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D Malcolm

Publications and source records attributed to D Malcolm.

36 records · Page 2Linked to original sources

Dissociation between hepatosplenic and marrow iron in liver cirrhosis.

Histochemical study of tissue iron in the various parts of the reticuloendothelial system in 15 subjects with cirrhosis was performed. Stainable iron in the liver and spleen sections, generally in large quantities, was found in 13 of 15 cases. Paradoxical association of hepatosplenic siderosis with depletion of marrow iron reserves was observed in seven subjects. In all seven, gross gastrointestinal blood loss had occurred during life and the source of bleeding from one or more anatomic lesions was identified at the time of autopsy. Depletion of marrow iron reserves in these seven subjects can be attributed to two factors: first, the available marrow iron stores were used for erythropoiesis; second, the ample hepatosplenic iron deposits could not be mobilized for transport to the bone marrow. Thus, hepatosplenic iron in cases of cirrhosis seems to be sequestered from its normal metabolic pathways.

Adult↗

Hemosiderosis in hemodialysis patients. An autopsy study of 50 cases.

The distribution of stainable iron stores was investigated in various organs of 50 hemodialysis patients with chronic renal disease. Massive iron deposits were found in the liver and spleen. Among 18 patients with severe hepatosplenic siderosis, iron deposits were abundant in the adrenal glands, lymph nodes, and lungs and were sparse in the heart, kidneys, and pancreas. There was an absence or scarcity of stainable iron in bone marrow of 19 pats. In five of these marrow-iron-depleted patients, serum concentrations of ferritin were high. In long-term hemodialysis patients, a variety of factors make massive iron overloads of various organs a likely occurrence, severe hepatosplenic siderosis may occur in marrow-iron-depleted patients, and serum ferritin levels in this setting may not always accurately reflect the status of marrow iron store.

Adult↗

Intraventricular thrombosis in polycythemia vera: A cause of intractable cardiac failure.

The occurrence of thrombotic events is central to the course of polycythemia vera. Myocardial, cerebral, peripheral, and pulmonary infarctions are frequent and are consequences of throbmoses in small and medium caliber arteries. Thrombosis in large caliber arteries is a rare event. Thrombosis within the chambers of the heart has not been hitherto reported. This report documents the occurrence of massive left ventricular thrombosis in a patient with polycythemia vera. The throbmus reduced the left ventricular capacity by about 75% and caused intractable congestive heart failure.

Aged↗

Lead poisoning.

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Humans↗

The lead problem.

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Environmental Pollution↗