Secretor state of patients with insulin dependent or non-insulin-dependent diabetes mellitus.
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Biomedical subjects
Publications and source records attributed to A Collier.
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In order to investigate whether the ability of peripheral blood monocytes to bind bacteria is impaired in diabetes, we studied carbohydrate-binding ("lectin-like") receptors and the receptor for the Fc portion of immunoglobulin on monocytes from 25 male Type 1 (insulin-dependent) diabetic patients and 10 age-matched healthy control subjects. Peripheral blood monocytes from the diabetic patients expressed lower levels of "lectin-like" receptors compared to the control subjects, whereas the expression of the receptor for the Fc portion of immunoglobulin was similar in both populations. There was no correlation between the degree of "lectin-like" binding activity and plasma glucose concentration or glycaemic control. Recognition of unopsonized bacteria by the "lectin-like" receptor is impaired in Type 1 diabetes; this may affect the efficient elimination of potential pathogens.
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We describe two insulin-dependent diabetic females who presented with severe hypoglycaemia associated with atrial fibrillation which reverted to sinus rhythm after intravenous dextrose. Atrial fibrillation has not previously been reported as a complication of hypoglycaemia in insulin-dependent diabetic patients.
Numerous platelet abnormalities, particularly hyperaggregation, have been described in diabetic patients, and it has been suggested that these may contribute towards the pathogenesis of microvascular complications. In the present study, the changes that occur in ADP-induced aggregation, sensitivity to a stable prostacyclin analogue (Iloprost), aggregation-induced thromboxane B2 production and platelet cyclic AMP levels were investigated in 9 young insulin-dependent diabetics, in which the glycaemic control significantly improved in one group (n = 5; HbA1 from 11.9-9.0%) over a 6 month period. With improvement of glycaemic control there was no significant change in the concentration of ADP required to produce 50 percent of the maximum aggregation wave response. However, there was a significant increase in the responsiveness of platelets to Iloprost and increased platelet thromboxane B2 production. There was no significant difference between the basal platelet cAMP levels before or after exposure to Iloprost. This study suggests that with improved short-term glycaemic control, although there are changes in platelet function, there may be no alteration in the homeostatic balance.
Acquired immunodeficiency syndrome (AIDS) is the lethal end stage of a sexually transmitted disease caused by a virus that is producing the major epidemic of our century. In this article we describe the history and epidemiology of AIDS and the disease states associated with infection with the human immunodeficiency virus (HIV), the apparent cause of AIDS. We review what is known about disease pathogenesis and present an overview of clinical management issues. In the absence of vaccine or therapy to prevent and eradicate this viral infection, we present formative educational approaches for its control.
After all previous antihypertensive treatment had been stopped, blood pressure and glucose tolerance were measured in 16 hypertensive non-insulin treated diabetics before and again six weeks after treatment with captopril, an angiotensin-converting enzyme inhibitor. Supine blood pressure fell from 184 +/- 4.1/103 +/- 2.6 to 165 +/- 5.2/88 +/- 2.1 mmHg (P less than 0.001) and erect from 179 +/- 5.2/102 +/- 3.2 to 158 +/- 5.6/87 +/- 2.6 mmHg (P less than 0.005). The area under the oral glucose tolerance curve fell from 2313.6 +/- 154 to 2192.8 +/- 146 mmol/min/l (P less than 0.02). There was no change in plasma insulin, total glycosylated haemoglobin or fructosamine. Four patients who failed to show lowering of supine diastolic pressure below 95 mmHg were additionally given oral frusemide with further improvement in blood pressure and no alteration in carbohydrate intolerance. It was concluded that captopril alone is usually an effective antihypertensive agent in non-insulin dependent diabetes with the addition of frusemide benefiting resistant cases. Glucose intolerance did not worsen with either captopril alone or captopril plus frusemide.
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Platelet aggregation to collagen in 12 Type 1 (insulin-dependent) diabetic patients with background retinopathy and 12 Type 1 diabetic patients with proliferative retinopathy was compared with an age- and sex-matched control group. An analogue of prostaglandin H2, 11,9 epoxymethano-prostaglandin H2, which directly stimulates thromboxane receptors, and EP 092, which is a competitive thromboxane A2 receptor antagonist, were used to investigate changes at platelet thromboxane receptor level in these groups. The concentration of collagen (EC50) required to give 50% of maximum aggregation did not differ between the two diabetic groups and the control group. However, platelets from the proliferative retinopathy group were significantly more sensitive to the thromboxane mimetic (11,9 epoxymethano-prostaglandin H2) (p less than 0.005) than the background retinopathy and control groups. This change may be a factor in the development of proliferative retinopathy.
This study was designed to assess the density characteristics of platelets from controls (N = 10) and three groups of diabetics (N = 32) exhibiting various degrees of glycemic control. With continuous gradients of Percoll, platelets from controls and diabetics (N = 8) with an HbA1 less than or equal to 9% formed a band extending from 1.0625 g/ml to 1.0925 g/ml with a mean platelet density of 1.0775 g/ml. In the two groups of diabetics with HbA1 greater than or equal to 10%, there was an increase in the proportion of low-density platelets recovered on the gradients and the mean platelet density was reduced to 1.0750 g/ml (HbA1 = 10-13%) and 1.070 g/ml (HbA1 greater than or equal to 14%). All three groups of diabetics had normal levels of intraplatelet ATP/ADP and beta-thromboglobulin. It is unlikely that in vivo degranulation of platelets after activation was responsible for the altered density profiles. We propose that abnormal platelet subpopulations with low density but normal intraplatelet granule content were responsible for the changed density profiles.
