MRCP shows improvement over last year, explanation?

[Guest guest]

Hey everyone,

I post here infrequently but have a question about the results of a

recent MRCP. Last year I was diagnosed after MRCP / ERCP and had a one

year follow up MRCP last week. The doctor's office sent me a letter

saying that this year's study showed improvement over last year. How

is this possible? I'm obviously thrilled that things look better but I

thought things were either stable or got worse. Anyone else experience

this? I go back to my doctor in February so I'll be sure to grill him

then.

Thank,

[Guest guest]

Hi ,

I don't know if my guess comes even close but in my son's MRCP there

seem to be some signs that show whether the inflammation near the bile

ducts is active or not. Could the improvement be that there is less

inflammation in some are where there was more of it last year meaning

that the disease is not as active?

Taru-Mari, mom of Eemeli (10), PSC 7/2003

--- " mosstheman47 " wrote:

The doctor's office sent me a letter saying that this year's study

showed improvement over last year. How is this possible?

[Guest guest]

Hi ;

Yes, the " dogma " seems to be that there is little evidence for any

improvement in cholangiographic appearance during the normal course of

PSC, see for example:

LaRusso NF, Shneider BL, Black D, Gores GJ, SP, Doo E, Hoofnagle

JH 2006 Primary sclerosing cholangitis: summary of a workshop.

Hepatology 44: 746-764

" Standard doses of ursodeoxycholic acid (UDCA) lead to improvements in

biochemical abnormalities but not in histology, cholangiographic

appearance or survival. "

But if you read the literature more carefully, there are isolated

reports of significant improvement in cholangiograms with certain

therapies. This is one example (see CASE 1 in the article below), but

there are others that I would be glad to share with anyone interested:

_______________________

J. Pediatr. Gastroenterol. Nutr. 27: 580-583 (1998)

Oral vancomycin: treatment of primary sclerosing cholangitis in

children with inflammatory bowel disease.

KL, KM

Division of Pediatric Gastroenterology and Nutrition, Department of

Pediatrics, Lucile Salter Packard Children's Hospital at Stanford

University, Palo Alto, California, U.S.A.

Received January 14, 1998; revised April 3, 1998; accepted April 19,

1998.

Address correspondence and reprint requests to Dr. K.L. , department

of Pediatrics, Stanford University, 750 Welch Road, Suite 116, Palo

Alto, CA 94304, U.S.A.

Primary sclerosing cholangitis is a rare hepatobiliary condition of

unknown cause characterized by inflammation of the extrahepatic and

intrahepatic bile ducts that causes focal narrowing, dilatation, or

obliteration by local periductal fibrosis. The disease is one of the

leading indications for liver transplantation in adults, because it

usually progresse to cirrhosis, portal hypertension, and liver failure

(1).

Seventy-five percent of patients with sclerosing cholangitis have

inflammatory bowel disease, especially ulcerative colitis (2).

Sclerosing cholangitis has rarely been observed in children with

immunodeficiency, histiocytosis X, cystic fibrosis, Alagille's

syndrome, celiac disease, reticulum cell sarcoma, and sickle cell

anemia (3).

Independent of the cause, there has been no satisfactory treatment (2).

Drugs that have been ineffective have included D-penicillamine (4),

corticosteroids (5), cyclosporine (6), methotrexate (7), and colchicine

(5). Ursodeoxycholic acid has been associated with some improvement in

clinical manifestations of primary sclerosing cholangitis in a few

studies (8-10), but has not been effective in other studies (11, 12).

This report describes three children with sclerosing cholangitis and

inflammatory bowel disease whose liver tests and symptoms improved when

treated with oral vancomycin.

