FS nor MPS.

During the study period, none of the SLE patients exhibited renal

insufficiency nor was there evidence of myositis. None of the SLE

patients had creatine phosphokinase (CPK) or aldolase levels outside of

the 'normal range'. The mean CPK level for all 25 patients was 126 U 1-1

(normal range 32-236 U 1-1). The mean aldolase level for the eight SLE

patients tested was 4.8 U 1[sup -1 (normal range 1-8 U 1-1). As a

control group, 12 patients with uncomplicated monoarticular

osteoarthritis (OA) (four hip, six knee and two shoulder) were also

studied. There were three men (ages 44, 48 and 53 years) and nine women

(mean age 50 years and range 42-64 years) in the OA group (see Table 1).

None of the OA or SLE patients was taking diuretics or uricosuric drugs.

None was bulimic, anorexic or using laxatives inappropriately. No

patient was cachetic or on a 'crash' diet at the time of the study. None

was taking vitamin supplements. All had simultaneous plasma and red

blood cell (RBC) Mg determinations.

Methods

All 25 SLE patients had venous blood drawn for both RBC and plasma Mg

levels. The samples were drawn into a heparinized tube from a peripheral

vein. They were immediately refrigerated and then transported to a

reference laboratory (National Medical Services, Willow Grove, PA, USA)

where the assays were performed. The plasma and RBC Mg levels using

washed cells were determined by using direction dilution techniques and

atomic absorption [ 14, 15] and the results here reported in mg dl-1.

RESULTS

The mean RBC Mg level for the SLE patients without FS or MPS was 4.50 mg

dl-1 with a standard deviation of 0.72 mg dl-1 whereas the mean RBC Mg

level for the SLE patients with FS was 4.63 mg dl-1 with a standard

deviation of 0.68 mg dl-1. There was no statistically significant

difference between these two groups. The mean RBC Mg level for all the

SLE patients was 4.60 mg dl-1 with a standard deviation of 0.70 mg dl-1,

which is statistically significantly different from that of the

reference controls (5.5 mg dl-1 and standard deviation 0.65 mg dl-1) and

12 osteoarthritis controls (5.30 mg dl-1 and standard deviation 0.62 mg

dl-1). A comparison of the means tests showed a z score of 4.60 and p <

0.001. The plasma Mg levels for the SLE patients were not significantly

different from the reference controls and also the osteoarthritis

controls. The mean plasma Mg level for the SLE patients was 2.00 mg

dl-1, which is not statistically significantly different from the mean

plasma Mg level for the reference controls and for the 12 osteoarthritis

controls (2.05 and 2.00 mg dl-1, respectively).

Clinical Vignette

A 35-year-old white female with a history of SLE for 9 years presented

with a 3-month history of gradually increasing myalgias. There was no

change in diet or exercise nor was she taking any new medications. Her

SLE had been well controlled on prednisone (5 mg/day) and azathioprine

(150 mg/day). She required occasional prescriptions for non-steroidal

anti-inflammatory medications such as Salsalate of up to 3 g/day for

arthralgias. On physical examination the patient had normal blood

pressure. An examination of the head, ears, eyes, nose and throat was

unrevealing. In particular, there was no alopecia, oral ulcers or malar

rash. A cardiopulmonary examination was unremarkable. An abdominal

examination was benign. A musculoskeletal examination revealed no signs

of synovitis, bony ankylosis or joint effusions. There was fairly good

range of motion of all the joints: however, there was some diffuse

tenderness on palpation of the muscles. There were only four of 18

fibromyalgia tender points noted (bilateral trapezius, right second rib

and left gluteus medius). She did not fulfil the ACR criteria [ 13] for

FS. Laboratory values revealed normal renal function and normal levels

of sodium, potassium, chloride and bicarbonate. Her erythrocyte

sedimentation rate (ESR) was normal (10 mm). Her CPK and aldolase were

also within the normal range (164 and 4.0 U 1-1, respectively). However,

her RBC Mg level was noted to be 3.8 mg dl-1 (reference mean 5.5 mg dl-1

with a range of 4.2-6.8 mg dl-1). Her plasma Mg level was 1.7 mg dl-1

(reference mean 2.05 mg dl-1 with a range of 1.6-2.5 mg dl-1). The

patient's dose of prednisone was not increased nor was there a change in

the dose or type of immunosuppressant. Rather, she was treated with six

weekly injections of magnesium sulphate (1 g intramuscularly) as had

been described previously in the treatment of CFS [ 2]. After the first

series of six injections the patient's RBC Mg level increased to 4.3 mg

dl-1, barely within the normal reference range. However, the patient's

myalgias improved significantly but did not completely subside. It was

not until a second course of six weekly injections of magnesium sulphate

(1 g intramuscularly) that the patient's myalgias almost disappeared.

Her RBC Mg level increased to 5.4 mg dl-1. The patient was treated

continuously with an oral magnesium supplement (magnesium chloride

(Slow-Mag) 64 ma, one tablet, three times a day with food). The

subsequent RBC Mg level 6 months after the initiation of the oral

magnesium supplementation was 5.2 mg dl-1. The patient remains free of

myalgias.

DISCUSSION

As in the case of other painful conditions [ 1-3], statistically

significant differences in Mg levels between SLE patients and controls

tended to be seen much more readily using RBC Mg levels as the measure

of total body Mg stores as opposed to the plasma Mg level. Most

clinicians tend to use either serum or plasma Mg levels and in doing so

may overlook Mg deficiency in some patients, a potentially reversible

problem. It can be very dangerous to treat symptoms such as myalgias in

SLE patients with an increase of corticosteroids and/or

immunosuppressants without checking the RBC Mg level first. If an SLE

patient's myalgias are due to a flare of this inflammatory connective

tissue disease, it is certainly prudent to treat with medication geared

towards controlling the inflammation. However, if the patient's myalgias

are due to Mg deficiency, treatment with an increased dose of

corticosteroids would likely be ineffective. In fact, the literature

suggests that corticosteroid treatment may even intensify the Mg

deficiency [ 16-21]. It could also cause complications such as avascular

necrosis of the bone [ 22], osteoporosis [ 23], a hastening of the

development of cataracts [ 24] and other side-effects [ 25]. The use of

immunosuppressants is also not without risk. They can cause bone marrow

suppression [ 26], liver toxicity [ 27] and other side-effects [ 28].

These potential problems may be acceptable if one is treating a flare of

SLE. However, if the myalgias are due to hypomagnesemia, an increase in

corticosteroids and/or a modification of immunosuppressants therapy

could expose the patient to needless risk.

Since the pain threshold tends to decrease as the total Mg levels

decrease [ 5], it seems only reasonable to check for hypomagnesemia in

patients with an unexplained increase in chronic pain. This includes SLE

patients whose myalgias may be due to different causes on different

occasions. Oral Mg products suitable for supplementation are available

over the counter, are relatively inexpensive and the Mg levels can be

monitored to avoid potential toxicity particularly in those SLE patients

with renal insufficiency.

It is not known why Mg levels tend to drop in patients with chronic pain

problems such as FS, MPS, EMS and SLE. It has been suggested [ 3] that

there may be a problem with Mg availability and/or utilization at the

tissue level as opposed to a suboptimal dietary intake or an increased

excretion of Mg. Whatever the mechanism, Mg deficiency should not go

unnoticed. To fail to consider Mg deficiency in the differential

diagnosis of neuromuscular problems in SLE might expose such patients to

undue risk and expense particularly if myalgias are mistakenly

attributed to inflammation.

TABLE 1. Individual RBC determination (mg dl-1)

SLE patients (n = 25) OA controls (n = 12)(a)

6.8

6.2

5.6

5.4. 5.4 5.4, 5.4

5.3 5.3©

5.2 5.2

5.1 5.1

5.0

4.9, 4.9, 4.9 4.9

4.8, 4.8 4.8

4.7, 4.7 4.7

4.6, 4.6, 4.6( 4.6

4.5

4.3

4.0

3.9

3.8

3.0

2.8

(a) Twelve osteoarthrities patients with monoarticular disease.

( Mean = 4.6 mg dl-1 and standard deviation = 0.65

mg dl-1.

Reference range mean = 5.5 mg dl-1.

REFERENCES

[1]Romano TJ, Stiller, JW. Magnesium deficiency in fibromyalgia

syndrome. J Nutr Med 1994;4: 165-7.

[2] IM, MJ, Dowson D. Red blood cell magnesium and chronic

fatigue syndrome. Lancet 1991; 337: 757-60.

[3]Romano TJ. Magnesium deficiency in patients with myofascial pain. J

Myofascial Ther 1994; 1: 11-12.

[4]Clauw DJ, Ward K, B, et al. Magnesium deficiency in the

eosinophilia-myalgia syndrome. Arthritis Rheumat 1994; 37: 1331-4.

[5]Webb WI, Gehi M. Electrolyte and fluid imbalance: neuropsychiatric

manifestations. Psychosomatics 1981; 22: 199-203.

[6]Clauw D, Ward K, Katz P, et al. Muscle intracellular magnesium levels

with pain tolerance in fibromyalgia (FM) (abstract). Arthritis Rheumat

1994; S213: 324.

[7]Matthay RA, Schwartz ML Petty TL, et al. Pulmonary manifestations of

systemic lupus erythematosus: review of 12 cases of acute lupus

pneumonitis. Medicine 1974; 54: 397-409.

[8]Haupt M, GW, Hutchins GM. The lung in systemic lupus

erythematosus: analysis of the pathogenic changes in 120 patients. Am J

Med 1981; 71: 791-9.

[9]Brigden W, Bywaters EGL, Less of MH, et al. The heart in systemic

lupus erythematosus. Br Heart J 1960; 22: 1-7.

[10] RP. Steroid use in systemic lupus erythematosus in systemic

lupus erythematosus. In: Lahita RG ed. New York: Wiley & Sons,

1987, pp. 889-922.

[11]Klippel JH. Immunosuppressive therapy in systemic lupus

erythematosus. In: Lahita RG ed. New York: Wiley & Sons, 1987, pp.

923-45.

[12]Tan EM, Cohen AS, Fries JF, et al. The 1982 revised criteria for the

classification of systemic lupus erythematosus. Arthritis Rheumat 1982;

25: 1271-7.

