Summary. Eighty‐eight cases of severe pancytopcnia closely following the onset of apparently typical viral hepatitis have been described. We report two additional patients. Remarkable features of the syndrome are the rapid, high mortality (88%) and the fact that the age and sex distribution parallel that of hepatitis, not that of other wries of aplastic anaemia. Although viral damage to haematopoietic cells can be demonstrated in vitro, chromosonies in our patients were normal after short‐term culture of peripheral lyrnpliocytes. Therapeutically, androgens may be of some benefit despite the high mortality. No adequate explanation for the association is available, but infectious hepatitis should be accepted as a potential cause of aplastic anacmia.
The X-linked anaemia of mice (gene symbol, sla) is hypochromic and microcytic, and the stainable iron stores are reduced. Chemical estimates of total body iron content and serum iron concentration show low values and the total serum iron binding capacity is elevated in anaemic mice. Rapid plasma iron clearance and increased iron utilization provide further confirmation of iron deficiency in anaemic animals. Alterations in activity of haem-containing enzymes have been sought in the heart, liver and kidney of anaemic mice, and slightly decreased activity found only in kidney cytochrome oxidase.The blood volume of mice with X-linked anaemia is increased in spite of decreased red cell mass, and thus the anaemia is in part due to dilution. The cause of the increased blood volume has not been elucidated, but it may be related to splenic enlargement. In contrast to iron depleted humans and experimental animals, mice with X-linked anaemia show impaired rather than increased intestinal iron absorption, indicating that the anaemia is a consequence of iron malabsorption. The defect in iron absorption may be an isolated one, since evidence of impaired retention of orally administered radio-iodinated tciolein, radio-zinc, radio-copper and radio-cobalt has not been found. It is suggested that the genetically-determined defect in the intestinal mucosa of mice with X-linked anaemia may be due to deficiency of either an enzyme or a carrier substance necessary for the normal transfer of iron from the intestinal mucosal cell to the plasma.The X-linked anaemia of mice is inherited as a recessive trait. The mutation arose in a mixed stock of mice following radiation, and the locus was shown to be near Tabby (Ta) and Brindled (Mo") on the X chromosome (Falconer & Isaacson, 1962). The gene symbol is sla, standing for sex-linked anaemia. The anaemia is hypochromic and microcytic (Grewal, 1962;Bannerman & Pinkerton, 1967). In young hemizygous male (sla/ -) and homozygous female (sla/sla) animals the haemoglobin concentration is generally between 5 and 8 g / I m ml. Spontaneous improvement may occur with age, and a rapid rise in haemoglobin and haematocrit follows
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