CASE 1

The patient was a 15-year-old boy who has had colitis and sclerosing

cholangitis for 2.5 years. In August 1993, he had diarrhea, a 20-lb

weight loss, diffuse abdominal pain, and jaundice. Serum studies showed

total bilirubin, 4.2 mg/dl; direct bilirubin, 1.8 mg/dl; aspartate

aminotransferase, 261 IU/l; gamma-glutamyl transpeptidase (GGT), 716

IU/l; and albumin 2.7 g/dl. Results of examination of a liver biopsy

specimen were consistent with sclerosing cholangitis with mixed

polymorphonuclear neutrophils and lymphocytic infiltrate in the bile

ducts and portal areas, proliferation of pseudoductules, and moderate

portal fibrosis without further bridging (Fig. 1A). An endoscopic

retrograde cholangiopancreatographic (ERCP) study showed early

sclerosing cholangitis with several intra- and extrahepatic strictures

(Fig. 2A). Cultures of bile, small bowel, and colon revealed no

pathogens. Colonoscopy with analysis of biopsy specimens showed

diffuse, nonspecific, acute, and chronic colitis. From December 1993 to

June 1994, he was intermittently treated with 250 mg oral vancomycin

four times daily for stools that were persistently positive for

Clostridium difficile toxin but negative for other pathogens. Diarrhea,

anorexia, and abdominal pain resolved during vancomycin therapy, his

erythrocyte sedimentation rate (ESR) and serum liver test results

reached normal levels. Since June 1994, he has had continued therapy

with 300 mg ursodeoxycholic acid twice daily and had multiple stool

studies for C. difficile toxin, polymerase chain reaction for C.

difficile, cultures, and examination for ova and parasites that were

negative for pathogens. Intermittently, he had symptoms including

bloody diarrhea, abdominal pain, and anorexia associated with abnormal

blood studies (ESR, GGT, and alanine aminotransferase [ALT]) and was

given multiple treatments of oral vancomycin (Fig. 3). His symptoms and

blood test results normalized during vancomycin therapy and worsened

within 2 to 4 weeks after vancomycin was discontinued (Fig. 4).

Compared with the liver biopsy specimens obtained during cessation of

vancomycin therapy, the specimens obtained during vancomycin therapy

demonstrated less portal inflammation and portal fibrosis (Fig. 1B). An

ERCP study performed during vancomycin therapy revealed a normal

biliary tract (Fig. 2B). More recently, symptoms and abnormal

laboratory test results were treated with oral metronidazole or

ciprofloxacin instead of oral vancomycin. There were no changes in

symptoms or laboratory test findings during administration of these

antibiotics.

CASE 2

A 14-year-old girl had Crohn's disease of the large and small bowel and

sclerosing cholangitis. At age 5 years, she had had bloody diarrhea and

showed severe colitis on colonoscopy and skip lesions in the duodenum

and small bowel in an upper gastrointestinal series. At age 8 years,

she had an elevated serum GGT concentration of 1351 IU/l, and analysis

of a liver biopsy specimen showed portal fibrosis and bile ductular

proliferation consistent with sclerosing cholangitis. An ERCP showed

mild intrahepatic and extrahepatic bile duct narrowing that was

indicative of early sclerosing cholangitis. During the past 6 years,

she has been maintained on 50 mg 6-mercaptopurine daily, 500 mg

sulfalazine three times daily, and 300 mg ursodeoxycholic acid three

time daily. For 5 years until May 1995, the GGT level ranged from 59 to

285 IU/l, and the ESR from 18 to 60 mm/hr. From May 1995, until oral

vancomycin therapy was begun in August 1995, she had bloody diarrhea,

right upper quadrant abdominal pain without fever or tenderness, and

abnormal blood test results with GGT, 468 to 818 IU/l; ALT 57 to 84

IU/l; and ESR, 60 to 103 mm/hr. In July, 1995, abdominal ultrasound

showed a dilated common bile duct (6 mm in diameter). Before vancomycin

therapy was initiated, stool cultures, C. difficile toxin, and

examination for ova and parasites were negative. During therapy with

125 mg vancomycin three times daily for 3 months beginning in August

1995, GGT, ALT and ESR decreased to near normal values (Fig. 4). Within

2 weeks after introduction of vancomycin, she became asymptomatic with

normal findings in abdominal ultrasound (4 mm diameter of bile duct).

For the 6 months after treatment with oral vancomycin and while

continuing therapy with 6-mercaptopurine, sulfalazine, and

ursodeoxycholic acid, she was asymptomatic. However, during the past

year she has been poorly compliant with pharmacologic therapy and has

had recurrence of right upper quadrant pain with elevation of ESR, ALT,

and GGT, which have not responded to oral vancomycin treatment.