[13]Wolfe F, Smythe HA, Yunus MB, et al. The American College of

Rheumatology 1990 Criteria for the classification of fibromyalgia.

Report of the multicenter criteria committee. Arthritis Rheumat 1990;

33: 160-72.

[14]Tietz NW, ed. Fundamentals of clinical chemistry, 3rd edn.

Philadelphia: WB Saunders, 1987, pp. 17-18.

[15]Brown SS, FL, Young DS, eds. Chemical diagnosis of disease.

Amsterdam: Elsevier/North Holland, Biomedial Press, 1979, p. 440.

[16]Aikawa JK, Harms DR, Reardon JZ. Effect of cortisone on magnesium

metabolism in the rabbit. Am J Physiol 1960; 199: 229-30.

[17]Lutwak L, Hurt C, Reid JM. Effect of corticoids on magnesium

metabolism in man (abstract). Clin Res 1961, 9: 181.

[18]Huszak I, Heiner L. Changes of the magnesium content of the serum

following ACTH loads in patients suffering from multiple sclerosis.

Psychiat Neurol Basel 1964; 148: 245-52.

[19]Massry SG, Coburn JW. The hormonal and non-hormonal control of renal

excretion of calcium and magnesium. Nephron 1973; 10: 66-112.

[20]Gelach K, Morowitz DA, Kirsner JB. Symptomatic hypomagnesemia

complicating regional enteritis. Gastroenterology 1970; 59: 567-74.

[21]Mader IJ, Iseri LT. Spontaneous hypopotassemia, hypomagnesemia,

alkalosis and tetany due to hypersecretion of cortisone-like

mineralcorticoid. Am J Med 1955; 19: 976-88.

[22]Zizic TM, Marcoux C, Hungerford DS, et al. Corticosteroid therapy

associated with ischemic necrosis of bone in systemic lupus

erythematosus. Am J Med 1985; 79: 596-604.

[23]Lukert BP, Raisz LG. Glucocorticoid-induced osteoporosis.

Pathogenesis and management. Ann Intern Med 1990; 112: 352-64.

[24]Lubkin VL. Steroid cataract: a review and a conclusion. J Asthma Res

1977; 14: 55-9.

[25]Axelrod L. Adrenal corticosteroids. In: RR, Green DJ, eds.

Handbook of drug therapy. New York: Elsevier North-Holland, 1979, p.

809.

[26]Bacon BR, Treuhaft WH, Goodman AM. Azathioprine-induced

pancytopenia. Occurrence in two patients with connective tissue

diseases. Arch Intern Med 1981; 141: 223-6.

[27]DePinho RA, Goldberg CS, Lefkowitch JH. Azathioprine and the liver.

Evidence favoring idiosyncratic mixed cholestatic-heparo cellular injury

in humans. Gastroenterology 1984; 86: 162-5.

[28]Schein PS, Winokur SH. Immunosuppressive and cytotoxic therapy:

