Case-control studies.
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Biomedical subjects
Publications and source records attributed to R L Cumming.
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A 39 year old man who presented with classical Henoch-Schönlein purpura was shown to have mediastinal nodular sclerosing Hodgkin's lymphoma. The Henoch-Schönlein purpura resolved after treatment of the lymphoma.
Aluminium balance studies were carried out on eight patients with various immunological disorders who were receiving plasma exchange with albumin solutions known to be contaminated with aluminium. Four patients with impaired renal function (creatinine clearance less than 50 ml/min) retained between 60% and 74% of the aluminium infused during a single plasma exchange. Transiliac bone biopsy specimens from three patients in this group had a high content of aluminium and showed histological evidence of current or previous bone disease related to aluminium. Two of these patients suffered intermittent bone pain. The main route of excretion of injected aluminium was in urine, only a small proportion of the total input being removed in the "plasma bag" during plasma exchange. The extent of aluminium retention and bone deposition was not reflected by the plasma aluminium concentration before or after plasma exchange. Treatment of five patients with intravenous desferrioxamine increased the plasma aluminium concentration and urinary output of aluminium in those with evidence of aluminium retention. These studies show that patients with poor renal function receiving treatment with albumin contaminated with aluminium retain the metal and deposit it in bone, where it may eventually cause aluminium bone disease. Plasma exchange should be used with caution in patients with renal impairment.
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Hairy cell leukaemia affecting primarily the spleen is a very rare feature of this disease at presentation. Splenectomy in such cases would seem to provide a cure. We report a case of primary splenic hairy cell leukaemia in which clinical and haematological remission were achieved after splenectomy, and we review the literature.
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An association linking multiple myeloma with a higher incidence of carcinomatous tumours has been reported. The following case report describes a man diagnosed as having bronchogenic carcinoma found also to have myelomatosis. Aspects of this association are discussed.
1. Ferritin was isolated from human and horse spleen and liver, and apoferritin prepared therefrom. 2. The electrophoretic mobilities of the four apoferritins were determined on polyacrylamide gels and on cellulose acetate strips, and all found to be equal. 3. Homologous ferritins share reactions of identity in immunodiffusion experiments, whereas heterologous ferritins show only partial identity. 4. The subunit molecular weight of each of the apoferritins was determined by polyacrylamide-gel electrophoresis in sodium dodecyl sulphate and by chromatography on agarose columns in 6m-guanidine-HCl. A value of approx. 18500 was found in all cases. The proteins all had sedimentation coefficients of 17-18S. It thus seems that they have identical quaternary structures. 5. The amino acid compositions of the proteins revealed distinct differences both between organs and between species. This was confirmed by analysis of the tryptic peptide patterns, where it was found that about one-third of the peptides were common to the four proteins and the other two-thirds varied from protein to protein. 6. It is concluded that the apoferritins present in the liver and spleen of human and horse are both organ- and species-specific. 7. The apoferritin isolated from the liver of a patient with idiopathic haemochromatosis was identical with normal human liver apoferritin by the criteria described above.
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1. The mechanism of the stimulation of ferritin synthesis by iron in vivo has been studied in rat liver. Ferritin synthesis and turnover was measured by [(14)C]leucine incorporation. 2. Actinomycin D had no inhibitory effect, after administration of iron, on [(14)C]leucine incorporation into ferritin but appeared to augment the effect of iron on ferritin synthesis. 3. Cycloheximide completely abolished the stimulation by iron of [(14)C]leucine into ferritin and was subsequently utilized to show that iron acts in vivo by translational induction of apoferritin synthesis, rather than by stabilization of apoferritin or its precursors. 4. This conclusion was confirmed by showing that 2 days after acute bleeding, when iron was in the process of being removed from hepatic ferritin stores, ferritin synthesis was decreased whereas breakdown rates were unchanged.
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