CASE 3

A 14-year-old boy with Crohn's disease of the stomach, small bowel, and

colon and sclerosing cholangitis. At age 11 years he had bloody

diarrhea, weight loss, and abnormal findings in liver tests (GGT 291

IU/l and ALT 206 IU/l). Endoscopic studies showed severe acute and

chronic inflammation of the entire colon, antrum and duodenum. Findings

in analysis of a liver biopsy specimen were consistent with sclerosing

cholangitis, showing proliferation and large bile ducts with intense

lymphoplasmacytic infiltrate and fibrous tissue surrounding the bile

ducts. He did not undergo an ERCP study. He was steroid dependent and

had abnormal cramping pain, nausea, and bloody diarrhea if his

prednisone dose was decreased below 15 mg daily. He was maintained with

75 mg 6-mercaptopurine daily for 2 years. During the past year, before

vancomycin therapy was begun, his GGT ranged from 350 to 1189 IU/l, ALT

from 49 to 499 IU/l, and ESR from 19 to 84 mm/hr. During therapy with

250 mg oral vancomycin three times daily for 2 weeks, and then twice

daily for 4 weeks, he remained asymptomatic while therapy with

prednisone, which had initially been prescribed at 40 mg daily, was

tapered. His GGT, ALT and ESR levels became normal (Fig. 4). For the 6

months of vancomycin and steroid therapy, while continuing 6-

mercaptopurine, he was asymptomatic and had normal levels of ESR, ALT

and GGT. In September 1996, he had bloody diarrhea, abdominal pain, and

vomiting for 2 weeks associated with an increase in ALT to 130 IU/l,

GGT to 148 IU/l, and ESR to 55 mm/hr. Stool cultures and C. difficile

toxin revealed no pathogens. Within 24 hours after 250 mg oral

vancomycin was administered (three times daily), he became asymptomatic

and within 6 weeks his ALT, GGT, and ESR readings were normal. For the

past 14 months he has been asymptomatic with normal levels of ALT, GGT,

and ESR.

DISCUSSION

The causes of inflammatory bowel disease and sclerosing cholangitis are

unknown. Infectious mechanisms have been proposed, but there have been

no specific infectious agents identified. Many antibiotics have been

tried, but none have been effective (2). Oral vancomycin has not been

previously used in the treatment of sclerosing cholangitis or

inflammatory bowel disease.

Vancomycin is bactericidal for staphylococci, streptococci including

enterococci, diptheroids, Listeria monocytogenes, and species of

Clostridium, Lactobacillus, Actinomyces, and Bacillus. It is not active

against Gram-negative bacilli, mycobacteria, or fungi. Vancomycin is

poorly absorbed after oral administration (13).

Enteric bacterial infection has been considered a cause of primary

sclerosing cholangitis. In one study, investigators reported portal

bacteremia in patients with ulcerative colitis who had colonic surgery

(14). However, others did not find portal vein phlebitis, a typical

feature of portal bacteremia, in most patients with primary sclerosing

cholangitis (15). Because lithocholic acid, a hepatotoxic bile acid, is

generated by intestinal flora, primary sclerosing cholangitis may be

caused by abnormal production of toxic bile acids by gut flora (16).

However, the composition and concentrations of bile acids have been

normal in the bile and portal blood of patients with sclerosing

cholangitis and inflammatory bowel disease (17). Animal studies have

provided evidence that enteric bacteria produce toxic proinflammatory

agents, such as N-formylmethionyl peptides, which can be absorbed,

enter the enterohepatic circulation, and appear undegraded in the bile,

which causes periportal inflammation and hepatocyte damage (18). In

addition, a ubiquitous bacterial cell wall polymer, peptidoglycan-

polysaccharide, has been shown in a rat model of bacterial overgrowth

to play a role in causing hepatobiliary disease that resembles primary

sclerosing cholangitis (19). From these data, we can hypothesize that

oral vancomycin may kill the enteric bacteria that produce these

biliary toxic inflammatory agents that are absorbed. The recurrence of

symptoms and abnormal laboratory findings observed in these patients

after vancomycin was discontinued suggests that the antibiotic did not

completely eradicate the infection or that there was reinfection.

Further prospective studies will be necessary before the indications,

dosage, length of time for treatment, and potential long-term benefits

of oral vancomycin can be determined.

Fig. 1. Specimens from liver biopsies performed in patient in Case 1

before oral vancomycin therapy (A) and after oral vancomycin therapy

( (hematoxylin-eosin, magnification x100). Liver biopsy specimens

show significantly less focal bridging fibrosis and portal inflammation

after oral vancomycin treatment ( compared with that in the specimens

obtained before treatment (A).