long-term complications. Ann Intern Med 1975; 82: 84-95.

~~~~~~~~

By THOMAS J. ROMANO MD PHD, 30 Medical Park, Wheeling, WV 26003, USA

_____

Copyright of Journal of Nutritional & Environmental Medicine is the

property of Carfax Publishing Company and its content may not be copied

or emailed to multiple sites or posted to a listserv without the

copyright holder's express written permission. However, users may print,

download, or email articles for individual use.

Source: Journal of Nutritional & Environmental Medicine, Jun97, Vol. 7

Issue 2, p107, 5p

Item: 9711141130

[This message contained attachments]

________________________________________________________________________

Message: 7

Date: Sat, 9 Nov 2002 21:35:48 -0700

From: " Heer " <idagirl@...>

Subject: Fw: Systemic lupus erythematosus and lupus-like syndromes.

5/13/95

----- Original Message -----

From: Kathynye@...

Kathynye@...

Sent: Friday, November 08, 2002 6:22 AM

Subject: POST: Systemic lupus erythematosus and lupus-like syndromes.

5/13/95

Subj: Lupus

Date: 11/8/2002 8:08:11 AM Eastern Standard Time

From: kathynye@...

Record: 14

Title: Systemic lupus erythematosus and lupus-like syndromes.

Subject(s): SYSTEMIC lupus erythematosus -- Diagnosis

Source: BMJ: British Medical Journal, 5/13/95, Vol. 310 Issue 6989,

p1257, 5p, 5c, 2bw

Author(s): Hay, Elaine M.; Snaith, L.

Abstract: Focuses on the diagnosis of systemic lupus

erythematosus. Characteristic generalized arthralgia; Mucocutaneous

manifestations; Sever fatigue; Development of diseases of major organs;

Preventing lupus flares; Symptomatic and supportive treatment; Pregnancy

with systemic lupus erythematosus.

AN: 9510221484

ISSN: 0959-8146

Full Text Word Count: 3215

Database: Academic Search Elite

Section: ABC of Rheumatology

SYSTEMIC LUPUS ERYTHEMATOSUS AND LUPUS-LIKE SYNDROMES

Contents

Clinical presentation

Arthralgia

Mucocutaneous manifestations

Fatigue

Major organ disease

Investigations

Management

Preventing lupus flares

Symptomatic and supportive treatment

Disease modifying drugs

Outcome with systemic lupus erythematosus

Pregnancy with systemic lupus erythematosus

Antiphospholipid syndrome

Subacute cutaneous lupus erythematosus

Discoid lupus erythematosus

Incipient lupus

Neonatal lupus syndrome

Drug induced lupus

Overlap syndromes

Classification criteria for systemic lupus erythematosus (revised

1982[1])

Factors that increase probability of associated connectivetissue disease

in patients with Raynaud's phenomenon

Kidney biopsy in systemic lupus erythematosus

Patient support groups

Treatments for systemic lupus erythematosus

Corticosteroid treatment for a severe lupus flare

Drugs implicated in causing lupus-like syndromes

Clinical features of overlap syndromes

Systemic lupus erythematosus is one of a family of interrelated and

overlapping autoimmune rheumatic disorders that includes rheumatoid

arthritis, scleroderma, polymyositis, dermatomyositis, and Sjogren's

syndrome. The disease can present as a wide variety of clinical

features, reflecting the many organ systems that can be affected. This

clinical diversity is matched serologically by a wide spectrum of

autoantibodies, which tend to cluster in relation to the clinical

pattern.

Systemic lupus erythematosus is rare: a general practice with 10 000

registered patients is unlikely to have more than three or four patients

with the disease at any one time. It is nine times more common in women

than in men, and nine times more common in Afro-Caribbeans and Asians

than in white patients. Thus, general practitioners' experience will

vary greatly according the ethnic mix of their registered population.

Clinical presentation

Consider systemic lupus erythematosus in a young woman presenting with

" seronegative rheumatoid arthritis "

Because lupus is so uncommon, one difficulty is considering the

possibility in the first place, particularly if the presentation is

atypical or the patient is elderly or male. Differentiating lupus from

similar disorders can be difficult, particularly early in the course of

the disease, because many of the clinical features are common

non-specific complaints. Although classification criteria for lupus are

widely accepted, they are more appropriate for classifying patients in

clinical trials or epidemiological studies than for making a diagnosis

in individual patients. Lupus should be considered when characteristic

clinical features--most commonly arthralgia, mucocutaneous

manifestations, and fatigue--occur in combination or evolve over time.

Arthralgia

Generalized arthralgia, with pronounced morning stiffness but little to

find on examination, is characteristic, and pain may be considerable.

Although symptoms may mimic early rheumatoid arthritis, joint swelling

(synovitis) is much less noticeable. About 20% of patients will develop

deformity (Jaccoud-type arthropathy) of the hands owing to tendons being

affected. This is reversible in its early stages, but it can become

permanent and joint instability may require surgery.

Mucocutaneous manifestations

A wide variety of manifestations is possible. The classic malar

" butterfly " rash is the textbook presentation; it usually presents

abruptly after exposure to sunlight and lasts for several days or weeks.

However, most facial rashes presenting in primary care are not caused by

lupus. More common causes include acne rosacea and the parvovirus

" slapped cheek " rash.

Rapid hair loss can be a useful marker of active disease and can lead to

alopecia. The hair will, however, regrow when the disease remits unless

the scalp is scarred. Ulceration of the mouth or, less commonly, the

nose or vagina may or may not be painful, but it is also usually self

limiting. Raynaud's phenomenon occurs in about half of patients at

presentation, but it is less common and usually milder than with

scleroderma or related syndromes. Conversely, most patients who present

to their general practitioner with Raynaud's syndrome will not have

systemic lupus erythematosus. If they are positive for antinuclear

antibodies they are likely to eventually develop a connective disease.

Fatigue

Severe fatigue in conjunction with some of the above symptoms may

reflect a flare up of the disease. Chronic fatigue, however, is almost

invariable in established systemic lupus erythematosus and may reflect

underlying depression or cardiovascular deconditioning.

Major organ disease

Patients greatly fear developing diseases of major organs such as the

kidneys or central nervous system. Reassuringly, these do not occur in

most patients, and when they do they are usually a relatively early

feature. Nevertheless, they are potentially life threatening and are

associated with a poorer prognosis overall.

Renal disease occurs in 20-50% of all patients at some time during their

disease, but end stage renal failure is rare (<5%). The start of disease

may be insidious, and patients should therefore have regular dipstick

testing of their urine for protein to facilitate early and aggressive

treatment.

" Cerebral lupus " is probably overdiagnosed. For example, anxiety and

depression are common but are usually caused by psychological stresses

associated with a painful, unpredictable, chronic illness rather than

reflecting cerebral lupus. Management should focus on personal social

problems such as isolation or marital stress. Headaches have a wide

variety of possible causes. " Tension headache " can be difficult to

distinguish from " lupus headache " --both may be unremitting and

unresponsive to simple analgesics. The latter is extremely uncommon,

however, and is usually associated with other features of active

disease. Migraine is more common in patients with lupus than in the

general population, particularly in patients with antiphospholipid

antibodies.

Cardiopulmonary disease--Pleurisy and pericarditis may be presenting

features, and pleuritic pain may mimic that of infection or embolism.

Although lung disease is uncommon, it is difficult to treat.

Investigations

The erythrocyte sedimentation rate should not be relied on to dictate

treatment decisions

Blood tests are useful for confirming the diagnosis of systemic lupus

erythematosus and for differentiating between various subsets of the

disease but are less useful for monitoring disease activity. The most

useful screening tests are a complete blood count, erythrocyte

sedimentation rate, and testing for antinuclear antibody.

If the test for antinuclear antibodies is negative, systemic lupus

erythematosus is extremely unlikely

There is often a normochromic normocytic anaemia when the disease is

active. Leucopenia or lymphocytopenia is common and is useful for

differentiating between systemic lupus erythematosus and rheumatoid

arthritis. Thrombocytopenia is an uncommon but well recognized

complication of lupus. Measuring C reactive protein can be a useful test

for distinguishing between a lupus flare and infection: it usually

remains normal in a flare, unless accompanied by serositis or synovitis,

but is elevated in infection. The erythrocyte sedimentation rate will be

elevated in both and occasionally remains considerably elevated when the

disease seems to be clinically quiescent.

More than 95% of patients with systemic lupus erythematosus have

antinuclear antibodies. However, such antibodies may be found in other

autoimmune disorders and (in low concentration) in chronic infection and

elderly people. Fewer than half of patients with lupus have antibodies

to double stranded DNA at presentation: thus it is not a good screening

test. However, rising tires of these antibodies, particularly if

accompanied by failing concentrations of C3 and C4, may herald the start

of renal disease. C3 and C4 are insensitive diagnostically. Antibodies

to soluble cellular antigens (such as La, Ro, U1 RNP, and Jo-1) can be

useful for distinguishing between lupus subsets.[23] Antiphospholipid

antibodies (such as anticardiolipin antibodies or lupus anticoagulant)

identify a subset of patients at particular risk of thromboembolic

complications or fetal loss.

Management

Firstly, patients need explanation and reassurance, as the liability to

episodic flare engenders insecurity and apprehension. It should be

emphasized that serious complications are rare and that most patients

have a normal life expectancy.

Preventing lupus flares

Patients should avoid exposure to sunlight (including sunbeds), which,

as well as precipitating acute or subacute skin lesions, may also cause

a generalized lupus flare. Sunscreens with a high protection factor

(factor 15 or higher) effective against ultraviolet A and B should be

applied liberally, and long sleeved clothes and sun hats should be worn

in sunny weather. Topical corticosteroid preparations are sometimes

helpful for chronic skin lesions but should be used sparingly to avoid

thinning of the skin.

Oral contraceptive pills containing low doses of oestrogen are probably

safe with mild lupus but should be used with caution by patients with

severe lupus since they can theoretically cause a flare. They are

contraindicated in patients with migraine, hypertension, a history of

thrombosis, or high tires of anticardiolipin antibodies.

Progestogen-only oral contraceptives are safe. Intrauterine devices

should be avoided if possible because of an increased risk of infection.

The evidence for use of hormone replacement therapy is not yet clear

enough to be able to give general advice: probably the best policy is

cautious introduction of low dose oestrogen when the disease is

quiescent with closer than usual monitoring.

Differentiating between a lupus flare and infection can be difficult.

Infection is an important cause of mortality in patients with systemic

lupus erythematosus, particularly in those taking corticosteroids or

immunosuppressive drugs. Furthermore, intercurrent infection can

precipitate a lupus flare. Hence it is important to maintain a high

index of suspicion and regard any flu-like or feverish episode lasting

more than a day or two as infection unless proved otherwise.

Sulphonamides should usually be avoided because they may cause rash or

sudden profound neutropenia.

Symptomatic and supportive treatment

Most common symptoms of systemic lupus erythematosus can be safely

treated symptomatically. Arthralgia, headaches, and non-specific chest

pains may be helped by non-steroidal anti-inflammatory drugs or simple

analgesics. Blood pressure should be checked regularly and hypertension

treated intensively, particularly if there is renal disease.

Disease modifying drugs

Corticosteroids have transformed the outlook for patients with lupus but

at a considerable price: much of the increased mortality late in the

course of the disease (due to infection, cardiovascular disease, or

fracture complications) may be attributable to these drugs. Once an

acute episode is under control the dose of corticosteroid should be

slowly reduced; complete withdrawal is optimal, but many patients are

best managed with a small maintenance dose of perhaps 5 mg or less a

day. The dose of prednisolone should not be increased for non-specific

constitutional symptoms in the absence of corroborative physical signs

or abnormal laboratory results, even though this may make the patient

feel better. Few lupus complications require immediate corticosteroid

treatment--it is often best to wait and see for a day or two to avoid

frequent increases in dose for non-specific symptoms. Arthralgia in

systemic lupus erythematosus responds poorly to low dose prednisolone

and usually does not warrant a high dose.

Antimalarial drugs--Chloroquine phosphate (250 mg daily or alternate

days) or hydroxychloroquine (200-400mg daily) is the mainstay of

treatment for skin or joint disorders. At these doses ocular

complications are extremely rare, but it is prudent to use the lowest

effective dose. Rheumatologists and ophthalmologists continue to

disagree about the need for routine screening. Hydroxychloroquine is

safer, though more expensive, than chloroquine. The total dose of

chloroquine should not exceed 300 g, but it is not clear whether there

should be such a limit for hydroxychloroquine.

Immunosuppressive drugs--Azathioprine, methotrexate, and

cyclophosphamide are generally reserved for life threatening diseases of

major organs such as the kidneys. They should be instituted and

monitored at specialist centers, with appropriate counselling given

about the short and long term side effects. Cyclophosphamide, whether

continuous oral, pulse, or intravenous, is of proved benefit in treating

renal lupus but is often associated with side effects that can be severe

(such as infertility, premature menopause, or bladder cancer). Gamete

storage should be offered before start of treatment when possible. Mesna

should be used to reduce the risk of bladder toxicity with intravenous

treatment, but oral mesna is not feasible for patients receiving

continuous oral treatment. All these immunosuppressive drugs have the

potential to suppress bone marrow activity, and frequent checks of

complete blood count and differential white cell count are mandatory.

Outcome with systemic lupus erythematosus

Early studies reported that fewer than half of patients survived five

years after diagnosis, but this figure has steadily improved. Recent

studies report five year survival rates of 86-88% and 10 year survival

rates of 76-87%. Patients who are non-white, male, or at the extremes of

the age range fare worst. Most patients with lupus die from causes

unrelated to the disease, but deaths (such as those due to infection or

ischaemic heart disease) are increasingly related to treatment. Renal

replacement therapy ensures that death from renal failure is uncommon.

Pregnancy with systemic lupus erythematosus

There is no evidence for reduced fertility in patients with systemic

lupus erythematosus, and pregnancy presents little hazard for the mother

if the lupus is mild or stable. Pre-existing renal disease may, however,

worsen during pregnancy, and complications such as hypertension may be

more difficult to control. Pre-eclamptic toxaemia may be difficult to

distinguish from renal flare.

There is an increased rate of fetal loss, particularly during the second

trimester, in patients with high titres of antiphospholipid antibodies.

Pregnancies in such women should be monitored carefully in specialist

units. Overall, there is no increased risk of fetal abnormalities, but

drug treatment during pregnancy may pose problems. Antimetabolites are

contraindicated because of teratogenesis, but low dose prednisolone,

chloroquine, and azathioprine are probably safe.

Antiphospholipid syndrome

This may occur in patients with coexisting systemic lupus erythematosus

or occur alone (primary antiphospholipid syndrome). It is characterized

by thrombosis, livedo reticularis, and sometimes thrombocytopenia

together with the lupus anticoagulant or antiphospholipid antibodies.

Subacute cutaneous lupus erythematosus

Intense photosensitivity and antibodies to La and Ro are the essential

features of this relatively rare syndrome.

Discoid lupus erythematosus

In this condition lesions are obviously discoid, systemic features are

rare and mild, and autoantibodies are low in titre.

Incipient lupus

Some patients do not progress to very active disease, and their

condition is characterized by mild arthralgia, rashes, or serositis with

weak positivity for antinuclear antibodies.

Neonatal lupus syndrome

A small proportion of babies born to mothers with systemic lupus

erythematosus (which is often mild and may even have been unrecognized)

develop the neonatal lupus syndrome. This syndrome appears to be

restricted to babies whose mothers have antibodies to Ro (SS-A) or La

(SS- antigens. A self limiting skin rash, which may be severe, is the

most common presentation. Rarely, babies may have permanent heart block

secondary to a conduction defect, which may require treatment with a

cardiac pacemaker.

Drug induced lupus

Lupus-like syndromes may occasionally be induced by some drugs. They

mostly consist of arthralgia with positivity for antinuclear antibodies,

and renal disease is rare. Antibodies to DNA are rare, but antihistone

antibodies are characteristic. The syndrome usually resolves when the

offending drug is withdrawn, but antinuclear antibodies persist for

months after.

Overlap syndromes

It has been suggested that the only true lupus syndrome consists of

nephritis, photosensitivity, serositis, and antibodies to DNA. While

this might be too purist a view, it is often difficult to categorise

patients; criteria such as those for systemic lupus erythematosus[1] or

those suggested for mixed connective tissue disease[4] do not cover all

situations. Convention, however, prefers some form of categorization,

and the syndromes usually termed overlap (though some prefer the term

undifferentiated connective tissue disease) tend to have certain

characteristic features. Patients also prefer their doctor to be able

attach a label to their condition that is acceptable to others and

carries some certainty with regard to prognosis and management.

Prognosis is on a case by case basis, depending on the rate of

progression and severity and nature of involvement of organ systems.

Management is similar in principle to that for systemic lupus

erythematosus: the pattern of involvement dictating the treatment. It is

clear that mixed connective tissue disease, for example, is not a robust

syndrome; clinical expression tends to focus on a scleroderma-like,

rheumatoid-like, or myositis-like syndrome, often with cardiopulmonary

features dictating the outcome.

PHOTO (COLOR): Jaccoud-type arthropathy; non-erosive deformity of

fingers owing to tendons being affected.

PHOTO (COLOR): Classic malar " butterfly " rash of systemic lupus

erythematosus after exposure to sunlight (reproduced with patient's

permission).

PHOTO (COLOR): Parvovirus " slapped cheek " rash.

PHOTO (BLACK & WHITE): Radiograph showing changes of restrictive lung

disease in patient with lupus-- " shrinking lung " appearance and linear

shadows. Pulmonary function tests may eventually stabilize, but

pulmonary hypertension occasionally develops.

PHOTO (BLACK & WHITE): Magnetic resonance image showing avascular

necrosis of hips. Avascular necrosis may affect any joint, and treatment

with high dose corticosteroid is a particular risk factor.

PHOTO (BLACK & WHITE): Severe lupus glomerulonephritis: appearance

confirms end stage renal failure with glomerular loss. Continued

treatment with immunosuppressive drugs and high dose corticosteroids is

unlikely to achieve any improvement in function and would probably

result only in further toxicity. (With less histological change, further

immunosuppression might be justified to delay need for dialysis).

Classification criteria for systemic lupus erythematosus (revised

1982[1])

To be classified as having systemic lupus erythematosus, patients must

have at least four of the following criteria in the course of their

disease:

* Malar rash * Discold rash

* Photosensitivity * Oral ulcers

* Arthritis * Serositis

* Renaldisorder * Neurological

disorder

* Haematological * Immunological

disorder disorder

* Presence of anti-nuclear antibodies

Factors that increase probability of associated connectivetissue disease

in patients with Raynaud's phenomenon

* Onset of condition in childhood or old age

* Asymmetrical manifestation of symptoms

* Severe disease threatening viabllity of peripheries

* Associated with other symptoms such as arthralgia, fatigue,

rash, etc

* Associated with abnormal results of blood tests (such as raised

erythrocyte sedimentation rate, anaemia, presence of antinuclear

antibodies)

Kidney biopsy in systemic lupus erythematosus

* May not be crucial for diagnosis of lupus glomerulonephritis if

confirmatory features are present--known active systemic lupus

erythematosus, urinary sediment with protein, casts, haematuria, and

negative urine cultures

* Important as a guide to management when there is doubt as to the

reversibility of renal damage

Patient support groups

* Support groups for patients with lupus can be most helpful [or

providing reassurance and reducing a patient's sense of isolation

* Further details can be obtained from: Lupus UK 51 North Street,

Romford, Essex RM1 1BA Telephone (01708) 731251

The clinical diversity of systemic lupus erythematosus makes it one of

the most difficult autoimmune rheumatic disorders to manage. General

practitioners play a vital role in supporting patients with lupus and

coordinating treatment, which can easily become fragmented among various

hospital specialists. Close liaison between specialists and general

practitioners is crucial for optimal patient care

Treatments for systemic lupus erythematosus

Non-steroidal anti-inflammatory drugs For symptomatic relief

Antimalarial drugs (chloroquine, hydroxychloroquine) For rashes,

arthritis, and malaise

Corticosteroids For severe flare For maintenance treatment (in low

doses)

Immunosuppressive drugs (azathioprine, methotrexate, cyclophosphamide,

etc) For severe flare (in conjunction with corticosteroids)

Additional treatments

For hypertension

For infection

For cerebral lupus (such as anticonvulsants)

For thrombosis

For haematological disorders (such as splenectomy)

Corticosteroid treatment for a severe lupus flare

Continuous oral treatment Starting dose of prednisolone is usually

0-75-1 mg/kg Treatment continued at same dose for 4-10 weeks depending

on clinical response Careful reduction can then be attempted

Intravenous pulses Methylprednisolone 0-5-1-5 g repeated 1-3 times

Suppresses symptoms and may modify outcome, but avascular necrosis

remains a risk

Intramuscular or oral mini pulses Such as 100-125 mg prednisolone

acetate intramuscularly Safer and cheaper than and probably as effective

as other methods for symptomatic relief

Drugs implicated in causing lupus-like syndromes

Common

* Hydralazine

* Procainamide

* Anticonvulsants (phenytoin, hydantoins, primidone)

* Isoniazid Rare

Rare

* Chlorpromazine

* Penicillamine

* actolol

* Antithyroid drugs (propylthiouracil, methylthiouracil)

* Methyldopa

Clinical features of overlap syndromes

* Raynaud's phenomenon

* " Sausage " digits

* Periungual vascular distortion

* Hyperglobulinaemia and presence of antibodies to several soluble

nuclear and cytoplasmic antigens

* Relative lack of cerebrosis, antibodies to DNA, and immune

complex glomerulonephritis

* Eventual outcome of cardiopulmonary disease

PHOTO (COLOR): Livedo reticularis in patient with antiphospholipid

syndrome.

PHOTO (COLOR): Sausage fingers of patient with mixed connective tissue

disease.

1. Tan EM, Cohen ES, Fries JF, Masi AT, McShane DJ, Rothfield NF,

et al. The 1982 revised criteria for the classification of systemic

lupus erythematosus. Arthritis Rheum 1982;25:1271-7.

2. Maddison PJ. Autoantibody profile. Oxford textbook of

rheumatology. Vol 1. Oxford: Oxford University Press, 1993:389-96.

3. Isenberg DA, Horsfall AC. Systemic lupus erythematosus. Oxford

textbook of rheumatology. Vol 2. Oxford: Oxford University Press,

1993:733-55.

4. Alarcon-Segovia D, Cardiel MH. Comparison between 3 diagnostic

criteria for mixed connective tissue disease: a study of 593 patients. y

Rheumatol 1989;16:328-34.

