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Biomedical subjects

M A Howard

Publications and source records attributed to M A Howard.

At least 91 records · Page 5Linked to original sources
PubMed1979

Abnormal factor VIII in chronic renal failure.

Factor VIII procoagulant activity (VIII-C), related antigen (VIII-AG), and von Willebrand factor (VIII-vWf) were measured in 38 patients with chronic renal failure (CRF), in 19 patients with normal renal function from a general medical ward, and in 17 normal subjects. Wide variation in the levels of factor VIII (FVIII) functions were found in the group of CRF patients. There was no correlation between the levels of the three individual activities of FVIII in renal disease. The levels of the three functions were elevated in the patient controls and no significant differences were found between the two groups of patients, although both groups were significantly different from the normal subjects. Increased electrophoretic mobility (EM) was detected in 22 of the 38 patients with CRF (58%) compared to seven of the 19 patients controls (37%). These studies suggest caution in interpretation of changes in FVIII status in patients with other clinical disorders, such as liver disease.

Antigens↗
PubMed1978

Demonstration of a platelet bypass mechanism in the clotting system using an acquired anticoagulant.

A lupus-type anticoagulant which causes strong inhibition of the partial thromboplastin time with kaolin (PTTK), the stypven time, and the thrombin generation tests has been investigated. All tests for platelet function were normal, as were all specific coagulation factor assays with the exception of a slightly reduced factor XI in this patient. A diethylaminoethyl-cellulose-immunoglobulin (DEAE-cellulose-IgG) fractionation of the patient's plasma produced two peaks containing inhibitory activity in the PTTK test. The first of these peaks had a cloudy appearance, suggesting the presence of immunoglobulin aggregates. Studies with IgG aggregates prepared from normal IgG and from the patient's IgG demonstrated that such aggregates were not the cause of inhibition. It was possible to neutralize the inhibitory activity of the purified IgG but not platelet-poor plasma (PPP) with a rabbit anti-IgG. The inhibition of the patient's PPP in the thrombin generation, the contact product, and the stypven time tests were corrected by the inclusion in the test system of platelets activated either by aggregation due to adenosine diphosphate (ADP) or formalin fixation and washing. These studies lend support to earlier findings that platelets interact at several sites in the coagulation cascade.

Antibodies↗
PubMed1973

Hereditary giant platelet syndrome: a disorder of a new aspect of platelet function.

The platelets of three patients with the hereditary giant platelet syndrome of Bernard and Soulier failed to aggregate in response to either ristocetin or bovine fibrinogen. The results of aggregation experiments using mixtures of platelets and plasma suggest that a reaction between a plasma factor deficient in von Willebrand's disease and a platelet component lacking in our patients, and leading to platelet aggregation independently of adenosine diphosphate (ADP), is essential for normal haemostasis.

Adenosine Diphosphate↗