Fig. 2. An endoscopic retrograde cholangiopancreatographic study

performed in the patient in Case 1 before oral vancomycin therapy

showing (arrows) biliary strictures (A) and after oral vancomycin

therapy showing (arrows) biliary strictures are no longer present (.

Fig. 3. The effects of multiple treatment of oral vancomycin on the

blood studies (ALT, GGT, ESR) in Case 1 are shown.

Fig. 4. The effects of oral vancomycin on blood studies (GGT, ESR, ALT)

of three children with inflammatory bowel disease and sclerosing

cholangitis are shown.

REFERENCES

1. Porayko MK, Wiesner RH, LaRusso NF, Ludwig J, MacCarty RL, Steiner

BL, Twomey CK, Zinsmeister AR 1990 Patients with asymptomatic primary

sclerosing cholangitis frequently have progressive disease.

Gastroenterology 98: 1594-1602.

2. Lee YM, Kaplan MM 1995 Primary sclerosing cholangitis. N. Engl. J.

Med. 332: 924-933.

3. Balistreri WF. Bove KE 1994 Sclerosing cholangitis. In (Suchy FJ,

ed.) Liver diseases in children. St. Loius: Mosby-Year Book, pp. 622-

637.

4. LaRusso NF, Wiesner RH, Ludwig J, MacCarty RL, Beaver SJ,

Zinsmeister AR 1988 Prospective trial of penicillamine in primary

sclerosing cholangitis. Gastroenterology 95: 1036-1042.

5. Lindor KD, LaRusso NF, Wiesner RH 1989 Prednisone and colchicine are

not of benefit after two years in patients with primary sclerosing

cholangitis. Hepatology 10: 638.

6. Weisner RH, Steiner B, LaRusso NF, Lindor KD, Baldus NP 1991 A

controlled clinical trial evaluating cyclosporine in the treatment of

primary sclerosing cholangitis. Hepatology 14: 63A.

7. Knox TA, Kaplan MM 1994 A double-blind controlled trial of oral-

pulse methotrexate therapy in the treatment of primary sclerosing

cholangitis. Gastroenterology 106: 494-499.

8. Beuers U, Spengler U, Kruis W, Aydemir U, Wiebecke B, Heldwein W,

Weinzierl M, Pape GR, Sauerbruch T, Paumgartner G 1992 Ursodeoxycholic

acid for treatment of primary sclerosing cholangitis: a placebo-

controlled trial. Hepatology 16: 707-714.

9. O'Brien CB, Senior JR, Arora-Mirchandani R, Batta AK, Salen G 1991

Ursodeoxycholic acid for the treatment of primary sclerosing

cholangitis: a 30-month pilot study. Hepatology 14: 838-847.

10. S, Bansi D, Hunt N, Christie J, Fleming K, Chapman R 1997

High dose ursodeoxycholic acid (UDCA) in primary sclerosing cholangitis

(PSC): results after two years of a randomized double-blind, placebo

controlled tiral. Gastroenterology 112: A1335.

11. Lo SK, Hermann R, Chapman RW et al 1992 Ursodeoxycholic acid in

primary sclerosing cholangitis: a double-blind placebo controlled

trial. Hepatology 16: A92.

12. Van Thiel DH, HI, Gavaler JS 1992 Ursodeoxycholic acid

(UCDA) therapy for primary sclerosing cholangitis. Hepatology 16: A62.

13. Di Febo G, Calabrese C, Matassoni F 1992 New trends in non-

absorbable antibiotics in gastrointestinal disease. Ital. J.

Gastroenterol. 24: S10-S13

14. BN, Dykes PW, Falker FC 1961 A study of liver disorder in

ulcerative colitis. Postgrad. Med. J. 37: 245-248.

15. Ludwig J, Barham SS, LaRusso NF, Elveback LR, Wiesner RH, McCall JT

1981 Morphologic features of chronic hepatitis associated with primary

sclerosing cholangitis and chronic ulcerative colitis. Hepatology 1:

632-640.

16. Carey JB 1964 Bile acids, cirrhosis, and human evolution.

Gastroenterology 46: 490-493.

17. Siegel JH, S, JS 1977 Bile acids in liver disease

associated with inflammatory bowel disease. Digestion 15: 469-481.