~~~~~~~~

By Elaine M Hay, L Snaith

The ABC of Rheumatology is edited by L Snaith.

Elaine M Hay is senior lecturer in community rheumatology at the

Staffordshire Rheumatology Centre, Stoke on Trent, and L Snaith

is senior lecturer in rheumatology at the Institute for Bone and Joint

Medicine, University of Sheffield Medical School.

_____

Copyright of British Medical Journal is the property of BMJ Publishing

Group and its content may not be copied or emailed to multiple sites or

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individual use.

Source: British Medical Journal, 5/13/95, Vol. 310 Issue 6989, p1257, 5p

Item: 9510221484

November 11, 2002

Hey J how are you girl? It is nice to have someone appreciate what I do once

in awhile !

Let us know how you are please!

----- Original Message -----

From: " JHH7 " <rogerlh@...>

< >

Sent: Sunday, November 10, 2002 2:32 PM

Subject: Re: Digest Number 1059

> Hi ,

>

> Thank you so much for posting these articles on Lupus!!! They are so

> helpful!!! The article Message: 7 was one of the best articles I have

read,

> as it was so clear and articulate.

>

> Thank you again for all you do!!

>

> --------------------------------------------------------------------------

--

> ------

> 6. Fw: Magnesium deficiency in systematic lupus erythematosus.

> From: " Heer " <idagirl@...>

> 7. Fw: Systemic lupus erythematosus and lupus-like syndromes.

> 5/13/95

> From: " Heer " <idagirl@...>

>

> Subj: MG levels

> Date: 11/8/2002 8:05:25 AM Eastern Standard Time

> From, kathynye@...

> Title: Magnesium deficiency in systematic lupus erythematosus.

>

> Subject(s): MAGNESIUM deficiency diseases; SYSTEMIC lupus

> erythematosus -- Diagnosis

> Source: Journal of Nutritional & Environmental Medicine, Jun97, Vol. 7

> Issue 2, p107, 5p, 1 chart

> Author(s): Romano, J.

> Abstract: Discusses the effects of reduced erythrocyte magnesium

> (Mg) deficiency in patients with systematic lupus erythematosus (SLE).

> Common symptom of the disorder; How to determine if SLE patients are

> also prone to hypomagnesemia; Results of the study.

> AN: 9711141130

> ISSN: 1359-0847

> Full Text Word Count: 2470

> Database: Academic Search Elite

> Section: ORIGINAL RESEARCH

> MAGNESIUM DEFICIENCY IN SYSTEMIC LUPUS ERYTHEMATOSUS

>

> Reduced erythrocyte magnesium (Mg) levels have been reported in

> fibromyalgia syndrome (FS), chronic fatigue syndrome (CFS), myofascial

> pain syndrome (MPS) and eosinophilia myalgia syndrome (EMS). These

> disorders have chronic pain as a common symptom. Chronic pain also

> affects some patients with systemic lupus erythematosus (SLE). To

> determine if SLE patients are also prone to hypomagnesemia, red blood

> cell (RBC) and plasma Mg levels were measured in all SLE patients seen

> in a general rheumatology practice in a 3-year period. There were 25

> such patients with a mean age of 47 years. Thirteen SLE patients had FS

> and 12 did not have either FS or MPS. The mean RBC Mg level for the SLE

> patients was 4.60 mg dl-1, statistically significantly lower than that

> of the reference controls and 12 osteoarthritis controls. It did not

> matter whether the SLE patients had ES or MPS. This finding has

> implications for diagnosis and treatment.

>

> Keywords: magnesium, myalgias, lupus, pain.

>

> INTRODUCTION

>

> Reduced erythrocyte magnesium (Mg) levels have been reported in

> fibromyalgia syndrome (FS) [ 1], chronic fatigue syndrome (CFS) [ 2],

> myofascial pain syndrome (MPS) [ 3] and eosinophilia myalgia syndrome

> (EMS) [ 4]. These four disorders have chronic pain and/or fatigue as a

> common denominator. Furthermore, it has been proposed that low Mg levels

> predispose patients to myalgias [ 5] and that low muscle Mg levels

> correspond to a low pain threshold [ 6]. Systemic lupus erythematosus

> (SLE) is also a condition that can be characterized by chronic pain in

> some patients. Lupus patients have often been described as having

>

> myalgias, arthralgias and pain resulting from inflammation of such

> structures as the lung pleura and/or pericardium [ 7-9]. If patients

> experience pain because of a flare of this systemic inflammatory

> connective tissue disease the treatment would typically be medications

> such as glucocorticosteroids or even immunosuppressants [ 10, 11].

> However, if low Mg is causing or contributing to increased pain in SLE

> patients without any concomitant increase in inflammatory activity, the

> use of these medications would not be expected to ease the pain and

> could perhaps be counterproductive because of side-effects. With this in

> mind the Mg levels were checked in SLE patients in a general

> rheumatology practice.

