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Biomedical subjects

S Shilo

Publications and source records attributed to S Shilo.

At least 19 recordsLinked to original sources
PubMed1998

Hypoglycemia in hospitalized nondiabetic older patients.

OBJECTIVES: To analyze the clinical characteristics, associated risk factors, and outcome of hypoglycemia in nondiabetic hospitalized older patients. DESIGN: A retrospective case control study. PARTICIPANTS: Sixty patients, aged 65 years and older, in the acute medical and geriatric wards who developed hypoglycemia. A control group was composed of 83 older patients, sex and age matched, in orthopedic and surgery wards who were undergoing corrective surgery for hip fracture or hernioplasty. MEASUREMENTS: For all patients, data for the following variables were abstracted from the charts: age, sex, degree of hypoglycemia, clinical presentation of hypoglycemia, number and duration of hypoglycemia episodes, nutritional state, and blood chemistry analysis. Risk factors were defined as nutritional state, heart failure, renal or liver disease, malignancy, and infection or sepsis. RESULTS: Mean blood glucose in hypoglycemic cases was 38.9 +/- 7 mg/dL. Symptoms and signs of hypoglycemia were noted in only 38.4% (23/60) of patients. All identified risk factors except cachexia were found significantly more frequently in the hypoglycemic patients than in the control group. Mean total number of risk factors was greater in the hypoglycemic group than in the control group, 2.97 +/- 1.1 versus 1.64 +/- .8, respectively (P < .001). In a multivariant logistic model, low plasma albumin level, liver disease, malignancy, and congestive heart failure were significant predictors of hypoglycemia. In-hospital mortality rate was higher among the hypoglycemic patients, 48% versus 18.1% (P < .001), and was independent of the degree of hypoglycemia or the number of hypoglycemic episodes. Mortality was correlated significantly with the number of risk factors (3.4 +/- 1.1 vs 2.5 +/- 1.1; P = .006). Hypoglycemia remained a significant predictor of mortality (OR = 3.67; 95% CI, 1.2-11.2) even after the adjustment for other risk factors. CONCLUSIONS: Hypoglycemic episodes occur even among nondiabetic hospitalized older patients. Symptoms and signs of hypoglycemia were noted in only two-fifths of the patients. Albumin less than 3.0 g%, liver disease, renal insufficiency, malignancy, congestive heart failure, and sepsis were statistically significant predictors of developing hypoglycemia. The overall mortality rate was significantly higher among the hypoglycemic patients and was independent of hypoglycemia levels. Mean total number of risk factors was significantly higher among those who died compared with hypoglycemic patients who survived. Based on the present study, the estimated odds of mortality in an older patient with hypoglycemia were 3.67 times higher than in those without hypoglycemia.

Age Factors↗
PubMed1991

[Pyogenic cervical osteomyelitis following pneumonia].

A 65-year-old man was admitted because of severe cervical pain radiating to both shoulders and bouts of fever, which followed pneumonia. Bone scan showed increased focal uptake in C6-7, while computerized tomography showed destruction of the 7th intervertebral disk, with bone sequesters and soft tissue swelling. Fine needle aspiration drew purulent material with gram-positive bacteria on direct staining. Culture grew Staphylococcus aureus, coagulase positive. Treatment with IV cloxacillin for 3 weeks, followed by oral treatment for another 3, resulted in complete remission.

Aged↗
PubMed1990

Compensated hypothyroidism presenting with galactorrhoea.

Compensated hypothyroidism was diagnosed in a 36-year-old female who presented with breast tenderness and mild galactorrhoea. T4 was 5.8 mcg dl-1 and T3RU was 22.5%, while TSH and prolactin were very mildly elevated (6.5 mU ml-1 and 26.1 ng ml-1, respectively). The TRH test showed an exaggerated response. TSH increased to 43 mU ml-1, and prolactin levels reached 161 ng ml-1. Treatment with T4 decreased the TSH and prolactin levels to within the normal range, and prevented the galactorrhoea. The case presented here demonstrates that galactorrhoea can be present even with mild hypothyroidism.

Adult↗
PubMed1990

Islet hormonal regulation of glucose turnover during exercise in type 1 diabetes.

