Balanced (2q minus; 14q plus) translocation.
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Biomedical subjects
Publications and source records attributed to M G Fitzgerald.
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Despite widespread doubts about the quantitative validity or clinical usefulness of lymphocyte response to phytohaemagglutinin (PHA), a satisfactory quantitative test of such responsiveness suitable for the clinical recognition of immunological defects has been developed here. This was achieved by exploring and controlling technical and other variables in the culture of lymphocytes and the quantitation of their response to phytohaemagglutinin. The aspects evaluated included intraperson as well as person-to-person variations, non-lymphocytic cell content, lymphocyte number, PHA batch, atmospheric conditions, culture duration, and quantitation of response. As a result of the information gained from these studies, together with the normal dose-response curve previously established (Fitzgerald, 1971), a satisfactory quantitative and reproducible method suitable for routine clinical use has been realized. This has been applied to the investigation of patients with suspected immunological deficiency disorders, and significant deviations from the normal have been shown. In addition, a PHA dose-response ratio derived from the responses of normal individuals and patients gives a practical quantitative expression of such defects.
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Blood ketone bodies, serum insulin levels, and plasma free fatty acids were examined in a series of patients with "non-ketotic diabetic coma" and compared with the findings in ketoacidotic subjects. Serum insulin levels in six "non ketotic" patients ranged between 1 and 25 muu./ml. and were not significantly different from levels reported in patients with ketoacidosis. In addition, plasma free fatty acids were shown to be unrelated to the degree of ketonaemia. The investigation shows that neither the levels of serum insulin nor those of free fatty acids can explain the absence of hyperketonaemia in some cases.
During eight weeks of a recent influenza epidemic 29 patients with ketoacidosis were admitted to the General Hospital, Birmingham. This was an exceptionally large number of cases. Of these, 14 had complained of a cough, nine had clinical evidence of respiratory infection, and four extensive bronchopneumonia. Hypokalaemia was present on admission in several instances and caused respiratory failure and death in three patients. Since the dangers of initial hypokalaemia are increased during the treatment of ketoacidosis, especially when sodium bicarbonate is used, serum potassium levels must be estimated initially and, if necessary, potassium chloride given intravenously at more frequent intervals than usual.
A survey of ketonuria in insulin-treated diabetics showed that its significance might vary according to the time of day at which the test was performed. Some of the patients had uncontrolled diabetes in the early morning, when severe hyperglycaemia and hyperketonaemia occurred together, while later during the same day or night an episode of hypoglycaemia caused hyperketonaemia, indicating that too much insulin had been given. Correct assessment of the significance of ketonuria is obviously important, because some patients would probably require a decrease rather than an increase of insulin dosage. Ketonuria does not necessarily indicate impending ketoacidosis.
Diabetic retinopathy was present in 7.5% of 5,157 newly diagnosed patients seen at the Birmingham General Hospital Diabetic Clinic between 1960 and 1967. Although die condition becomes commoner with increasing age it is found in 1.5% of patients aged 20 to 39 years. The aetiology is discussed, the conclusion being that in young as in elderly diabetics asymptomatic diabetes of long duration is the main factor.
Lactic acidosis is occasionally responsible for metabolic acidosis in diabetics. It may occur in the presence of normal blood levels of the ketone bodies, and such cases are often described as having "non-ketotic diabetic acidosis." Lactic acid may contribute to the metabolic acidosis in patients with true diabetic ketoacidosis, but the blood lactate concentrations in these patients are not usually very high. In some patients the ketoacidosis is replaced by a lactic acidosis during treatment. This usually occurs in association with a serious underlying disorder and is associated with a poor prognosis. A transient increase in blood lactate concentration was in fact observed in most patients after the beginning of treatment, but the significance of this finding is uncertain.