Re: Mild chronic pancreatitis to

[Guest guest]

,

Attached is a good article on Chronic Pancreatitis that you may wish to read.

It's only one of several that I have stored in my files, as I've been

researching

CP and it's related problems for three years now and have quite a " library " of

information saved.

What I'm going to say now is you probably won't like, but I do believe that

people should be well educated about their illnesses and doctors often don't

tell us the things we need to know in order to deal with them. I've learned to

be very proactive about my diseases, and having knowledge about them is

one way a person can be effective in asking for and securing appropriate

treatment.

Although your CP is mild now and not giving you much problem, there is a

good chance that this lull is only temporary, and that you may have troubles

with it in the future. I know this isn't the news that you wanted to hear, but

I

am basing this assumption on facts that I've read in my medical research.

One thing that I believe you need to think about is that there may be a familial

connection to this disease, as you said that your aunt died from pancreatic

cancer. There is a good possibility that your CP is the result of genetic

causes, and if I were you, I would ask for genetic testing, especially since the

actual cause of your pancreatitis has not been established.

Chronic pancreatitis is a progressively degenerative disease. Each acute

attack or episode of pain, what we often call a flare up, causes additional

damage to the gland. You were told that calcification was already seen in

your pancreas in the first CT-scan. Every time we have an exacerbation,

more damage is done, and more calcifications develop. Over time, the

damage progresses and the patient eventually reaches advanced stages of

the disease.

Research says that the time frame for this damage to reach it's final stages of

pancreas burn out can be anywhere from 5-25 years. I've already proven

those statistics as incorrect, since my burn-out happened near the end of my

second year!

The progressive part of the disease affects everyone differently, and some

cases are mild, where others are severe. The best you can do for yourself is

to arm yourself with knowledge and understanding of CP and just continue on

as you have been. Your healthiness with your physical activity should benefit

you, for as long as you can tolerate it. I was a very athletic prior to my

diagnosis, swimming, hiking, skiing and biking on a regular basis. I do believe

this has helped me now in my ability to recover from an attack quicker than

someone who has not had that type of althletic lifestyle.

Your body will tell you what you can do, and if you reach a point where any

activity causes pain or discomfort, then you know it's time to slow down with

that pursuit.

Being strict with yourself with a low fat diet is said to be most beneficial.

Many

gastroenterologists recommend a daily intake of no more than 30 grams of

fat. In my first two years with CP I ate no more than 20 grams of fat each

day, with each meal or snack containing no more than 6-8 grams of fat. You

may also find that protein gives you some problems.....this, too, has been

known to be difficult for the pancreatic enzymes to digest. That's why the

enzyme supplements contain protease, in addition to amylase and lipase.

The fact that your lipase is still elevated may mean that there is still some

inflamation going on. Mine was elevated for over a year, and the doctors said

that this was due to the pseudocysts I have. I don't know the reason for

yours, but it usually indicates that there's still some activity going on.

Your diet and Creon won't necessarily prevent you from having further

damage, but they will help you to take the load of digestion off of the

pancreas, thus hoping to offset the onset of another episode of inflamation.

The pancreatic enzyme supplements will also help you to avoid the pain that

eating often causes afterward. While it's difficult to find the precise causes

that trigger an attack, we do know that alcohol, high fats, high protein and

excessive exercise can trigger an episode. In your case, since your body is

used to your running activity, I wouldn't call your running excessive activity.

I hope that some of this information is helpful for you.. The article isn't the

best one that I have, but it will get you started with some information that you

probably didn't know. Please feel free to ask ANY questions, or jump in and

comment on anything you wish to. We're here to help you, and I hope we

can.

With love, hope and prayers,

Heidi

Heidi H. Griffeth

South Carolina State Rep.

SE Regional Rep., PAI

Note: All comments or advice are based on personal experience or opinion

only, and should never be substituted for consultation with a medical

professional.

The article below lists the different causes for pancreatitis.