A decline in plasma insulin and an increase in glucagon are known to occur during intense and/or prolonged exercise. However, it is not established whether changes in insulin and glucagon secretion are involved in the precise matching of hepatic glucose production to the enhanced glucose uptake by muscle during brief, low intensity exercise. We studied the effects of 30-min cycle exercise at 40% of maximal aerobic capacity in healthy subjects and C-peptide-deficient subjects with type 1 diabetes (IDDM) using [3-3H]glucose to estimate glucose turnover. Diabetic subjects were studied during continuous iv insulin infusion, which normalized glucose kinetics before experimental perturbations. In control (saline-infused) experiments, endogenous glucose appearance (Ra) increased by 80-90% above baseline to match the increase in glucose disappearance in both normal and IDDM subjects, even though the latter exercised at fixed levels of plasma free insulin, averaging 203 +/- 19 pmol/L. In other experiments, somatostatin was infused, and glucagon (1.0 ng/kg.min) and insulin (at two different rates) were maintained at constant levels. Infusion of insulin in normal subjects at doses sufficient to maintain constant peripheral plasma insulin was associated with no apparent effect on glucose turnover (plasma insulin, 80 +/- 21 pmol/L, compared to 52 +/- 5 pmol/L during saline; P = NS). However, insulin infusion at doses that normalized the portal insulin concentration (approximately 208 pmol/L) together with glucagon replacement inhibited the rise in glucose production in both normal and IDDM subjects. There were similar 45-55% reductions (P less than 0.03) of the increase in Ra seen with exercise in control experiments. When peripheral plasma free insulin (and presumably portal levels as well) were increased by about 20% in this experimental setting in IDDM (278 +/- 43 pmol/L), the suppression of Ra was even more profound, and Ra failed to increase at all with exercise. We conclude that the hormonal regulation of Ra in brief duration exercise in man does not necessitate the decrements in portal venous insulin observed under more intense exercise conditions as long as an exercise-induced glucagon secretory response can occur. Glucagon secretion alone cannot prevent hypoglycemia when portal venous insulin concentrations are increased by minimal amounts, such as in insulin-treated diabetics.

Adult↗
PubMed1990

Abnormal growth hormone responses to hypoglycemia and exercise in adults with type I diabetes.

Abnormal regulation of growth hormone (GH) secretion has been reported in some patients with insulin-dependent diabetes (IDD). We compared the GH responses in 32 healthy subjects (age 25 +/- 2 SE years) and in 23 IDD patients (28 +/- 1.9 years old, diabetes duration 10.4 +/- 2 years, and glycohemoglobin levels 9.3 +/- 2.0%). During acute, severe hypoglycemia (glucose less than 40 mg/dl), the mean GH levels were similar. When prolonged mild hypoglycemia was induced (58.0 +/- 2.0 mg/dl in the controls and 54.0 +/- 2.0 mg/dl in the IDD patients), the mean GH levels were similar, although the increase in GH was delayed in the latter group. During brief (30 min) exercise at 40-50% of VO2max, GH rose comparably in both groups (IDD patients maintained euglycemia with basal insulin infusion). However, with more prolonged and intense exercise using a glucose clamp to maintain euglycemia, GH rose to 5.4 +/- 2.2 ng/ml in controls and 26.4 +/- 12.6 ng/ml in the diabetics (P less than 0.05). When the combination of intense exercise and hypoglycemia (approximately 55 mg/dl) was used, GH rose to a peak of 21.7 +/- 2.7 ng/ml in the controls and to 33 +/- 3.0 ng/ml in the diabetics (P = NS). Our data show that in insulin-infused IDD patients made euglycemic for these experiments: a) The GH response to acute, severe hypoglycemia was identical to that in the controls and the response to mild, prolonged hypoglycemia was delayed, but of similar magnitude compared with controls; b) Exercise-induced GH responses were observed in both groups, but exaggerated in the diabetics at a higher exercise intensity; c) Hypoglycemia during exercise produced an additive effect on GH secretion in the controls but not in the IDD patients. We conclude that the wide range of abnormal GH secretory responses in type I diabetes reflects a central, possibly hypothalamic, defect in GH regulation.

Adult↗
PubMed1989

Regulation of counterregulatory hormone secretion in man during exercise and hypoglycemia.

