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A case of an IgA deficient child who developed several autoimmune diseases namely, celiac disease, pernicious anemia, autoimmune thyroiditis and autoimmune thrombocytopenic purpura is reported; the possible connections and etiology of these phenomena is briefly discussed. Individuals with selective IgA deficiency should no longer be considered "normal".
Previous studies of the effect of scandium on the tissue distribution of Ga-67 suggest that Ga-67 makes its initial in vivo entry into normal and malignant tissues by different routes. (Scandium blocking of plasma protein Ga-67 binding increased Ga-67 excretion, decreased its uptake in normal tissues, but had little effect on rodent tumors.) In further studies we have used other methods to alter the plasma binding of Ga-67. Iron saturation of plasma produced effects on Ga-67 tissue distribution similar to those observed with scandium. On the other hand, increasing Ga-67 plasma binding through induction of anemia and administration of apotransferrin produced the reverse of the effects observed with scandium and iron. We conclude that the initial in vivo entry of Ga-67 into tumor tissue involves mainly an unbound or loosely bound form of Ga-67, whereas its uptake by normal soft tissues is strongly promoted by its binding to transferrin.
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Five episodes of iron deficiency anemia associated with pruritus were observed in 4 women. In contrast to the majority of cases in the literature the pruritus in our patients was localized and not generalized. It disappeared 1--14 days after the beginning of iron replacement. --Iron deficiency should be considered in the differential diagnosis of both generalized and localized pruritus. The literature suggests that pruritus associated with low serum iron levels in malignancy may respond to iron therapy
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The pool size of erythroid burst-(BFUe) and colony-forming units (CFUe) has been evaluated in normal or hypoxia-induced polycythemic mice at sequential times after either transfusion or administration of purified erythropoietin (Ep). The present investigations were focused on the in vitro tritiated thymidine (3H-TdR) suicide index of the erythroid precursors in these two experimental models. After transfusion an early but transient decline of the DNA sythesis index was observed in the BFUe pool, whereas this parameter showed a later, more prolonged decrease within the CFUe population. Symmetric patterns were documented after Ep injection: an early, transient elevation of the 3H-TdR sensitivity at the BFUe level and a late, more persistent rise within the CFUe compartment. In all experiments no modification of this indes was observed within the pool of the CFUe. These fluctuations of BFUe and CFUe cycling were temporally consistent with modifications of their respective pool size, as previously reported. Thus, variations of the pool size may be at least partially mediated by the cycling activity. Furthermore, early fluctuations of BFUe proliferative rate indicate that, after erythroid perturbations, this pool may initially be sensitive to and regulated by modifications of Ep activity. Later, however, compensatory mechanisms allow the BFUe to escape from this early Ep influence, thus leading its cycling activity and pool size to return to normality and stabilize.
Eight intramuscular injections of 200 mg/kg of iron (DFe), given as iron dextran twice weekly in the week before and the three weeks after intravenous infection with about 10(7.5) colony-forming units of Mycobacterium avium, significantly prolonged (by about 11 days) the mean 'time-to-death' of immature male fowl (Gallus domesticus) compared with corresponding regimes using dextran (Dx) only or saline, When a proportion of the birds were examined 21 days after infection many of the abnormalities associated with the disease, including a marked hypochromic anaemia, were less severe in DFe-treated than in the Dx- or saline-treated chicks and there were about 10- to 85-fold fewer viable tubercle bacilli in the liver and spleen of the DFe-treated birds.
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Chicks aged 15 days were infected orally with 10(6-4) living Salmonella gallinarum. Iron from iron dextran or ferric ammonium citrate (DFe and CFe respectively), in doses of 2-0 or 0-4 mg/kg given intramuscularly at the time of infection, had no effect on subsequent mortality compared with infected controls. Increasing the amount of CFe to the maximum (20 mg/kg) that was non-toxic intramuscularly was also ineffective but when the dose of DFe was increased to 20 or 50 mg/kg the survival rate rose sharply. If given at other times in relation to the time of infection, or more frequently, 50 mg/kg or more of DFe was less active. The increased survival rate among infected chicks given 50 mg/kg of DFe at the time of infection was accompanied by decreases in the severity of the morbid changes in the disease, and by reductions of between c 10- to 100-fold in the numbers of viable S gallinarum in the liver, spleen or blood at the height of the acute infection. DFe (50 mg/kg) given at the time of infection also eliminated the difference in the survival rate noted previously between infected chicks fed respectively with diets containing fish or meat meal as the sole source of supplementary protein.
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Histochemical studies were performed on tissues from piglets of different ages treated orally with iron dextran soon after birth. The mucosal cells in the distal region of the small intestine were heavily laden with stainable iron granules during the first three days after the iron administration. The absorptive epithelial cells are desquamated within seven to ten days after birth. Consequently, the number of iron granules gradually diminishes during the first seven days after treatment and no iron granules are demonstrated 12 days after the administration of iron. The iron dextran complex is pinocytosed in newborn piglets and then transported via the lymphatic system. Thus the sinusoidal lining cells of the body and mesenteric lymph nodes are already heavily laden with iron granules 24 hours after oral treatment. This iron store is released only slowing during the first weeks of life. Great amounts of iron granules are demonstrated in the liver and spleen macrophages during the first week after the administration of iron. Due to the rapid utilization of iron in growing piglets these iron stores diminish sharply during the weeks following birth. The distribution of stainable iron in the lymph nodes, liver and spleen seven days after intramuscular injection of iron dextran in newborn piglets was comparable to that for oral administration at that stage of the experiment.
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