Hypochromic Anemias of the Tropics Associated with Pyridoxine and Nicothnic Acid Deficiency

Two cases of hypochromic anemia with erythronormoblastic marrows and giant stab-cells are reported. Both cases deteriorated when only on iron treatment; the first responded to pyridoxine therapy and the second to nicotinic acid.

Neither of the patients had diarrhea or steatorrhea and all were on the normal tropical hospital diet, similar to that given to the other patients who responded to iron therapy alone. The patients were under our constant control and were in the hospital from three to four weeks and had no other treatment. The diet of these two patients before they entered hospital did not appear to differ from that of other Africans with whom we have been dealing.

The presence of G.S.C. in the marrow is in our opinion associated with a deficiency of folic acid, due either to malabsorption following the anemia or low intake associated with poor appetite. In many cases G.S.C. disappear during treatment with iron alone, perhaps due to improvement in absorption or appetite. In others supplementary folic acid is necessary.^31,32,34

Bone marrow biopsy done in eight other cases of pellagra showed no giant stab-cells and the marrow was normal except for an increase in plasma cells and eosinophils.

We do not think that pyridoxine or nicotinic acid were responsible for their presence in these cases, since giant stab-cells are found in all megaloblastic anemias and in some cases of hypochromic anemia, as well as in other conditions where there is no evidence of either pyridoxine or nicotinic acid deficiency.

There was nothing significant about the serum proteins which were within normal range; the albumin globulin ratio was, however, reversed in both patients (tables 1 and 2) and remained so on discharge from hospital. This reversed A/G ratio is common in many Africans and Indians, is not related to anemia and may be associated with diet or be genetically determined.^31-32,35,36

Until the exhibition of pyridoxine and nicotinic acid the patients were making no progress, but afterwards they made an uninterrupted cure and were discharged from the hospital feeling well.

The reticulocytosis was the expected one for the blood count and hemoglobin level, and as will be seen from figures 1 and 2 did not occur until after either pyridoxine or nicotinic acid had been given.

As in Dinning’s and Day’s pyridoxine deficient rats we also found in our pyridoxine-treated patients that there were increased R.B.C. counts and low hemoglobins with the mean corposcular hemoglobin of 20γγg. and 17 γγg.

In eight other cases of typical pellagra there was, however, no sign of anemia at all, the hemoglobin range being between 15 to 16 Gm. per 100 ml.

At this altitude (6,000 feet) "pure" iron deficient anemia is rather rare³² and it was no surprise to us that these two cases failed to respond to iron therapy alone and that they needed other factors.

Pyridoxine appears in some way to be associated with hemopoiesis. Its absence does not in all cases give rise to anemia but sometimes produces abnormalites in red and white cell maturation and hemoglobin production in man and animals.

The role of nicotinic acid in hemopoiesis is obscure.

We realize that two swallows do not make a summer, and we have no idea how important a part pyridoxine and nicotinic acid play in hemopoiesis. Since, however, such pyridoxine and nicotinic acid-responding cases are rather infrequent we thought it worthwhile to record these two cases.