Chronic Pancreatitis

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

Larry , MD

Objectives

* To understand the relationship of acute to chronic pancreatitis

* To be aware of the etiology, pathogenesis and epidemiology of chronic

pancreatitis

* To know the principles of therapy of chronic pancreatitis

Acute Pancreatitis

I. Classification

* Chronic pancreatitis is divided into two clinical types: pancreatitis and

chronic relapsing pancreatitis

* In both, regardless of the cause, the gland is permanently damaged,

morpho-logically and functionally

* Relapsing indicates that the progressive destruction of the pancreas is

punctuated by discrete episodes of acute inflammation associated with pain

* In a classic example of chronic relapsing pancreatitis, alcoholic

pancreatitis,

the gland incurs irreversible damage and the patient generally suffers

recurrent painful attacks resembling acute pancreatitis

* In contrast, the type referred to simply as chronic pancreatitis is often

illustrated by idiopathic disease, in which the gradual destruction of the

gland,

with resulting pancreatic insufficiency, often proceeds without discrete painful

exacerbation

II. Etiology

* Ethanol

* In the U.S. and other industrialized countries, alcohol accounts for more

than 90% of all cases of chronic pancreatitis

* The amount of alcohol consumed appears to determine the outcome in any

particular person

* The susceptibility of the pancreas to alcohol differs widely, a minimum of

100g/d is needed

* Tropical Form

* Hypercalcemia

* Heredity

* Tumor

* Pancreas Divisum

* Cystic Fibrosis

* Trauma

* Unknown Causes

III. Pathology

* The 1984 Marseille classifications recognized two general pathologic types:

chronic pancreatitis and chronic obstructive pancreatitis

* Alcoholic pancreatitis is an example of the former, tumor-associated chronic

pancreatitis of the latter

* Morphologic appearance is similar in both types

* Initially, the pancreas enlarges and is soft; then it becomes gradually harder

as fibrosis develops

* With advancing atrophy, the gland eventually shrinks

* A cardinal feature of chronic pancreatitis is the presence of protein plugs

and calcifications

* Proteinaceous material precipitates in the ducts and ductules, initially

consisting mainly of pancreatic enzyme protein and a glycoprotein

* In late stages, calcium carbonate is added to the precipitates, giving rise to

stones (pancreatic calculi)

* These produce the well known x-ray appearance of pancreatic calcifications

* Protein plugs and calculi are rare in chronic obstructive pancreatitis

IV. Pathogenesis

* The vast majority of cases of chronic pancreatitis, regardless of cause,

exhibit very similar morphologic and histologic features, which clearly

distinguish them from chronic obstructive pancreatitis, leading to the notion

that various " etiologic types " share a common pathogenic mechanism

* The presence of microscopic ductal plugs is the most common feature of

chronic pancreatitis

* Whether the obstruction caused by those plugs results in the episodic acute

attacks of early chronic pancreatitis is difficult to ascertain

* Nonetheless, precipitates of proteinaceous material in the canalicular

ductules constitute the initial abnormality in chronic pancreatitis

* Those precipitates are made up of pancreatic enzyme protein and a

glycoprotein, pancreatic stone protein (PSP)

* Later, calcium carbonate is added

* Thus, protein plugs appear to be the precursors of pancreatic stones

* Approximately half of the patients who present with morphologic changes of

chronic pancreatitis already have pancreatic calcifications on abdominal x-ray

examination

* Most develop calcifications with gradual progression of the disease, so that

15 years after presentation, radiographic evidence of calcifications is well

above 90%

* Chronic obstructive pancreatitis is the result of occlusion of the main

pancreatic duct

* Any obstructing lesion--a tumor, a scar resulting from trauma, papillary

inflammation, a congenital structure--is a potential cause

* Fibrosis is accompanied by uniform acinar atrophy

* Exocrine insufficiency ensues, but it's partially reversible if the

obstruction is

removed

V. Clinical picture

The clinical picture of chronic pancreatitis is dominated by three features;

abdominal pain, maldigestion, and diabetes.