>

> PATIENTS AND METHODS

>

> Patients

>

> During the period September 1992 to May 1995 inclusive, 25 SLE patients

> were evaluated and treated in a general rheumatology practice. All the

> patients fulfilled 1982 American College of Rheumatology (ACR) criteria

> for SLE [ 12]. There were four males and 21 females with a mean age of

> 47 years (range 18-64 years). Thirteen SLE patients (one male and 12

> females) fulfilled the ACR criteria for FS [ 13]. The remaining 12

> patients (three males and nine females) had neither FS nor MPS.

>

> During the study period, none of the SLE patients exhibited renal

> insufficiency nor was there evidence of myositis. None of the SLE

> patients had creatine phosphokinase (CPK) or aldolase levels outside of

> the 'normal range'. The mean CPK level for all 25 patients was 126 U 1-1

> (normal range 32-236 U 1-1). The mean aldolase level for the eight SLE

> patients tested was 4.8 U 1[sup -1 (normal range 1-8 U 1-1). As a

> control group, 12 patients with uncomplicated monoarticular

> osteoarthritis (OA) (four hip, six knee and two shoulder) were also

> studied. There were three men (ages 44, 48 and 53 years) and nine women

> (mean age 50 years and range 42-64 years) in the OA group (see Table 1).

> None of the OA or SLE patients was taking diuretics or uricosuric drugs.

> None was bulimic, anorexic or using laxatives inappropriately. No

> patient was cachetic or on a 'crash' diet at the time of the study. None

> was taking vitamin supplements. All had simultaneous plasma and red

> blood cell (RBC) Mg determinations.

>

> Methods

>

> All 25 SLE patients had venous blood drawn for both RBC and plasma Mg

> levels. The samples were drawn into a heparinized tube from a peripheral

> vein. They were immediately refrigerated and then transported to a

> reference laboratory (National Medical Services, Willow Grove, PA, USA)

> where the assays were performed. The plasma and RBC Mg levels using

> washed cells were determined by using direction dilution techniques and

> atomic absorption [ 14, 15] and the results here reported in mg dl-1.

>

> RESULTS

>

> The mean RBC Mg level for the SLE patients without FS or MPS was 4.50 mg

> dl-1 with a standard deviation of 0.72 mg dl-1 whereas the mean RBC Mg

> level for the SLE patients with FS was 4.63 mg dl-1 with a standard

> deviation of 0.68 mg dl-1. There was no statistically significant

> difference between these two groups. The mean RBC Mg level for all the

> SLE patients was 4.60 mg dl-1 with a standard deviation of 0.70 mg dl-1,

> which is statistically significantly different from that of the

> reference controls (5.5 mg dl-1 and standard deviation 0.65 mg dl-1) and

> 12 osteoarthritis controls (5.30 mg dl-1 and standard deviation 0.62 mg

> dl-1). A comparison of the means tests showed a z score of 4.60 and p <

> 0.001. The plasma Mg levels for the SLE patients were not significantly

> different from the reference controls and also the osteoarthritis

> controls. The mean plasma Mg level for the SLE patients was 2.00 mg

> dl-1, which is not statistically significantly different from the mean

> plasma Mg level for the reference controls and for the 12 osteoarthritis

> controls (2.05 and 2.00 mg dl-1, respectively).

>

> Clinical Vignette

>

> A 35-year-old white female with a history of SLE for 9 years presented

> with a 3-month history of gradually increasing myalgias. There was no

> change in diet or exercise nor was she taking any new medications. Her

> SLE had been well controlled on prednisone (5 mg/day) and azathioprine

> (150 mg/day). She required occasional prescriptions for non-steroidal

> anti-inflammatory medications such as Salsalate of up to 3 g/day for

> arthralgias. On physical examination the patient had normal blood

> pressure. An examination of the head, ears, eyes, nose and throat was

> unrevealing. In particular, there was no alopecia, oral ulcers or malar

> rash. A cardiopulmonary examination was unremarkable. An abdominal

> examination was benign. A musculoskeletal examination revealed no signs

> of synovitis, bony ankylosis or joint effusions. There was fairly good

> range of motion of all the joints: however, there was some diffuse

> tenderness on palpation of the muscles. There were only four of 18

> fibromyalgia tender points noted (bilateral trapezius, right second rib

> and left gluteus medius). She did not fulfil the ACR criteria [ 13] for

> FS. Laboratory values revealed normal renal function and normal levels

> of sodium, potassium, chloride and bicarbonate. Her erythrocyte

> sedimentation rate (ESR) was normal (10 mm). Her CPK and aldolase were

> also within the normal range (164 and 4.0 U 1-1, respectively). However,

> her RBC Mg level was noted to be 3.8 mg dl-1 (reference mean 5.5 mg dl-1

> with a range of 4.2-6.8 mg dl-1). Her plasma Mg level was 1.7 mg dl-1

> (reference mean 2.05 mg dl-1 with a range of 1.6-2.5 mg dl-1). The

> patient's dose of prednisone was not increased nor was there a change in

> the dose or type of immunosuppressant. Rather, she was treated with six

> weekly injections of magnesium sulphate (1 g intramuscularly) as had

> been described previously in the treatment of CFS [ 2]. After the first

> series of six injections the patient's RBC Mg level increased to 4.3 mg

> dl-1, barely within the normal reference range. However, the patient's

> myalgias improved significantly but did not completely subside. It was

> not until a second course of six weekly injections of magnesium sulphate

> (1 g intramuscularly) that the patient's myalgias almost disappeared.

> Her RBC Mg level increased to 5.4 mg dl-1. The patient was treated

> continuously with an oral magnesium supplement (magnesium chloride

> (Slow-Mag) 64 ma, one tablet, three times a day with food). The

> subsequent RBC Mg level 6 months after the initiation of the oral

> magnesium supplementation was 5.2 mg dl-1. The patient remains free of

> myalgias.

>

> DISCUSSION

>

> As in the case of other painful conditions [ 1-3], statistically

> significant differences in Mg levels between SLE patients and controls

> tended to be seen much more readily using RBC Mg levels as the measure

> of total body Mg stores as opposed to the plasma Mg level. Most

> clinicians tend to use either serum or plasma Mg levels and in doing so

> may overlook Mg deficiency in some patients, a potentially reversible

> problem. It can be very dangerous to treat symptoms such as myalgias in

> SLE patients with an increase of corticosteroids and/or

> immunosuppressants without checking the RBC Mg level first. If an SLE

> patient's myalgias are due to a flare of this inflammatory connective

> tissue disease, it is certainly prudent to treat with medication geared

> towards controlling the inflammation. However, if the patient's myalgias

> are due to Mg deficiency, treatment with an increased dose of

> corticosteroids would likely be ineffective. In fact, the literature

> suggests that corticosteroid treatment may even intensify the Mg

> deficiency [ 16-21]. It could also cause complications such as avascular

> necrosis of the bone [ 22], osteoporosis [ 23], a hastening of the

> development of cataracts [ 24] and other side-effects [ 25]. The use of

> immunosuppressants is also not without risk. They can cause bone marrow

> suppression [ 26], liver toxicity [ 27] and other side-effects [ 28].

> These potential problems may be acceptable if one is treating a flare of

> SLE. However, if the myalgias are due to hypomagnesemia, an increase in

> corticosteroids and/or a modification of immunosuppressants therapy

> could expose the patient to needless risk.

>

> Since the pain threshold tends to decrease as the total Mg levels

> decrease [ 5], it seems only reasonable to check for hypomagnesemia in

> patients with an unexplained increase in chronic pain. This includes SLE

> patients whose myalgias may be due to different causes on different

> occasions. Oral Mg products suitable for supplementation are available

> over the counter, are relatively inexpensive and the Mg levels can be

> monitored to avoid potential toxicity particularly in those SLE patients

> with renal insufficiency.

>

> It is not known why Mg levels tend to drop in patients with chronic pain

> problems such as FS, MPS, EMS and SLE. It has been suggested [ 3] that

> there may be a problem with Mg availability and/or utilization at the

> tissue level as opposed to a suboptimal dietary intake or an increased

> excretion of Mg. Whatever the mechanism, Mg deficiency should not go

> unnoticed. To fail to consider Mg deficiency in the differential

> diagnosis of neuromuscular problems in SLE might expose such patients to

> undue risk and expense particularly if myalgias are mistakenly

> attributed to inflammation.

>

> TABLE 1. Individual RBC determination (mg dl-1)

>

> SLE patients (n = 25) OA controls (n = 12)(a)

>

> 6.8

> 6.2

> 5.6

> 5.4. 5.4 5.4, 5.4

> 5.3 5.3©

> 5.2 5.2

> 5.1 5.1

> 5.0

> 4.9, 4.9, 4.9 4.9

> 4.8, 4.8 4.8

> 4.7, 4.7 4.7

> 4.6, 4.6, 4.6( 4.6

> 4.5

> 4.3

> 4.0

> 3.9

> 3.8

> 3.0

> 2.8

>

> (a) Twelve osteoarthrities patients with monoarticular disease.

>

> ( Mean = 4.6 mg dl-1 and standard deviation = 0.65

> mg dl-1.

>

> © Mean = 5.3 mg dl-1 and standard deviation = 0.62

> mg dl-1.

>

> Reference range mean = 5.5 mg dl-1.

>

> REFERENCES

>

> [1]Romano TJ, Stiller, JW. Magnesium deficiency in fibromyalgia

> syndrome. J Nutr Med 1994;4: 165-7.

>

> [2] IM, MJ, Dowson D. Red blood cell magnesium and chronic

> fatigue syndrome. Lancet 1991; 337: 757-60.

>

> [3]Romano TJ. Magnesium deficiency in patients with myofascial pain. J

> Myofascial Ther 1994; 1: 11-12.

>

> [4]Clauw DJ, Ward K, B, et al. Magnesium deficiency in the

> eosinophilia-myalgia syndrome. Arthritis Rheumat 1994; 37: 1331-4.

>

> [5]Webb WI, Gehi M. Electrolyte and fluid imbalance: neuropsychiatric

> manifestations. Psychosomatics 1981; 22: 199-203.

>

> [6]Clauw D, Ward K, Katz P, et al. Muscle intracellular magnesium levels

> with pain tolerance in fibromyalgia (FM) (abstract). Arthritis Rheumat

> 1994; S213: 324.

