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Biomedical subjects

B M Singh

Publications and source records attributed to B M Singh.

At least 73 records · Page 4Linked to original sources
PubMed1980

Epilepsia partialis continua associated with nonketotic hyperglycemia: clinical and biochemical profile of 21 patients.

In 21 patients, epilepsia partialis continua (EPC) was an early symptom of nonketotic hyperglycemia and occurred during an initial phase of hyponatremia and mild hyperosmolality. EPC persisted for an average of 8 days, and its duration correlated predominantly with the degree of hyponatremia. Depression of consciousness and cessation of seizures occurred with increasing severity of hyperglycemia and hyperosmolality. In 9 patients, EPC was the first symptom leading to the diagnosis of diabetes mellitus. Four patients died of serious associated illness. The majority of the patients had evidence of a localized structural cerebral lesion. Metabolic disturbances including hyperglycemia, mild hyperosmolality, hyponatremia, and lack of ketoacidosis contribute to the development of EPC in areas of focal cerebral damage.

Adult↗
PubMed1980

Hypertensive cerebrovascular disease and normal pressure hydrocephalus.

A hypertensive patient with clinical and laboratory features of normal pressure hydrocephalus (NPH) but with evidence of bilateral multiple cerebral infarcts on computed tomography (CT) did not benefit from shunting. In six reported cases of hypertensive cerebrovascular disease with NPH, the result of shunting was not predictable and was generally disappointing. Laboratory criteria to predict which cases of NPH will benefit from shunting remain controversial. The chances of improvement after shunting are slight when there is CT evidence of bilateral multiple cerebral infarcts, even though other clinical and laboratory data might suggest NPH.

Aged↗
PubMed1976

Prognosis in unstable angina.

A retrospective study was made of 158 patients with unstable angina admitted to a coronary care unit over a 4-year period. Twenty patients (13 per cent) had myocardial infarcts while in hospital, and of these 3 died; three others died without preceding evidence of myocardial infarction. There was thus an acute mortality rate of 4 per cent. Patients with persisting angina after the first 24 hours and those without a previous history of myocardial ischaemia were more likely to develop a myocardial infarct or to die in hospital. Follow-up information, ranging from 3 to 7 years, was available in 144 of 152 hospital survivors. Patients older than 60 years (P less than 0-05), with cardiomegaly (P less than 0-01) and with pulmonary venous congestion (P less than 0-05) were found to have significantly increased long-term mortality. Long-term mortality was also found to rise with increasing coronary prognostic index. The average mortality rate for the whole group of hospital survivors was about 5 per cent per annum. Of the 111 patients who were alive at follow-up, 19 (17%) had had a myocardial infarct after leaving hospital, and a similar number had moderate or severe angina.

Age Factors↗
PubMed1968

Epidemiological, clinical, and biochemical study of endemic dental and skeletal fluorosis in punjab.

The incidence of dental fluorosis in 46,000 children in the Punjab was assessed and compared with the fluoride content of their water supplies. Ten villages were selected for more detailed studies of skeletal as well as dental fluorosis.Factors other than the fluoride contect of the drinking water which were found to influence the incidence and the severity of fluorosis were the chemical composition of the water and in particular its calcium content; the duration of exposure; sex and occupation; nutritional status; and climatic and geological variations. The role of fluoride-containing foodstuffs has yet to be assessed.

Adolescent↗
PubMed1966

Endemic fluorosis.

Explore the source record for details and available documents.

Fluoride Poisoning↗
PubMedDate not supplied

Effects of autonomic neuropathy on glucose, fatty acid, and ketone body metabolism following insulin withdrawal in patients with insulin-dependent diabetes.

It has been postulated that sympathetic denervation due to autonomic neuropathy may protect against the development of diabetic ketoacidosis in patients with insulin-dependent diabetes. We tested this hypothesis by withdrawing exogenous insulin from five men with established insulin-dependent diabetes and severe symptomatic autonomic neuropathy. Six men also with insulin-dependent diabetes of more than 5-years duration but no clinical evidence of neuropathy served as controls. Normoglycemia was maintained during the night before the study using a variable intravenous insulin infusion that was terminated at 0800 h the following morning (time 0 min). During a 600-min observation period following termination of the insulin infusion the rise (mean +/- SEM) in blood glucose concentration between 0 min and 600 min was comparable between the autonomic neuropathy and control groups (8.2 +/- 1.3 versus 8.3 +/- 1.1 mmol/L; p > 0.1). The rise in plasma nonesterified fatty acids was significantly less for the autonomic neuropathy patients (0.96 +/- 0.06 versus 1.65 +/- 0.14 mmol/L; p < 0.01) with a similar trend for the rise in total ketone body concentration (2.74 +/- 0.85 versus 3.72 +/- 0.38 mmol/L). Capillary pH at 600 min, however, was not significantly different between the groups (23 +/- 2 versus 20 +/- 1 mmol/L). In conclusion, plasma fatty acids and ketone body concentrations rise less rapidly following withdrawal of insulin in patients with insulin-dependent diabetes and autonomic neuropathy suggesting that such patients may have a degree of protection against the development of diabetic ketoacidosis.

Adult↗
PubMedDate not supplied

The effect of glucose and insulin infusion on the fall of ketone bodies during treatment of diabetic ketoacidosis.

During the treatment of diabetic ketoacidosis intravenous glucose is infused when blood glucose has fallen to around 14 mmol l-1. The use of hypertonic (10%) glucose has been recommended in order to hasten the clearance of blood ketone bodies. In a randomized controlled study 17 patients presenting with severe diabetic ketoacidosis were allocated to one of two regimens of intravenous glucose and insulin when blood glucose had fallen to less than 14 mmol l-1. Nine patients were given 5% glucose containing 10 U l-1 insulin and 8 patients received 10% glucose with 40 U l-1 insulin. Fluid was infused at a rate of 250 ml h-1 for 6 h. At the start of the infusions blood glucose had fallen from levels at presentation to 12.8 +/- 1.1 mmol l-1 (mean +/- SE) in the group which subsequently received the low infusion rate and to 13.7 +/- 0.9 mmol l-1 in the subsequent high infusion rate group. With glucose/insulin infusion blood glucose after 6 h was 11.5 +/- 0.9 mmol l-1 (low infusion rate group) and 15.7 +/- 1.3 mmol l-1 (high infusion rate group). This difference between groups at 6 h was significant (p less than 0.05). Over the 6 h of infusion the fall in blood total ketone bodies was significantly greater in the group receiving the higher rate of glucose/insulin infusion (7.34 +/- 0.57 vs 5.18 +/- 0.57 mmol l-1; p less than 0.05). Despite the greater fall in total ketone bodies in this group there was no difference in the improvement in capillary blood pH or bicarbonate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