* Abdominal pain

* More than 90% of patients experience abdominal pain

* Often it begins insidiously

* It is intermittant or continuous, with fluctuations in intensity

* More than half the patients suffer episodic attacks of pain indistinguishable

from that of acute pancreatitis

* By the time the first attack occurs, the gland is already permanently

damaged

* Subsequent attacks are milder and shorter lived, and the pain then

becomes chronic

* The pain of chronic pancreatitis is upper abdominal

* Pain location correlates with that of disease, being epigastric when mainly

the head of the pancreas is inflamed and left-sided when the disease is

primarily in the tail

* The pain frequently radiates to the back, and occasionally to the left

shoulder

* Maldigestion

* As structural destruction of the pancreas occurs, pancreatic function

gradually declines

* Only when exocrine function is substantially impaired, maldigestion

becomes clinically overt

* This process takes many years, during which digestion is normal

* If weight loss occurs during that period, it is usually due to poor nutrition

* Intake is limited because of pain induced by eating

* Steatorrhea is the most obvious manifestation of pancreatic maldigestion

* Stools are loose, bulky and particularly malodorous

* The amount of fecal fat depends on two factors

* Severity of exocrine insufficiency

* Amount of dietary fat

* Exocrine insufficiency results from inadequate secretion of pancreatic

enzymes due to acinar cell destruction, and inadequate delivery of pancreatic

juice into the duodenum owing to ductal obstruction

* When duodenal lipase activity is less than 10% of normal, steatorrhea

becomes clinically manifest

* Steatorrhea is accompanied by azotorrhea, the loss of protein in the

stool--the latter supervenes when trypsin activity falls below 10% of normal

* Protein maldigestion occurs later than fat maldigestion in chronic

pancreatitis

* Diabetes

* Chronic pancreatitis causes injury to islet cells; eventually results in a

shortage of insulin with development of diabetes

* Ketoacidosis is unusual because complete absence of insulin secretion from

the diseased pancreas is rare and only small amounts of insulin are required

to prevent ketoacidosis

* Complications of diabetes are relatively infrequent

VI. Complications

* Pseudocyst

* Common Bile Duct Obstruction

* Pancreatic Ascites

* Pancreatic Pleural Effusion

* Splanchnic Venous Obstruction

VII. Diagnosis

* General principles

* When calcifications are present, the diagnosis of chronic pancreatitis is

easy, regardless of presentation

* It is also straightforward when the patient is known to consume excessive

amounts of alcohol and complains of pain typical of pancreatic origin or

presents with steatorrhea or diabetes

* In regions where tropical pancreatitis is prevalent, the diagnosis is readily

made

* Greater difficulty is encountered when pancreatitis is painless and no

calcifications appear on abdominal film

* Patients may come to medical attention because of hyperglycemia,

steatorrhea, or weight loss without other symptoms

* Physical examination

* During an acute attack, the abdomen is tender and the patients tend to lean

forward to alleviate pain

* Bowel sounds are often diminished owing to associated ileus, and there may

be nausea and vomiting

* The pulse is rapid and the blood pressure low, with third-space fluid losses

* Dyspnea may occur, often the result of a pleural effusion, usually

sympathetic, but sometimes from pancreatic juice tracking into the pleural

space through a fistula

* Scleral icterus can be present, caused by extrinsic biliary obstruction from

edema of the head of the pancreas or an adjacent pseudocyst

* It is usually transient but may persist if the pseudocyst does not resorb or a

phlegmon appears in the head of the pancreas, compressing the common

bile duct

* Except when painful exacerbations occur, the physical examination is of

limited value. Epigastric tenderness is often present and on occasion, a large

anterior pseudocyst may be palpated.

* Laboratory evaluation

* Amylase and Lipase

* Serum amylase and lipase levels are elevated at the onset of an acute

exacerbation of chronic pancreatitis

* Amylase value returns to normal within a few days, and the lipase elevation

persists a few days longer

* Other conditions, such as intestinal obstruction and infarction, acute

cholecystitis, and ectopic pregnancy also cause hyperamylasemia

* In later phases of chronic pancreatitis, when exacerbations are milder and

acinar destruction has become extensive, enzymesecretion is significantly

reduced, amylase and lipase elevations during exacerbations may be minimal

* Persistent hyperamylasemia should raise the suspicion of a pseudocyst

* Liver Function Tests

* Transaminase elevations are often noted in an acute exacerbation of

chronic pancreatitis

* Increased alkaline phosphatase and bilirubin result commonly from

compression of the common bile duct, due to pancreatic edema, during an

acute exacerbation, or to a pseudocyst

* When hyperbilirubinemia is accompanied by fever and chills, cholangitis

must be considered

* Tests of pancreatic structure

* Plain Films

* Ultrasonography and Computed Tomography

* Endoscopic Retrograde Cholangiopancreatography

* Tests of pancreatic function

* Measurement of pancreatic exocrine function is useful in the diagnosis of

chronic pancreatitis

* The severity of maldigestion, its contribution to weight loss, and the

efficacy

of pancreatic enzymes can be assessed

* Pancreatic function may be inferred by direct measurement of the

components of pancreatic secretion

* Enzyme activity may be estimated by the ability of the pancreas to cleave a

given substance

* Pancreatic integrity may be reflected by the level of pancreatic enzymes or

hormones secreted in the bloodstream or by recovering enzymes from the

stool

* Pancreatic dysfunction can be appreciated by the amount of undigested

nutrients recovered in the stool

* Invasive Tests

* The Secretin Test

* The Lundh Test

* Noninvasive Tests

* The NBT-PABA Test (Bentiromide Test)