>

> [7]Matthay RA, Schwartz ML Petty TL, et al. Pulmonary manifestations of

> systemic lupus erythematosus: review of 12 cases of acute lupus

> pneumonitis. Medicine 1974; 54: 397-409.

>

> [8]Haupt M, GW, Hutchins GM. The lung in systemic lupus

> erythematosus: analysis of the pathogenic changes in 120 patients. Am J

> Med 1981; 71: 791-9.

>

> [9]Brigden W, Bywaters EGL, Less of MH, et al. The heart in systemic

> lupus erythematosus. Br Heart J 1960; 22: 1-7.

>

> [10] RP. Steroid use in systemic lupus erythematosus in systemic

> lupus erythematosus. In: Lahita RG ed. New York: Wiley & Sons,

> 1987, pp. 889-922.

>

> [11]Klippel JH. Immunosuppressive therapy in systemic lupus

> erythematosus. In: Lahita RG ed. New York: Wiley & Sons, 1987, pp.

> 923-45.

>

> [12]Tan EM, Cohen AS, Fries JF, et al. The 1982 revised criteria for the

> classification of systemic lupus erythematosus. Arthritis Rheumat 1982;

> 25: 1271-7.

>

> [13]Wolfe F, Smythe HA, Yunus MB, et al. The American College of

> Rheumatology 1990 Criteria for the classification of fibromyalgia.

> Report of the multicenter criteria committee. Arthritis Rheumat 1990;

> 33: 160-72.

>

> [14]Tietz NW, ed. Fundamentals of clinical chemistry, 3rd edn.

> Philadelphia: WB Saunders, 1987, pp. 17-18.

>

> [15]Brown SS, FL, Young DS, eds. Chemical diagnosis of disease.

> Amsterdam: Elsevier/North Holland, Biomedial Press, 1979, p. 440.

>

> [16]Aikawa JK, Harms DR, Reardon JZ. Effect of cortisone on magnesium

> metabolism in the rabbit. Am J Physiol 1960; 199: 229-30.

>

> [17]Lutwak L, Hurt C, Reid JM. Effect of corticoids on magnesium

> metabolism in man (abstract). Clin Res 1961, 9: 181.

>

> [18]Huszak I, Heiner L. Changes of the magnesium content of the serum

> following ACTH loads in patients suffering from multiple sclerosis.

> Psychiat Neurol Basel 1964; 148: 245-52.

>

> [19]Massry SG, Coburn JW. The hormonal and non-hormonal control of renal

> excretion of calcium and magnesium. Nephron 1973; 10: 66-112.

>

> [20]Gelach K, Morowitz DA, Kirsner JB. Symptomatic hypomagnesemia

> complicating regional enteritis. Gastroenterology 1970; 59: 567-74.

>

> [21]Mader IJ, Iseri LT. Spontaneous hypopotassemia, hypomagnesemia,

> alkalosis and tetany due to hypersecretion of cortisone-like

> mineralcorticoid. Am J Med 1955; 19: 976-88.

>

> [22]Zizic TM, Marcoux C, Hungerford DS, et al. Corticosteroid therapy

> associated with ischemic necrosis of bone in systemic lupus

> erythematosus. Am J Med 1985; 79: 596-604.

>

> [23]Lukert BP, Raisz LG. Glucocorticoid-induced osteoporosis.

> Pathogenesis and management. Ann Intern Med 1990; 112: 352-64.

>

> [24]Lubkin VL. Steroid cataract: a review and a conclusion. J Asthma Res

> 1977; 14: 55-9.

>

> [25]Axelrod L. Adrenal corticosteroids. In: RR, Green DJ, eds.

> Handbook of drug therapy. New York: Elsevier North-Holland, 1979, p.

> 809.

>

> [26]Bacon BR, Treuhaft WH, Goodman AM. Azathioprine-induced

> pancytopenia. Occurrence in two patients with connective tissue

> diseases. Arch Intern Med 1981; 141: 223-6.

>

> [27]DePinho RA, Goldberg CS, Lefkowitch JH. Azathioprine and the liver.

> Evidence favoring idiosyncratic mixed cholestatic-heparo cellular injury

> in humans. Gastroenterology 1984; 86: 162-5.

>

> [28]Schein PS, Winokur SH. Immunosuppressive and cytotoxic therapy:

> long-term complications. Ann Intern Med 1975; 82: 84-95.

>

> ~~~~~~~~

>

> By THOMAS J. ROMANO MD PHD, 30 Medical Park, Wheeling, WV 26003, USA

>

> _____

>

> Copyright of Journal of Nutritional & Environmental Medicine is the

> property of Carfax Publishing Company and its content may not be copied

> or emailed to multiple sites or posted to a listserv without the

> copyright holder's express written permission. However, users may print,

> download, or email articles for individual use.

> Source: Journal of Nutritional & Environmental Medicine, Jun97, Vol. 7

> Issue 2, p107, 5p

> Item: 9711141130

>

> [This message contained attachments]

>

> ________________________________________________________________________

>

> Message: 7

> Date: Sat, 9 Nov 2002 21:35:48 -0700

> From: " Heer " <idagirl@...>

> Subject: Fw: Systemic lupus erythematosus and lupus-like syndromes.

> 5/13/95

>

> ----- Original Message -----

> From: Kathynye@...

> Kathynye@...

> Sent: Friday, November 08, 2002 6:22 AM

> Subject: POST: Systemic lupus erythematosus and lupus-like syndromes.

> 5/13/95

>

> Subj: Lupus

> Date: 11/8/2002 8:08:11 AM Eastern Standard Time

> From: kathynye@...

>

> Record: 14

> Title: Systemic lupus erythematosus and lupus-like syndromes.

> Subject(s): SYSTEMIC lupus erythematosus -- Diagnosis

> Source: BMJ: British Medical Journal, 5/13/95, Vol. 310 Issue 6989,

> p1257, 5p, 5c, 2bw

> Author(s): Hay, Elaine M.; Snaith, L.

> Abstract: Focuses on the diagnosis of systemic lupus

> erythematosus. Characteristic generalized arthralgia; Mucocutaneous

> manifestations; Sever fatigue; Development of diseases of major organs;

> Preventing lupus flares; Symptomatic and supportive treatment; Pregnancy

> with systemic lupus erythematosus.

> AN: 9510221484

> ISSN: 0959-8146

> Full Text Word Count: 3215

> Database: Academic Search Elite

> Section: ABC of Rheumatology

> SYSTEMIC LUPUS ERYTHEMATOSUS AND LUPUS-LIKE SYNDROMES

> Contents

> Clinical presentation

> Arthralgia

> Mucocutaneous manifestations

> Fatigue

> Major organ disease

> Investigations

> Management

> Preventing lupus flares

> Symptomatic and supportive treatment

> Disease modifying drugs

> Outcome with systemic lupus erythematosus

> Pregnancy with systemic lupus erythematosus

> Antiphospholipid syndrome

> Subacute cutaneous lupus erythematosus

> Discoid lupus erythematosus

> Incipient lupus

> Neonatal lupus syndrome

> Drug induced lupus

> Overlap syndromes

> Classification criteria for systemic lupus erythematosus (revised

> 1982[1])

> Factors that increase probability of associated connectivetissue disease

> in patients with Raynaud's phenomenon

> Kidney biopsy in systemic lupus erythematosus

> Patient support groups

> Treatments for systemic lupus erythematosus

> Corticosteroid treatment for a severe lupus flare

> Drugs implicated in causing lupus-like syndromes

> Clinical features of overlap syndromes

>

> Systemic lupus erythematosus is one of a family of interrelated and

> overlapping autoimmune rheumatic disorders that includes rheumatoid

> arthritis, scleroderma, polymyositis, dermatomyositis, and Sjogren's

> syndrome. The disease can present as a wide variety of clinical

> features, reflecting the many organ systems that can be affected. This

> clinical diversity is matched serologically by a wide spectrum of

> autoantibodies, which tend to cluster in relation to the clinical

> pattern.

>

> Systemic lupus erythematosus is rare: a general practice with 10 000

> registered patients is unlikely to have more than three or four patients

> with the disease at any one time. It is nine times more common in women

> than in men, and nine times more common in Afro-Caribbeans and Asians

> than in white patients. Thus, general practitioners' experience will

> vary greatly according the ethnic mix of their registered population.

>

> Clinical presentation

>

> Consider systemic lupus erythematosus in a young woman presenting with

> " seronegative rheumatoid arthritis "

>

> Because lupus is so uncommon, one difficulty is considering the

> possibility in the first place, particularly if the presentation is

> atypical or the patient is elderly or male. Differentiating lupus from

> similar disorders can be difficult, particularly early in the course of

> the disease, because many of the clinical features are common

> non-specific complaints. Although classification criteria for lupus are

> widely accepted, they are more appropriate for classifying patients in

> clinical trials or epidemiological studies than for making a diagnosis

> in individual patients. Lupus should be considered when characteristic

> clinical features--most commonly arthralgia, mucocutaneous

> manifestations, and fatigue--occur in combination or evolve over time.

>

> Arthralgia

>

> Generalized arthralgia, with pronounced morning stiffness but little to

> find on examination, is characteristic, and pain may be considerable.

> Although symptoms may mimic early rheumatoid arthritis, joint swelling

> (synovitis) is much less noticeable. About 20% of patients will develop

> deformity (Jaccoud-type arthropathy) of the hands owing to tendons being

> affected. This is reversible in its early stages, but it can become

> permanent and joint instability may require surgery.

>

> Mucocutaneous manifestations

>

> A wide variety of manifestations is possible. The classic malar

> " butterfly " rash is the textbook presentation; it usually presents

> abruptly after exposure to sunlight and lasts for several days or weeks.

> However, most facial rashes presenting in primary care are not caused by

> lupus. More common causes include acne rosacea and the parvovirus

> " slapped cheek " rash.

>

> Rapid hair loss can be a useful marker of active disease and can lead to

> alopecia. The hair will, however, regrow when the disease remits unless

> the scalp is scarred. Ulceration of the mouth or, less commonly, the

> nose or vagina may or may not be painful, but it is also usually self

> limiting. Raynaud's phenomenon occurs in about half of patients at

> presentation, but it is less common and usually milder than with

> scleroderma or related syndromes. Conversely, most patients who present

> to their general practitioner with Raynaud's syndrome will not have

> systemic lupus erythematosus. If they are positive for antinuclear

> antibodies they are likely to eventually develop a connective disease.