Thirteen hypetensive non-insulin dependent diabetics (9 male, 4 female, mean age 61.6 +/- 6 years) were given 6 weeks treatment with captopril in a dose range 75-150 mg/day. Each patient underwent a standard glucose tolerance test and had blood pressure profiles recorded before and after captopril. Supine systolic blood pressure (mmHg) improved from 181 (+/- 16) to 162 (+/- 17) and diastolic blood pressure from 103 (+/- 11) to 89 (+/- 9). A similar improvement was seen in erect systolic (174 +/- 19 to 156 +/- 19) and diastolic (103 +/- 14 to 87 +/- 11) blood pressures. Following treatment there was no significant change in glucose tolerance although the 120 minute plasma glucose value improved from 15.3 +/- 4.2 to 13.9 +/- 3.4 mmol/l (P less than 0.05). The drug was well tolerated and free of adverse effects. Captopril would therefore appear to be an effective and safe anti-hypertensive agent in non-insulin dependent diabetes and did not result in any deterioration of glucose tolerance.
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Giant cerebral evoked potentials have been observed in a case of brain stem tumor and in hydrocephaly. The mechanism of the amplitude augmentation has been discussed.
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Lower limb venous compliance and transcapillary escape rate of transferrin were measured in eight normotensive, insulin-dependent male diabetic patients and eight control subjects using a dual isotope technique. Technetium-99m labelled autologous erythrocytes were used to measure venous compliance and to correct for local changes in blood volume, whilst Indium-113m labelled transferrin was used to measure transcapillary escape of protein. The diabetic patients were found to have reduced venous compliance 1.5 (0.7 to 3.4) x 10(-2) mmHg-1 compared with controls 3.2 (2.4 to 4.1) x 10(-2) mmHg-1 (p less than 0.01). The diabetic patients were also found to have greater transcapillary escape of transferrin -2.7 (-1.5 to -5.3) x 10(-3), compared with control subjects -5.2 (-4.1 to -8.1) x 10(-3) (p less than 0.02) in response to increasing hydrostatic pressure. These results show reduced venous compliance in patients with a mean duration of diabetes of 15 years and with only at most, early complications of diabetes, and confirm previous observations showing increased transcapillary escape of protein.
Elevation of glomerular filtration rate (GFR) is a feature of diabetes mellitus in humans and in animal models. Angiotensin II has been implicated as a mediator of GFR in diabetes. The acute effect of inhibition of angiotensin converting enzyme with captopril on renal haemodynamic and endocrine parameters was therefore studied in 14 normotensive male Type 1 diabetic patients, and the responses compared with those in five normal male control subjects. Following captopril 12.5 mg orally the diabetic patients exhibited an acute fall in GFR from 122 +/- 3.8 to 113 +/- 4.5 ml min-1 1.73-m-2 (p less than 0.02) and a rise in renal plasma flow (RPF) from 670 +/- 57 to 797 +/- 46 ml min-1 1.73-m-2 (p less than 0.01) which resulted in a fall in filtration. This did not occur in normal control subjects. Natriuresis occurred only in normal control subjects. There was no change in urinary excretion of PGE2 or kallikrein in either group but excretion of 6-keto-PGF1 alpha fell in the diabetic patients. There was a significant correlation between glycosylated haemoglobin and baseline RPF (rs = -0.79, p less than 0.001) and filtration fraction (rs = 0.83, p less than 0.001) that persisted when the change in these variables following captopril was analysed. Our results are compatible with the response to ACE inhibition in diabetic patients being secondary to inhibition of angiotensin II and suggest that this response may be related to blood glucose control.
Hypoglycemia is a serious problem in insulin-treated diabetic patients. In this study the efficacy of intravenous glucagon (1 mg) was compared with that of intravenous dextrose (25 g) in the treatment of hypoglycemia in insulin-treated patients attending an accident and emergency department. In addition, the prevailing glycemic control of these patients was compared with patients routinely attending a diabetic outpatient clinic. Both intravenous glucagon and dextrose were effective in the treatment of hypoglycemic coma. There was a difference in the glycemic profile after intravenous glucagon compared with intravenous dextrose, and recovery of a normal level of consciousness after glucagon was slower than after dextrose (6.5 vs. 4.0 min, respectively; P less than .001), although the average duration of hypoglycemic coma was 1.4 h. The glucagon- and dextrose-treated groups had significantly lower HbA1 than comparable patients routinely attending the clinic (9.5 +/- 0.8 vs. 12.0 +/- 3.8%, respectively; P less than .001). In view of the ease of administration and the small risk of vascular and extravascular complications, intravenous glucagon appears to be a useful alternative to intravenous dextrose in the treatment of severe hypoglycemia.