18. Hobson CH, Butt TJ, Ferry DM, Hunter J, Chadwick VS, Broom MF 1988

Enterohepatic circulation of bacterial chemotactic peptide in rats with

experimental colitis. Gastroenterology 94: 1006-1013.

19. Lichtman SN, Okoruwa EE, Keku J, Schwab JH, Sartor RB 1992

Degradation of endogenous bacterial cell wall polymers by the muralytic

enzyme mutanolysin prevents hepatobiliary injury in genetically

susceptible rats with experimental intestinal bacterial overgrowth. J.

Clin. Invest. 90: 1313-1322.

__________________________

Publication Types:

Case Reports

Accession Number 00005176-199811000-00015.

Author , L.; , Kathleen M.

Institution Division of Pediatric Gastroenterology and Nutrition,

Department of Pediatrics, Lucile Salter Packard Children's Hospital at

Stanford University, Palo Alto, California, U.S.A.

Title Oral Vancomycin: Treatment of Primary Sclerosing Cholangitis in

Children with Inflammatory Bowel Disease.[Report]

Source Journal of Pediatric Gastroenterology & Nutrition. 27(5):580-

583, November 1998.

References 1. Porayko MK, Weisner RH, LaRusso NF, et al. Patients with

asymptomatic primary sclerosing cholangitis frequently have progressive

disease. Gastroenterology 1990;98:1594-602.

2. Lee Y-M, Kaplan MM. Primary sclerosing cholangitis. N Engl J Med

1995;332:924-33.

3. Balistreri WF, Bove KE. Sclerosing cholangitis. In: Suchy FJ, ed.

Liver diseases in children. St. Louis: Mosby-Year Book, 1994:622-37.

4. LaRusso NF, Wiesner RH, Ludwig J, MacCarty RL, Beaver SJ,

Zinsmeister AR. Prospective trial of penicillamine in primary

sclerosing cholangitis. Gastroenterology 1988;95:1036-42.

5. Lindor KD, LaRusso NF, Wiesner RH. Prednisone and colchicine are not

of benefit after two years in patients with primary sclerosing

cholangitis (abstract). Hepatology 1989;10:638.

6. Weisner RH, Steiner B, LaRusso NF, Lindor KD, Baldus NP. A

controlled clinical trial evaluating cyclosporine in the treatment of

primary sclerosing cholangitis (abstract). Hepatology 1991;14:63A.

7. Knox TA, Kaplan MM. A double blind controlled trial of oral pulse

methotrexate therapy in the treatment of primary sclerosing

cholangitis. Gastroenterology 1994;106:494-99.

8. Beuers U, Spengler U, Kruis W. Ursodeoxycholic acid for treatment of

primary sclerosing cholangitis. A placebo-controlled trial. Hepatology

1992;16:707-14.

9. O'Brien CB, Senior JR, Arora-Mirchandani R, Batta AK, Salen G.

Ursodeoxycholic acid for the treatment of primary sclerosing

cholangitis: A 30 month pilot study. Hepatology 1991;14:838-47 (Erratum

Hepatology 1992;15:566.

10. S, Bansi D, Hunt N, Christie J, Fleming K, Chapman R. High

dose ursodeoxycholic acid (UCDA) in primary sclerosing cholangitis

(PSC): Results after two years of a randomised doubleblind, placebo-

controlled trial (abstract). Gastroenterology 1997;112:A1335.

11. Lo SK, Herrmann R, Chapman RW, et al. Ursodeoxycholic acid in

primary sclerosing cholangitis: A double-blind placebo controlled trial

(abstract). Hepatology 1992;16:A92.

12. Van Thiel DH, HI, Gavaler JS. Ursodeoxycholic acid (UCDA)

therapy for primary sclerosing cholangitis (PSC): Preliminary report of

a randomized controlled trial (abstract). Hepatology 1992;16:A62.

13. Di Febo G, Calabrese C, Matassoni F. New trends in non-absorbable

antibiotics in gastrointestinal disease. Ital J Gastroenterol

1992;24:10-3.

14. BN, Dykes PW, FC. A study of liver disorder in

ulcerative colitis. Postgrad Med J 1961;37:245-8.

15. Ludwig J, Barham SS, LaRusso NF, Elveback LR, Weisner RH, McCall

JT. Morphologic features of chronic hepatitis associated with primary

sclerosing cholangitis and chronic ulcerative colitis. Hepatology

1981;1:632-40.