>

> Fatigue

>

> Severe fatigue in conjunction with some of the above symptoms may

> reflect a flare up of the disease. Chronic fatigue, however, is almost

> invariable in established systemic lupus erythematosus and may reflect

> underlying depression or cardiovascular deconditioning.

>

> Major organ disease

>

> Patients greatly fear developing diseases of major organs such as the

> kidneys or central nervous system. Reassuringly, these do not occur in

> most patients, and when they do they are usually a relatively early

> feature. Nevertheless, they are potentially life threatening and are

> associated with a poorer prognosis overall.

>

> Renal disease occurs in 20-50% of all patients at some time during their

> disease, but end stage renal failure is rare (<5%). The start of disease

> may be insidious, and patients should therefore have regular dipstick

> testing of their urine for protein to facilitate early and aggressive

> treatment.

>

> " Cerebral lupus " is probably overdiagnosed. For example, anxiety and

> depression are common but are usually caused by psychological stresses

> associated with a painful, unpredictable, chronic illness rather than

> reflecting cerebral lupus. Management should focus on personal social

> problems such as isolation or marital stress. Headaches have a wide

> variety of possible causes. " Tension headache " can be difficult to

> distinguish from " lupus headache " --both may be unremitting and

> unresponsive to simple analgesics. The latter is extremely uncommon,

> however, and is usually associated with other features of active

> disease. Migraine is more common in patients with lupus than in the

> general population, particularly in patients with antiphospholipid

> antibodies.

>

> Cardiopulmonary disease--Pleurisy and pericarditis may be presenting

> features, and pleuritic pain may mimic that of infection or embolism.

> Although lung disease is uncommon, it is difficult to treat.

>

> Investigations

>

> The erythrocyte sedimentation rate should not be relied on to dictate

> treatment decisions

>

> Blood tests are useful for confirming the diagnosis of systemic lupus

> erythematosus and for differentiating between various subsets of the

> disease but are less useful for monitoring disease activity. The most

> useful screening tests are a complete blood count, erythrocyte

> sedimentation rate, and testing for antinuclear antibody.

>

> If the test for antinuclear antibodies is negative, systemic lupus

> erythematosus is extremely unlikely

>

> There is often a normochromic normocytic anaemia when the disease is

> active. Leucopenia or lymphocytopenia is common and is useful for

> differentiating between systemic lupus erythematosus and rheumatoid

> arthritis. Thrombocytopenia is an uncommon but well recognized

> complication of lupus. Measuring C reactive protein can be a useful test

> for distinguishing between a lupus flare and infection: it usually

> remains normal in a flare, unless accompanied by serositis or synovitis,

> but is elevated in infection. The erythrocyte sedimentation rate will be

> elevated in both and occasionally remains considerably elevated when the

> disease seems to be clinically quiescent.

>

> More than 95% of patients with systemic lupus erythematosus have

> antinuclear antibodies. However, such antibodies may be found in other

> autoimmune disorders and (in low concentration) in chronic infection and

> elderly people. Fewer than half of patients with lupus have antibodies

> to double stranded DNA at presentation: thus it is not a good screening

> test. However, rising tires of these antibodies, particularly if

> accompanied by failing concentrations of C3 and C4, may herald the start

> of renal disease. C3 and C4 are insensitive diagnostically. Antibodies

> to soluble cellular antigens (such as La, Ro, U1 RNP, and Jo-1) can be

> useful for distinguishing between lupus subsets.[23] Antiphospholipid

> antibodies (such as anticardiolipin antibodies or lupus anticoagulant)

> identify a subset of patients at particular risk of thromboembolic

> complications or fetal loss.

>

> Management

>

> Firstly, patients need explanation and reassurance, as the liability to

> episodic flare engenders insecurity and apprehension. It should be

> emphasized that serious complications are rare and that most patients

> have a normal life expectancy.

>

> Preventing lupus flares

>

> Patients should avoid exposure to sunlight (including sunbeds), which,

> as well as precipitating acute or subacute skin lesions, may also cause

> a generalized lupus flare. Sunscreens with a high protection factor

> (factor 15 or higher) effective against ultraviolet A and B should be

> applied liberally, and long sleeved clothes and sun hats should be worn

> in sunny weather. Topical corticosteroid preparations are sometimes

> helpful for chronic skin lesions but should be used sparingly to avoid

> thinning of the skin.

>

> Oral contraceptive pills containing low doses of oestrogen are probably

> safe with mild lupus but should be used with caution by patients with

> severe lupus since they can theoretically cause a flare. They are

> contraindicated in patients with migraine, hypertension, a history of

> thrombosis, or high tires of anticardiolipin antibodies.

> Progestogen-only oral contraceptives are safe. Intrauterine devices

> should be avoided if possible because of an increased risk of infection.

> The evidence for use of hormone replacement therapy is not yet clear

> enough to be able to give general advice: probably the best policy is

> cautious introduction of low dose oestrogen when the disease is

> quiescent with closer than usual monitoring.

>

> Differentiating between a lupus flare and infection can be difficult.

> Infection is an important cause of mortality in patients with systemic

> lupus erythematosus, particularly in those taking corticosteroids or

> immunosuppressive drugs. Furthermore, intercurrent infection can

> precipitate a lupus flare. Hence it is important to maintain a high

> index of suspicion and regard any flu-like or feverish episode lasting

> more than a day or two as infection unless proved otherwise.

> Sulphonamides should usually be avoided because they may cause rash or

> sudden profound neutropenia.

>

> Symptomatic and supportive treatment

>

> Most common symptoms of systemic lupus erythematosus can be safely

> treated symptomatically. Arthralgia, headaches, and non-specific chest

> pains may be helped by non-steroidal anti-inflammatory drugs or simple

> analgesics. Blood pressure should be checked regularly and hypertension

> treated intensively, particularly if there is renal disease.

>

> Disease modifying drugs

>

> Corticosteroids have transformed the outlook for patients with lupus but

> at a considerable price: much of the increased mortality late in the

> course of the disease (due to infection, cardiovascular disease, or

> fracture complications) may be attributable to these drugs. Once an

> acute episode is under control the dose of corticosteroid should be

> slowly reduced; complete withdrawal is optimal, but many patients are

> best managed with a small maintenance dose of perhaps 5 mg or less a

> day. The dose of prednisolone should not be increased for non-specific

> constitutional symptoms in the absence of corroborative physical signs

> or abnormal laboratory results, even though this may make the patient

> feel better. Few lupus complications require immediate corticosteroid

> treatment--it is often best to wait and see for a day or two to avoid

> frequent increases in dose for non-specific symptoms. Arthralgia in

> systemic lupus erythematosus responds poorly to low dose prednisolone

> and usually does not warrant a high dose.

>

> Antimalarial drugs--Chloroquine phosphate (250 mg daily or alternate

> days) or hydroxychloroquine (200-400mg daily) is the mainstay of

> treatment for skin or joint disorders. At these doses ocular

> complications are extremely rare, but it is prudent to use the lowest

> effective dose. Rheumatologists and ophthalmologists continue to

> disagree about the need for routine screening. Hydroxychloroquine is

> safer, though more expensive, than chloroquine. The total dose of

> chloroquine should not exceed 300 g, but it is not clear whether there

> should be such a limit for hydroxychloroquine.

>

> Immunosuppressive drugs--Azathioprine, methotrexate, and

> cyclophosphamide are generally reserved for life threatening diseases of

> major organs such as the kidneys. They should be instituted and

> monitored at specialist centers, with appropriate counselling given

> about the short and long term side effects. Cyclophosphamide, whether

> continuous oral, pulse, or intravenous, is of proved benefit in treating

> renal lupus but is often associated with side effects that can be severe

> (such as infertility, premature menopause, or bladder cancer). Gamete

> storage should be offered before start of treatment when possible. Mesna

> should be used to reduce the risk of bladder toxicity with intravenous

> treatment, but oral mesna is not feasible for patients receiving

> continuous oral treatment. All these immunosuppressive drugs have the

> potential to suppress bone marrow activity, and frequent checks of

> complete blood count and differential white cell count are mandatory.

>

> Outcome with systemic lupus erythematosus

>

> Early studies reported that fewer than half of patients survived five

> years after diagnosis, but this figure has steadily improved. Recent

> studies report five year survival rates of 86-88% and 10 year survival

> rates of 76-87%. Patients who are non-white, male, or at the extremes of

> the age range fare worst. Most patients with lupus die from causes

> unrelated to the disease, but deaths (such as those due to infection or

> ischaemic heart disease) are increasingly related to treatment. Renal

> replacement therapy ensures that death from renal failure is uncommon.

>

> Pregnancy with systemic lupus erythematosus

>

> There is no evidence for reduced fertility in patients with systemic

> lupus erythematosus, and pregnancy presents little hazard for the mother

> if the lupus is mild or stable. Pre-existing renal disease may, however,

> worsen during pregnancy, and complications such as hypertension may be

> more difficult to control. Pre-eclamptic toxaemia may be difficult to

> distinguish from renal flare.

>

> There is an increased rate of fetal loss, particularly during the second

> trimester, in patients with high titres of antiphospholipid antibodies.

> Pregnancies in such women should be monitored carefully in specialist

> units. Overall, there is no increased risk of fetal abnormalities, but

> drug treatment during pregnancy may pose problems. Antimetabolites are

> contraindicated because of teratogenesis, but low dose prednisolone,

> chloroquine, and azathioprine are probably safe.

>

> Antiphospholipid syndrome

>

> This may occur in patients with coexisting systemic lupus erythematosus

> or occur alone (primary antiphospholipid syndrome). It is characterized

> by thrombosis, livedo reticularis, and sometimes thrombocytopenia

> together with the lupus anticoagulant or antiphospholipid antibodies.

>

> Subacute cutaneous lupus erythematosus

>

> Intense photosensitivity and antibodies to La and Ro are the essential

> features of this relatively rare syndrome.

