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Platelet kinectics (using 51Cr labelling) was measured in 66 tests on 59 patients with autoimmune thrombocytopenia (the majority with chronic Werlhof's disease plus cases of acute Werlhof's disease, Evans' syndrome and visceral lupus), measuring platelet survival time, platelet production, and splenic storage rate of platelets. Dependent on the severity of the disease, the elimination curve showed an abnormal course during the initial phase which - in comparison with the normal - indicated approximately a difference of the spleen-dependent part of the disappearance rate from the antibody-dependent destruction. Accordingly, platelet storage in the spleen was slightly supernormal in the studied diseases. On average, platelet destruction was increased to more than twice normal. In 36% of cases platelet production remained within normal range. On average, the least increase in platelet production occurred in the acute form of Werlhof's disease. Maximal storage capacity, which can be six times normal and above, was reached in only a few cases.

Patients with sideroblastic anaemia do not respond to iron or other common haematinics. Since the first report by Harris, Whittington, Weisman and Horrigan (1956) on ‘Pyridoxine‐Responsive Anemia in the Human Adult’, 30 additional cases have been reported in the literature (Gehrmann, 1963). The problem presented by these pyridoxine‐responsive anaemias is underlined by the fact that not all patients with sideroblastic anaemia respond to the administration of pyridoxine, and that in some patients with pyridoxine‐responsive anaemia the effect of treatment is incomplete whereas in others full regression of all abnormalities follows. These different responses to the administration of pyridoxine and certain distinguishing clinical and laboratory features suggest that at least two miscellaneous groups of pyridoxine‐responsive anaemias exist. The available data suggest that some of these patients are actually deficient in pyridoxine and this allows us to distinguish between ‘pyridoxine‐deficiency anaemia’ and so‐called pyridoxine‐responsive anaemia. All the reported cases in the literature can be classified into these two groups. Furthermore, it seems justified to distinguish within the group of pyridoxine‐responsive anaemias cases of either hereditary (‘anaemia sideroblastica hereditaria’) or acquired (‘anaemia refractoria sideroblastica’) origin. Features common to both pyridoxine‐deficiency and pyridoxine‐responsive anaemia are: (1) severe hypochromic anaemia with a dimorphic blood picture and a low reticulocyte count; (2) hyperferraemia and haemosiderosis; (3) maturation arrest of the erythroblasts with sideroblastosis (‘ring’ sideroblasts); (4) an increased iron disappearance rate but a decreased red‐cell uptake; (5) a slightly decreased or a normal red‐cell survival time; (6) absence of an abnormal haemoglobin, and (7) at least some correction of anaemia after the administration of pyridoxine. Present knowledge of these two groups will be discussed in the present report and supplemented by personal observations. Patients with pyridoxine‐responsive anaemia which develops during the course of isoniazid treatment will be excluded, since this drug can induce true pyridoxine deficiency by forming a water‐soluble iso‐nicotinyl hydrazone complex (Williams and Abdulian, 1956).

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