Talk:Glycogen storage disease type I
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Hi, I have a degree in biochemistry and I know that humans can't make glucose from acetyl-coa, as stated in the article.
:you are right; fixed; thanks and please contribute alteripse 22:25, 18 March 2007 (UTC)
Hello
type I GSD can exist in two forms; type IA and type IB, with a small difference in clinical picture, yet there is no mention of that here
:It's now mentioned beginning in the Genetics section of the article. We might want to first mention it earlier. RJFJR (talk) 22:27, 23 December 2017 (UTC)
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Why adding KCl ??
please answer is needed:
if you read physiology: potassium compete with hydrogen ions for excretion by the kidney.
and I am oriented that acidosis result eventually in hyperkalemia & hyperlalemia result eventually in acidosis.
why he recommended giving KCl in case of acidosis ! !
I believe that there was misunderstanding because the example given was repeated vomiting, so the source possibly was talking about the treatment of the vomiting, not the treatment of acidosis episode in GSD 1
yasir al-bayati — Preceding unsigned comment added by Yasir muhammed ali (talk • contribs) 19:20, 16 March 2018 (UTC)
Concerned about plagiarism
The following segment contains a reference to a page number, wikipedia pages do not have page numbers. I am concerned that this section of text, or the entire diagnosis section was lifted from another work.
Once the diagnosis is suspected, the multiplicity of clinical and laboratory features usually makes a strong circumstantial case. If hepatomegaly, fasting hypoglycemia, and poor growth are accompanied by lactic acidosis, hyperuricemia, hypertriglyceridemia, and enlarged kidneys by ultrasound, GSD I is the most likely diagnosis. The differential diagnosis list includes glycogenoses types III and VI, fructose 1,6-bisphosphatase deficiency, and a few other conditions (page 5), but none are likely to produce all of the features of GSD I.