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Biomedical subjects

E K Blackburn

Publications and source records attributed to E K Blackburn.

At least 19 recordsLinked to original sources
PubMed1978

Percutaneous liver biopsy and chronic liver disease in haemophiliacs.

Systematic screening of forty-seven haemophiliacs in Sheffield revealed abnormal liver-function tests in thirty-six (77%), with a tendency for these abnormalities to persist. To assess the importance of these abnormalities, percutaneous liver biopsy was carried out on eight symptom-free patients under factor-VIII cover. A wide spectrum of chronic liver disease was demonstrated, including chronic aggressive hepatitis and cirrhosis. The liver pathology bore no relation to clinical history or to biochemical findings. Hepatitis-B-virus markers were common, but evidence suggests that this is not the only factor contributing to the development of liver disease. The high incidence of chronic liver disease seems to be a recent development and is probably related to factor-concentrate replacement therapy.

Adult↗
PubMed1978

Cellular hyperviscosity as a cause of neurological symptoms in leukaemia.

Six patients with various forms of leukaemia had neurological signs and symptoms associated with an extremely high white blood cell count and increased whole blood (but not plasma) viscosity. All were treated by leucapheresis with an Aminco Celltrifuge. Rapid and complete reversal of all symptoms occurred in three patients and partial recovery in one. One patient died shortly after leucapheresis and another (from cerebral intravascular coagulation) two days later. It is concluded that a cellular hyperviscosity syndrome may cause neurological dysfunction in patients with extremely high white cell counts, and that leucapheresis, in carefully selected patients, can be an effective method of treatment.

Adult↗
PubMed1977

Heparinised clotting factor concentrates in patients with Christmas disease and liver disease.

Evidence has been sought of activation of the coagulation system in two groups of patients following the infusion of two heparinised clotting factor concentrates. No changes were detected in 13 patients with mild hepatic dysfunction. In six studies on patients with Christmas disease induced abnormalities occurred in only one. Activation of the coagulation mechanism did not occur in another individual who had received the same batch of material.

Blood Cell Count↗
PubMed1975

Serial changes in the coagulation system following clotting factor concentrate infusion.

Various parameters of the coagulation system have been monitored in patients with Christmas disease following the infusion of clotting factor concentrates. Significant reduction of clotting factor VIII and serum antithrombin III were observed in each of the five studies, whilst the plasma fibrinogen level fell in four subjects. The induced abnormalities were shortlived and there were no clinical sequelae. Further studies are required to assess the effects of similar concentrates in patients with liver disease.

Antithrombins↗
PubMed1975

Skin window studies in polycythaemia rubra vera.

The inflammatory response was studied in patients with primary polycythaemia by means of a modified skin window technique. In untreated patients, the overall cellularity was a prominent feature and, as compared with the controls, the 48 h preparations showed a significantly greater percentage of granulocytes with a corresponding decreased percentage of macrophages. In the peripheral blood of these patients, both total white cells and granulocyte counts were significantly higher than in the control subjects. A highly significant relationship between the blood and skin window neutrophils was demonstrated. In polycythaemia patients in remission, the results were generally similar to the controls, except that there was still a highly significant increase in the percentage of skin window basophils. The results provided no evidence of a defect in cell migration or in the phagocytic activity of macrophages in polycythaemia vera. Possible mechanisms of the cutaneous basophilia and its relevance to the manifestation of this disorder are discussed.

Adult↗
PubMed1974

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↗