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Anemia (megaloblastic)


Q-A 1

Q (t) We are searching informations concerning " megaloblastic anaemia " or " vitamin B 12 deficiency is a primary cause of megaloblastic anaemia ", but we didn't find anything right and precise.

Could you help us to get through ?

If possible, could you send us references to consult ?

A (t) We will give a general answer, concerning healthy as well as HIV infected persons. Then, we will indicate some features specific to HIV infection and AIDS.

Megaloblastic anaemia is an anaemia (blood hemoglobin level lower than 12g/100ml) with a very high mean globular volume (MGV) (higher than 120µm3). Megaloblasts can be observed on the myelogram, indicating an alteration of the DNA synthesis at the level of the red blood cell precursor. The origin may be obvious : folic acid deficiency (intake deficiency secundary to an important denutrition), malabsorption (secundary to a surgical resection of the small intestine, gastrectomy, intestine stenosis, intestinal fistula, and over all by intestine malabsorption, whatever the reason, which leads to diarrhea), relative deficiency (multipara women), in case of a chronic stimulation of the marrow, due to haemolytic or refractory anaemia, use deficiency (alcoholism, antifolic drugs).

In all these cases, folic acid dosage allows to confirm the diagnostic and the test treatment by folic acid is justified.

When the cause is not obvious, a Biermer disease may be suspected. The confirmation of this diagnostic is based on the existence of a vitamin B12 deficiency by blood dosage (acid folic level being normal in these case) and stomach anomalies (lack of chlorhydric acidity, stomach atrophy visualised by fibroscopy, lack of intrinsic factor (protein synthetised at the stomach level allowing the absorption of vitamin B12) in the gastric liquid, or Schilling test, revealing a drastic decrease of vitamine B112 absorption with a possible correction of the discorder by administration of intrinsic factor, and to eventually demonstrate the presence of anti intrinsic factor antibodies).

Apart from Biermer disease, other causes should be investigated : botriocephalic anaemia (over all in lake regions) in wich vitamin B12 is consumned by the worm (as well as in the case of an intestinal infection, particularly " anse borgne " syndrome), unknown intestinal malabsorption (whithout diarrhea and weight loss) often associated with a folic acid, vitamin B12 and iron deficiency. There is another form of rare megaloblastic anaemia, primitive and pre-leukemic that should be considered when the blood levels of the two vitamins are normal. There are also some rare genetic causes responsible for vitamin B12 malabsorption among children.

Concerning HIV infected persons, vitamin B12 blood level is frequently very low when T4 lymphocytes count is very low. Actually, some minors intestinal vitamin B12 absorption disorders may exist at early stages of the infection, due to the presence of HIV in intestinal cells. At an early stage of HIV infection, vitamin B12 deficiency is present for 24 to 36% of persons living in occidental countries. When vitamin B12 level is normalised by supplementation, an improvement of T4 lymphocytes count and cognitive functions is sometimes noted. A more recent study showed that the risk of evolution to AIDS is twice higher for persons with a low blood level of vitamin B12 (this study is summed up on our internet website <http://www.positifs.org/> C.22, chap. V paragraph 1). Another study that we also summed up (C.22, chapter V, paragraph 4) showed that vitamin B12 and folic acid blood levels are not influenced by oral supplementation, wich could be explained by a decrease of the intestinal absorption.

It has been also shown that for persons wich almost normal T4 lymphocytes level, low level of vitamin B12 is secundary to AZT treatment. Concerning AZT, an isolated and often moderate macrocytosis is frequently observed (without anaemia), signing a moderated marrow toxicity. (9709)



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1st version: October 1998.

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