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Biomedical subjects

F E Preston

Publications and source records attributed to F E Preston.

At least 253 records · Page 14Linked to original sources

Essential thrombocythaemia and peripheral gangrene.

Six patients are described in whom gangrene of one or more toes occurred as the presenting feature of essential thrombocythaemia. Spontaneous platelet aggregation was observed in platelet-rich plasma from four patients and platelet aggregation after the addition of adenosine diphosphate and collagen was highly abnormal in samples from all six. All of the patients described dramatic relief of pain within six hours of ingestion of aspirin and this coincided with disappearance of the spontaneous platelet aggregation and collagen-induced platelet aggregation. Treatment with phosphorus-32 corrected the platelet count and there were no further recurrences of peripheral vascular disease. Platelet function tests performed at the time all gave normal results. It is concluded that essential thrombocythaemia is an important and treatable cause of peripheral vascular disease.

Adenosine Diphosphate↗

The kidney and intravascular coagulation in myelomatosis.

In 15 out of 35 patients with myelomatosis histological examination showed intravascular fibrin within the glomeruli, and this was associated with proliferation of the mesangial complex in 12. The presence of intravascular fibrin and mesangial proliferation was not associated with any specific immunoglobulin abnormality or with the presence or absence of Bence Jones proteinuria. In addition to fibrin being present within glomerular capillaries it was also shown in intertubular capillaries in three cases of myelomatosis with acute tubular necrosis. It is suggested that intraglomerular coagulation and fibrin deposition may contribute to the genesis of renal failure in myelomatosis.

Acute Kidney Injury↗

Disseminated intravascular coagulation as a consequence of cerebral damage.

Three cases with intracranial lesions developed evidence of disseminated intravascular coagulation which was confirmed at necropsy. The factors engendering this state, including release of potent thromboplastin from neural tissue are discussed and the danger of this intermediary mechanism of disease increasing the mortality of intracranial disease is demonstrated. Careful haematological investigation of all patients with intracranial disease is therefore advised, especially if they manifest evidence of a bleeding tendency.

Adult↗

Intravascular coagulation and E. coli septicaemia.

Eight patients with E. coli septicaemia had oliguric renal failure which was associated with haematological evidence of intravascular coagulation. Five of these patients also had the characteristic blood picture of microangiopathic haemolytic anaemia. In an attempt to prevent further deposition of fibrin, intravenous heparin was administered to six patients, three of whom recovered fully and three died. The diagnosis of intravascular coagulation was subsequently confirmed by histological examination of necropsy material and it is suggested that some of the complications of E. coli septicaemia may be attributable to disseminated intravascular coagulation.

Anemia, Hemolytic↗