16. Carey JB Jr. Bile acids, cirrhosis, and human evolution.

Gastroenterology 1964;46:490-3.

17. Siegel JH, S, JS. Bile acids in liver disease

associated with inflammatory bowel disease. Digestion 1977;15:469-81.

18. Hobson CH, Butt TJ, Ferry DM, Hunter J, Chadwick VS, Broom MF.

Enterohepatic circulation of bacterial chemotactic peptide in rats with

experimental colitis. Gastroenterology 1988;94:1006-13.

19. Lichtman SN, Okoruwa EE, Keku J, Schwab JH, Sartor RB. Degradation

of endogenous bacterial cell wall polymers by the mutanolysin prevents

hepatobiliary injury in genetically susceptible rats with experimental

intestinal bacterial overgrowth. J Clin Invest 1992;90:1313-22.

Language English.

Document Type Case Report.

Journal Subset Clinical Medicine. Life Sciences.

ISSN 0277-2116

NLM Journal Code jl6, 8211545

PMID: 9822326

_______________________

Can you share with the group what you have been doing to get this great

result? What ever you are doing, keep doing it!

Best regards,

Dave R.

> Hey everyone,

>

> I post here infrequently but have a question about the results of a

> recent MRCP. Last year I was diagnosed after MRCP / ERCP and had a one

> year follow up MRCP last week. The doctor's office sent me a letter

> saying that this year's study showed improvement over last year. How

> is this possible? I'm obviously thrilled that things look better but I

> thought things were either stable or got worse. Anyone else experience

> this? I go back to my doctor in February so I'll be sure to grill him

> then.

[Guest guest]

-

Hi ,

Count me as one of the lucky few for whom an MRCP showed improvement.

After years of hospitalizations (at first I was lucky to go for a

month without a trip to the ER), we began to see improvement and now

some stability in the most recent one. I'm not questioning the

results, I'm just thankful for them!

Penny

-- In , " mosstheman47 "

wrote:

>

.. The doctor's office sent me a letter

> saying that this year's study showed improvement over last year. How

> is this possible? I'm obviously thrilled that things look better but I

> thought things were either stable or got worse. Anyone else experience

> this? I

>

>

[Guest guest]

Thanks for the responses! I finally got ahold of the radiologist

report and I've included it below. My limited understanding of this

is: the stricture in my common bile duct looks better and the

intrahepatic strictures are minor / questionable.

Is it true that ERCP produces better images than MRCP? Could this

explain why the MRCP shows " borderline findings " but the ERCP

confirmed my diagnosis?

Thanks,

<--- Report below: --->

Findings: The intrahepatic ducts are not dilated. On the coronal

source images, there are slight irregularities of the intrahepatic

ducts, corresponding to the subtle abnormality seen on the ERCP.

However this is of questionable significance. It could reflect mild

form of sclerosing cholangitis however is considered a borderline

finding.

On the the axial scans, the extrahepatic common duct, measures between

3 and 5mm, mildly prominent for patient's age (I'm 26 btw). As before

the gallbladder appears distended. No definitive gallstones are

identified. An area of signal loss seen on the coronal series 8, image

7 is of questionable relevance as it is only seen on one acquisition.

The common duct tappers normally within the head of pancreas. A normal

juncture between the pancreatic duct the bile duct is observed. Cystic

duct appears normal in diameter.

Liver size is normal. The postcontrast scans show normal, homogeneous

enhancement of the liver. Portal veins, hepatic veins are patent.

Pancreas, spleen, adrenal glands are normal. No evidence for delayed

enhancement of the common duct wall.

Impression:

1. Borderline prominent extrahepatic duct without evidence for a

distal stricture. This finding appears slightly improved when compared

to the previous MRCP.

2. Questionable minimal intrahepatic ductal irregularities suggestive

of mild strictures, considered a borderline finding.

-----

>

>

> Hey everyone,

>

> I post here infrequently but have a question about the results of a

> recent MRCP. Last year I was diagnosed after MRCP / ERCP and had a one

> year follow up MRCP last week. The doctor's office sent me a letter

> saying that this year's study showed improvement over last year. How

> is this possible? I'm obviously thrilled that things look better but I

> thought things were either stable or got worse. Anyone else experience

> this? I go back to my doctor in February so I'll be sure to grill him

> then.

>

> Thank,

>

>