We examined the role of the plasma glucose concentration per se in the secretion of counterregulatory hormones during exercise. Ten men (average age, 24 yr; maximal aerobic capacity, 31.8 mL/kg.min) were studied during two 50-min bicycle exercise periods at either normal glucose [87 +/- 1 (+/- SE) mg/dL (4.8 +/- 0.1 mmol/L)] or low glucose [59 +/- 1 mg/dL (3.3 +/- 0.1 mmol/L)]. The plasma glucose targets were achieved by exogenous insulin and variable glucose infusions. These results were compared to studies in which saline was infused. Exercise at normal glucose was associated with significant increments in plasma epinephrine (maximum 3- to 5-fold above baseline) and norepinephrine (2-fold), comparable to those that occurred during saline administration. Plasma GH increased only at the most intense exercise level, while plasma cortisol and glucagon did not increase significantly. In low glucose-exercise studies, the increase in plasma epinephrine during exercise was significantly greater than that at normal glucose (P less than 0.01), although proportional to basal preexercise levels (r = 0.73; P less than 0.001). Plasma glucagon increased almost 100%, and plasma cortisol and GH increased by 150% and 400%, respectively. Compared to the effect of the same degree of hypoglycemia in the absence of exercise, only plasma epinephrine (P = 0.002) and norepinephrine (P less than 0.001) displayed effects independent of hypoglycemia during exercise. When low glucose was reversed to normal at the midpoint of exercise, plasma epinephrine and glucagon returned to the levels obtained for the same duration of exercise at normal glucose, while norepinephrine, GH, and cortisol were only partially responsive to the rise in plasma glucose. These data suggest that 1) moderate exercise is a stimulus for a sympathoadrenal and GH response, but not a peripheral glucagon response; 2) during exercise and hypoglycemia, plasma epinephrine and norepinephrine are enhanced, while the glucagon response is entirely glucose dependent; and 3) the epinephrine response to hypoglycemia can be dissociated from that to exercise, suggesting differing control mechanisms. We conclude that the activation of counterregulatory hormones during exercise is regulated by glucose-independent mechanisms, although these responses may be augmented by concurrent hypoglycemia.

Adult↗
PubMed1987

Improved renal function following acute peritoneal dialysis in patients with intractable congestive heart failure.

Nine patients, six men and three women, 40 to 73 years of age, were included in the study. All of the patients had severe heart failure refractory to aggressive therapy including digitalis, diuretics, and vasodilators. Eight patients underwent one treatment of peritoneal dialysis while the remaining patient received two dialyses. The urine output was measured by an indwelling catheter; glomerular filtration rate (GFR) was determined by creatinine and inulin clearance, and renal blood flow (RBF) was determined by sodium paraamino hippurate (PAH) clearance. Following one peritoneal dialysis, the mean fluid loss/patient was 3,995 ml (range 3,200 to 5,100 ml). Dialysis was generally well tolerated. One patient, who had underlying hepatic cirrhosis and underwent two dialyses, developed hepatic failure and died 10 days after the second dialysis. At postmortem, peritonitis was discovered. All of the patients showed a marked subjective and objective clinical improvement. The mean plasma urea decreased from 154 to 71 mg/dl (P less than 0.005), and mean plasma creatinine decreased from 1.83 to 1.13 mg/dl (P less than 0.005). Blood pH was 7.30 before dialysis and increased to 7.37 (P less than 0.0125) after treatment. Mean urine output predialysis was 955 ml and increased to 1,472 ml post dialysis (P less than 0.0005). Creatinine clearance increased from 35 to 73 ml/min (P less than 0.0005). The mean inulin clearance increased from 33 ml/min predialysis to 69 ml/min post dialysis (P less than 0.0005), and mean PAH clearance increased from 96.7 to 362.5 ml/min (P less than 0.0005). Acute peritoneal dialysis is a safe and effective means for removing large quantities of excess fluid from patients with intractable heart failure.

Adult↗
PubMed1986

Glibenclamide induced prolonged hypoglycaemia.

Prolonged hypoglycaemia (serum glucose levels of 50 mg/dl and less, for more than 12 h in spite of treatment with periodic injections of hypertonic glucose) secondary to treatment with glibenclamide was found in 13 hospitalized patients. The mean daily dose of glibenclamide was 6.7 mg. In nine patients, the hypoglycaemia developed within 7 days of treatment. In two patients the tendency to hypoglycaemia lasted for more than 60 h in spite of continuous infusion of 5% or 10% glucose. Old age seems to be a crucial predisposing factor as none of the patients was under the age of 68 years. Contributing factors were renal failure and congestive heart disease. We feel that glibenclamide should be used with care in the elderly and in patients with renal or cardiac failure.

Aged↗
PubMed1986

Evolution of hypothyroidism in familial goitre due to deiodinase deficiency: report of a family and review of the literature.

We studied two sisters who developed large non-toxic goitres in adolescence. Deiodinase deficiency was diagnosed by a rapid thyroid uptake of radioactive iodine (RAI) at 2 hours associated with a marked fall in thyroidal 131I by 24 hours. Serial RAI scans in the second patient documented evolution of the iodine-deficient state. Conservation of intra-thyroidal iodine stores was maintained by avid iodine uptake and failure to release organified 131I. With progressive loss of inorganic iodine, hypothyroidism developed, associated with a rise in serum TSH which further exacerbated the loss of iodine. Treatment with L-thyroxine resulted in an improvement of thyroid function, but normalization was achieved only after small doses of Lugol's iodine were administered. These studies illustrate the variable nature and late onset of an inborn error of thyroid metabolism. This family supports an autosomal recessive mode of inheritance for deiodinase deficiency. We have documented progression from a euthyroid to hypothyroid state resulting from decompensation of iodine conservation mechanisms.