>

> Discoid lupus erythematosus

>

> In this condition lesions are obviously discoid, systemic features are

> rare and mild, and autoantibodies are low in titre.

>

> Incipient lupus

>

> Some patients do not progress to very active disease, and their

> condition is characterized by mild arthralgia, rashes, or serositis with

> weak positivity for antinuclear antibodies.

>

> Neonatal lupus syndrome

>

> A small proportion of babies born to mothers with systemic lupus

> erythematosus (which is often mild and may even have been unrecognized)

> develop the neonatal lupus syndrome. This syndrome appears to be

> restricted to babies whose mothers have antibodies to Ro (SS-A) or La

> (SS- antigens. A self limiting skin rash, which may be severe, is the

> most common presentation. Rarely, babies may have permanent heart block

> secondary to a conduction defect, which may require treatment with a

> cardiac pacemaker.

>

> Drug induced lupus

>

> Lupus-like syndromes may occasionally be induced by some drugs. They

> mostly consist of arthralgia with positivity for antinuclear antibodies,

> and renal disease is rare. Antibodies to DNA are rare, but antihistone

> antibodies are characteristic. The syndrome usually resolves when the

> offending drug is withdrawn, but antinuclear antibodies persist for

> months after.

>

> Overlap syndromes

>

> It has been suggested that the only true lupus syndrome consists of

> nephritis, photosensitivity, serositis, and antibodies to DNA. While

> this might be too purist a view, it is often difficult to categorise

> patients; criteria such as those for systemic lupus erythematosus[1] or

> those suggested for mixed connective tissue disease[4] do not cover all

> situations. Convention, however, prefers some form of categorization,

> and the syndromes usually termed overlap (though some prefer the term

> undifferentiated connective tissue disease) tend to have certain

> characteristic features. Patients also prefer their doctor to be able

> attach a label to their condition that is acceptable to others and

> carries some certainty with regard to prognosis and management.

>

> Prognosis is on a case by case basis, depending on the rate of

> progression and severity and nature of involvement of organ systems.

> Management is similar in principle to that for systemic lupus

> erythematosus: the pattern of involvement dictating the treatment. It is

> clear that mixed connective tissue disease, for example, is not a robust

> syndrome; clinical expression tends to focus on a scleroderma-like,

> rheumatoid-like, or myositis-like syndrome, often with cardiopulmonary

> features dictating the outcome.

>

> PHOTO (COLOR): Jaccoud-type arthropathy; non-erosive deformity of

> fingers owing to tendons being affected.

>

> PHOTO (COLOR): Classic malar " butterfly " rash of systemic lupus

> erythematosus after exposure to sunlight (reproduced with patient's

> permission).

>

> PHOTO (COLOR): Parvovirus " slapped cheek " rash.

>

> PHOTO (BLACK & WHITE): Radiograph showing changes of restrictive lung

> disease in patient with lupus-- " shrinking lung " appearance and linear

> shadows. Pulmonary function tests may eventually stabilize, but

> pulmonary hypertension occasionally develops.

>

> PHOTO (BLACK & WHITE): Magnetic resonance image showing avascular

> necrosis of hips. Avascular necrosis may affect any joint, and treatment

> with high dose corticosteroid is a particular risk factor.

>

> PHOTO (BLACK & WHITE): Severe lupus glomerulonephritis: appearance

> confirms end stage renal failure with glomerular loss. Continued

> treatment with immunosuppressive drugs and high dose corticosteroids is

> unlikely to achieve any improvement in function and would probably

> result only in further toxicity. (With less histological change, further

> immunosuppression might be justified to delay need for dialysis).

>

> Classification criteria for systemic lupus erythematosus (revised

> 1982[1])

>

> To be classified as having systemic lupus erythematosus, patients must

> have at least four of the following criteria in the course of their

> disease:

>

> * Malar rash * Discold rash

>

> * Photosensitivity * Oral ulcers

>

> * Arthritis * Serositis

>

> * Renaldisorder * Neurological

> disorder

>

> * Haematological * Immunological

> disorder disorder

>

> * Presence of anti-nuclear antibodies

>

> Factors that increase probability of associated connectivetissue disease

> in patients with Raynaud's phenomenon

>

> * Onset of condition in childhood or old age

> * Asymmetrical manifestation of symptoms

> * Severe disease threatening viabllity of peripheries

> * Associated with other symptoms such as arthralgia, fatigue,

> rash, etc

> * Associated with abnormal results of blood tests (such as raised

> erythrocyte sedimentation rate, anaemia, presence of antinuclear

> antibodies)

>

> Kidney biopsy in systemic lupus erythematosus

>

> * May not be crucial for diagnosis of lupus glomerulonephritis if

> confirmatory features are present--known active systemic lupus

> erythematosus, urinary sediment with protein, casts, haematuria, and

> negative urine cultures

> * Important as a guide to management when there is doubt as to the

> reversibility of renal damage

>

> Patient support groups

>

> * Support groups for patients with lupus can be most helpful [or

> providing reassurance and reducing a patient's sense of isolation

> * Further details can be obtained from: Lupus UK 51 North Street,

> Romford, Essex RM1 1BA Telephone (01708) 731251

>

> The clinical diversity of systemic lupus erythematosus makes it one of

> the most difficult autoimmune rheumatic disorders to manage. General

> practitioners play a vital role in supporting patients with lupus and

> coordinating treatment, which can easily become fragmented among various

> hospital specialists. Close liaison between specialists and general

> practitioners is crucial for optimal patient care

>

> Treatments for systemic lupus erythematosus

>

> Non-steroidal anti-inflammatory drugs For symptomatic relief

>

> Antimalarial drugs (chloroquine, hydroxychloroquine) For rashes,

> arthritis, and malaise

>

> Corticosteroids For severe flare For maintenance treatment (in low

> doses)

>

> Immunosuppressive drugs (azathioprine, methotrexate, cyclophosphamide,

> etc) For severe flare (in conjunction with corticosteroids)

>

> Additional treatments

> For hypertension

> For infection

> For cerebral lupus (such as anticonvulsants)

> For thrombosis

> For haematological disorders (such as splenectomy)

>

> Corticosteroid treatment for a severe lupus flare

>

> Continuous oral treatment Starting dose of prednisolone is usually

> 0-75-1 mg/kg Treatment continued at same dose for 4-10 weeks depending

> on clinical response Careful reduction can then be attempted

>

> Intravenous pulses Methylprednisolone 0-5-1-5 g repeated 1-3 times

> Suppresses symptoms and may modify outcome, but avascular necrosis

> remains a risk

>

> Intramuscular or oral mini pulses Such as 100-125 mg prednisolone

> acetate intramuscularly Safer and cheaper than and probably as effective

> as other methods for symptomatic relief

>

> Drugs implicated in causing lupus-like syndromes

>

> Common

>

> * Hydralazine

> * Procainamide

> * Anticonvulsants (phenytoin, hydantoins, primidone)

> * Isoniazid Rare

>

> Rare

>

> * Chlorpromazine

> * Penicillamine

> * actolol

> * Antithyroid drugs (propylthiouracil, methylthiouracil)

> * Methyldopa

>

> Clinical features of overlap syndromes

>

> * Raynaud's phenomenon

> * " Sausage " digits

> * Periungual vascular distortion

> * Hyperglobulinaemia and presence of antibodies to several soluble

> nuclear and cytoplasmic antigens

> * Relative lack of cerebrosis, antibodies to DNA, and immune

> complex glomerulonephritis

> * Eventual outcome of cardiopulmonary disease

>

> PHOTO (COLOR): Livedo reticularis in patient with antiphospholipid

> syndrome.

>

> PHOTO (COLOR): Sausage fingers of patient with mixed connective tissue

> disease.

>

> 1. Tan EM, Cohen ES, Fries JF, Masi AT, McShane DJ, Rothfield NF,

> et al. The 1982 revised criteria for the classification of systemic

> lupus erythematosus. Arthritis Rheum 1982;25:1271-7.

> 2. Maddison PJ. Autoantibody profile. Oxford textbook of

> rheumatology. Vol 1. Oxford: Oxford University Press, 1993:389-96.

> 3. Isenberg DA, Horsfall AC. Systemic lupus erythematosus. Oxford

> textbook of rheumatology. Vol 2. Oxford: Oxford University Press,

> 1993:733-55.

> 4. Alarcon-Segovia D, Cardiel MH. Comparison between 3 diagnostic

> criteria for mixed connective tissue disease: a study of 593 patients. y

> Rheumatol 1989;16:328-34.

>

> ~~~~~~~~

>

> By Elaine M Hay, L Snaith

>

> The ABC of Rheumatology is edited by L Snaith.

>

> Elaine M Hay is senior lecturer in community rheumatology at the

> Staffordshire Rheumatology Centre, Stoke on Trent, and L Snaith

> is senior lecturer in rheumatology at the Institute for Bone and Joint

> Medicine, University of Sheffield Medical School.

>

> _____

>

> Copyright of British Medical Journal is the property of BMJ Publishing

> Group and its content may not be copied or emailed to multiple sites or

> posted to a listserv without the copyright holder's express written

> permission. However, users may print, download, or email articles for

> individual use.

> Source: British Medical Journal, 5/13/95, Vol. 310 Issue 6989, p1257, 5p

> Item: 9510221484

>

September 25, 2005

> Hello!

> Does anyone use amber apothecary style bottles (the ones with glass

> stopper

> tops), to store essential oils?

> If so could you reccommend a supplier (online or mail order).

Hi Pixie,

I wasn't aware that SKS had the apothecary type - but maybe they

do - good site to be aware of in any case.

Bestbottles.com (Nemat International) does have apothecary bottles

in several sizes and colors - these are meant for retail sale not

storage, but maybe they'd suit you.

Good luck,

e

April 13, 2008

> Posted by: " Melita "

> leftcoastmelita@... video_gurl40

> Date: Sun Apr 13, 2008 7:02 am ((PDT))

>

> Has anyone tried Teff flour in anything?

I have. I like it---it's good. If you buy injera or

go to a restaurant where they have it, beware, because

most injera made in this country has wheat in it

because teff is so expensive.

Lori

" I wrestled with reality for 36 years, and I'm happy to say that I

finally won out over it. "

---Elwood P. Dowd

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