* Fecal Fat

VII. Treatment

* Diabetes

* Exogenous insulin, unopposed by glucagon (low or absent in pancreatic

disease), may cause hypoglycemia, so tight glycemic control is potentially

dangerous

* Since the development of diabetic vasculopathy is infrequent, it is

unnecessary to maintain blood sugar within the normal range

* Plasma glucose value of 200 to 250 mg/dl throughout the day is a desirable

target

* Therapy should control symptoms, principally polydypsia and polyuria and

prevent the excessive loss of calories in the urine

* This is important since many patients with pancreatic diabetes have poor

dietary habits, avoid eating because it aggravates pain, and most suffer from

steatorrhea

* Maldigestion

* Steatorrhea occurs when pancreatic lipase secretion falls below 10%

* To restore the duodenal lipase concentration to a level that prevents

steatorrhea 30,000 units of lipase is required with every meal

* Most enzyme preparations contain 3000-4000 units of lipase per tablet

* Seven or eight tablets per meal is needed. Reducing fecal fat to half original

amount with the administration of oral preparations is a reasonable goal

* Dietary measures are also recommended: reducing consumption of fat and

increasing protein

* Pain

* Management of Painful Complications

* Acute inflammation

* Pseudocyst

* Infected Necrosis

* Pancreatic Biliary Stricture

* Pancreatic Ascites and Pleural Effusions

* Medical Management of Chronic Pain

* General Considerations

* Since the various surgical procedures for pain relief are often unsuccessful,

or of limited and temporary benefit, patients suffering from chronic pancreatic

pain should be managed medically unless there are complications that

necessitate surgical therapy

* With marked deterioration of pancreatic function, pain may eventually

disappear

* In alcohol-induced disease, painless pancreatitis is often associated with

pancreatic dysfunction

* With chronic pancreatitis, the episodic inflammatory attacks become

progressively less frequent and less severe as the gland gradually loses its

ability to secrete enzymes

* Analgesia

* Mild pain should be managed medically

* Aside from abstinence from alcohol, medical management rests primarily on

the use of analgesics, prescribed in the smallest possible doses, to avoid

addiction

* Surgery for the palliation of pain must then be considered

* Pancreatic Enzyme

* A trial of pancreatic enzymes in large doses is warranted

* Pharmacologic doses exert a suppressive effect on pancreatic secretion by

a feedback mechanism involving proteases, trypsin, chymotrypsin, and

elastase when they reach the duodenum

* Suppression of pancreatic secretion relieves pain by limiting the increase in

pancreatic duct pressure

* Surgical Therapy

* General Considerations

* Patients with debilitating pain for whom medical management fails should be

considered for surgery, in an effort to better the quality of life and avoid

narcotic addition

* Drainage

* In order to remove the obstruction to the flow of pancreatic juice, and

therefore reduce intraductal pressure, the main pancreatic duct is opened

longitudinally along its entire length

* A defunctionalized loop of jejunum is slit longitudinally and sewn to the

pancreatic duct, so that pancreatic secretionsflow into the bowel

* Pain may be alleviated and pancreatic function, though not improved, is not

further compromised

* Denervation.

* Denervation procedures aim at interrupting the transmission of pain from

the pancreas through the sympathetic nerve fibers

* Since the majority of sensory nerves to the pancreas transverse the celiac

ganglia and splanchnic nerves, both transthoracic splanchnicectomy and

ganglionectomy have been used

* They offer variable degrees of pain relief

* Endoscopic Therapy

* Considerable progress has been achieved in applying endoscopic

techniques to the management of chronic pancreatitis

* It is possible to remove stones lodged in the pancreatic duct, directly by use

of a basket

* Removal of stones from the pancreatic duct may restore pancreatic flow and

relieve pain

* Stents may be placed in strictured areas of the pancreatic duct

* The technique is particularly useful when a single stenotic area is located in

the distal duct

* Inserting a stent may reduce intraductal pressure and reduce pain

* Removing obstructions early in chronic pancreatitis may retard the

progression of disease

* In cases of chronic pancreatitis associated with pancreas divisum,

endoscopic sphincterotomy of the minor papilla and stent placement across

the papilla are successful in decreasing the frequency and severity of the

attacks