Adult↗
PubMed1986

Iodine-induced hyperthyroidism in a patient with a normal thyroid gland.

Iodine-induced hyperthyroidism can develop even in the presence of an otherwise normal gland. One of the less common sources of iodine is tablets of seaweed, sold over the counter without prescription. We report the case of a 72 year old female who developed clinical and laboratory evidence of hyperthyroidism while ingesting sea-kelp (Vitalia) tablets. Six months after stopping the tablets, the symptoms and laboratory evidence of hyperthyroidism had disappeared. No evidence of pre-existing thyroid disease was found.

Aged↗
PubMed1986

Beta-adrenergic contribution to glucagon-induced glucose production and insulin secretion in uremia.

Spontaneous or propranolol-induced hypoglycemia can occur in uremic humans. We studied glucose kinetics (using [3-3H]glucose) in five uremic humans 24 h after hemodialysis and in seven normal controls. The effect of glucagon infusion at rates of 3, 6, 12, and 18 ng X kg-1 X min-1 at 60-min intervals was compared with either saline or beta-adrenergic blockade (propranolol infusion). In uremics, plasma glucose increased by 20-25% and by 40-50% at the 3 and 6 ng X kg-1 X min-1 glucagon doses, respectively, with no further increases at higher infusion rates. Glucose production increased transiently and in tandem with glucose uptake at each glucagon increment (P less than 0.0001). During beta-adrenergic blockade, the effect of glucagon in stimulating glucose production was blunted by 14-24% at the 6-18 ng X kg-1 X min-1 doses (P less than 0.05). During saline infusion, plasma insulin concentrations increased progressively to peak levels fourfold above basal at the 18 ng X kg-1 X min-1 dose. This increase in plasma insulin was virtually abolished by concomitant beta-adrenergic blockade (P = 0.0002). In contrast to uremic subjects, normal controls exhibited lesser degrees of hyperglycemia and hyperinsulinemia at all glucagon infusion rates. Propranolol infusion had no effect on the increments in glucose production and uptake nor on the plasma insulin response. These results suggest that in uremic humans propranolol independently reduces the hepatic response to glucagon and the insulin secretory response to hyperglycemia and/or hyperglucagonemia. These observations provide a possible mechanism for the adrenergic regulation of glucose homeostasis in uremia.

Adult↗
PubMed1986

Histomorphometric evaluation of reversible heparin-induced osteoporosis in pregnancy.

Transilial bone biopsy confirmed heparin-induced osteopenia in a 23-year-old postpartum patient. Histomorphometric measurements during the reversible stage of bone disease that followed discontinuation of the heparin sodium therapy revealed signs of recovery; these were superimposed on a loose trabecular structure typical of osteoporosis. The histomorphometric evidence of recovery correlated well with signs of clinical improvement. In the majority of patients, heparin therapy during pregnancy is innocuous; however, discontinuation of treatment is recommended at the earliest signs of osteoporosis.

Adult↗
PubMed1985

Atrioventricular and sinoatrial block in thyrotoxic crisis.

A 55 year old woman in thyrotoxic crisis developed atrial fibrillation, atrioventricular block, and sinoatrial block in rapid succession. All of these abnormalities resolved completely after antithyroid treatment. This course of events illustrates the profound effect of thyroid hormones on cardiac function. In view of the potential aggravation of atrioventricular conduction disturbance by beta adrenergic blocking agents, thyrotoxic patients should be carefully screened for electrocardiographic evidence of conduction disturbance before the administration of such drugs.

Electrocardiography↗
PubMed1985

Acute hemolytic anemia caused by severe hypophosphatemia in diabetic ketoacidosis.

Hypophosphatemia in diabetic ketoacidosis is well recognized, but is believed to be usually of moderate severity. We describe 2 patients in whom acute hemolytic anemia secondary to severe (0.19-0.35 mmol/l) hypophosphatemia has developed 1-2 days following treatment for diabetic ketoacidosis. Our experience indicates that severe hypophosphatemia requiring phosphate supplementation does occur in diabetic patients, and calls for increased awareness for the clinical and laboratory manifestations of this complication of diabetic ketoacidosis.

Acidosis↗