Edema & Other Interesting Facts Re:Malabsorption

[Guest guest]

Steve,

You wrote, " I have a serious problem with bloating and my MD's have me on

Lasix for this problem, knowing full well my main health issue is CP. "

A lot of doctors are not aware of the drug interactions and side effects that

many can cause. I also find that many health care providers do not understand

the different pathophysiology involved with different conditions, i.e.,

edema. There are generally five causes for edema: 1) increased hydrostatic

pressure, 2) lymphatic obstruction, 3) sodium retention, 4)

increased endothelial permeability, 5) hypoprotenemia. the last one being the

most

likely cause for persons with pancreatitis and subsequent malabsorption.

Diuresing someone who with protein malabsorption will not reduce the amount

of edema, but will likely throw the patient into an electrolyte imbalance. And,

as contrary as this sounds, giving someone more protein, will not resolve the

problem of malabsorption hypoprotenemia. It is complicated. Edema develops

from the impaired absorption of amino acids, the building blocks of proteins.

The body can't absorb " proteins " , per se, only, after they are broken down. It

is following the impaired absorption of amino acids that causes the protein

depletion and hypoprotenemia.

In normal malabsorption, the diet of choice is low fat, low carbohydrates,

and high protein.

In pancreatitis, protein precipitates can block the pancreatic duct.

Additionally, there is a diminished secretion of trypsin. When vitamin B12 from

the

protein is ingested, a nonspecific R-protein found in the GI fluids, binds with

it and does not allow its binding to intrinsic factor (IF) from the stomach.

The IF-VitB12 complex is necessary for the active absorption of the B12,

therefore resulting in Vit B12 malabsorption, a type of hypoprotenemia.

An interesting point about fat malabsorption, is that the steatorrhea

consists mainly of Triglycerides, esterified fats, in contrast to the

steatorrhea of

sprue, (which I mentioned in an earlier post), which are free fatty acids. It

is an interesting point when evaluating our Triglyceride levels and the

concurrent cause for pancreatitis. This is also an interesting point for those

considering trying a gluten free diet. For persons with pancreatitis, the fat

from

gluten breakdown, or sprue is the primary source of fats for our bodies. And,

as weird as it is, our bodies need fat to absorb fat soluble vitamins. So,

this source is suggesting that we do not eliminate the sprue from our diets.

Another interesting fact is that carbohydrate malabsorption is uncommon in

pancreatitis, since loss of 97% Amylase secretion is necessary for the

malabsorption of starch. That may account for a portion of why many have trouble

with

weight loss.

Yet another fact re: treating malabsorption is that the lipase enzyme taken

or produced by the body is irreversibly inactivated by a pH less than 4.0;

therefore, it is necessary to keep the gastric pH above 4.0 or more for at least

an hour pc, or after meals. Treatment is either to administer larger than

needed doses of lipase, antacids before the meal, or to administer an H2

blocker,

like tagamet. I found this interesting that there is a reason for the H2

blocker other than the complaints of gastric reflux. If you are having a trouble

with steatorrhea and you are not on an H2 blocker, this would suggest that you

might want to discuss with your health care provider.

Sodium Bicarbonate and Aluminum Hydroxide are the only antacids that are

effective in further reducing steatorrhea, if they are given before the meal.

Other antacids, like Magnesium-Aluminum Hydroxide or Calcium Carbonate tend to

increase steatorrhea. Hmmm?

This source of information comes from Guide to Pathophysiology, Lippincott &

, 2003 & Manual of Gastroenterology, Little Brown & Co. 2000

Karyn E. , RN

Executive Director, PAI

http://www.pancassociation.org

Pancreatitis Association International