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Biomedical subjects

S C Shah

Publications and source records attributed to S C Shah.

At least 19 recordsLinked to original sources
PubMed1996

Preliminary experience with use of a selective 5HT3 receptor antagonist (ondansetron) to prevent high dose chemotherapy induced emesis.

Ondansetron was used as an antiemetic along with dexamethasone during 16 cycles of highly or moderately ematogenic chemotherapy. There was major control in two cycles and complete control in the remaining 14. Side effects were minor and did not require discontinuation of the drug. This combination, therefore, appears to be safe and effective in preventing chemotherapy induced emesis.

Adult↗
PubMed1993

Lack of immune responsiveness to bovine serum albumin in insulin-dependent diabetes.

BACKGROUND: Epidemiologic studies have implicated the ingestion of cow's milk in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). Moreover, in a recent study, 100 percent of patients with new-onset IDDM had antibodies against bovine serum albumin (BSA), with a majority directed against a 17-amino-acid BSA peptide (ABBOS). Cellular immune mechanisms are thought to be the principal mediators of pancreatic beta-cell destruction in IDDM. METHODS: We measured the responses of peripheral-blood mononuclear cells to BSA and ABBOS or serum IgG anti-BSA antibodies (by particle-concentration fluorescence immunoassay) in 71 patients with IDDM, 55 subjects at various degrees of risk for IDDM, 36 patients with other autoimmune disorders (chronic autoimmune thyroiditis, rheumatoid arthritis, and systemic lupus erythematosus), and 48 normal subjects. RESULTS: The responses of peripheral-blood mononuclear cells to BSA or ABBOS were positive in 2 of 24 patients with new-onset IDDM, 1 of 25 first-degree relatives of patients with IDDM who were negative for islet-cell antibodies, 2 of 30 first-degree relatives of patients with IDDM who were positive for islet-cell antibodies, 1 of 28 patients with established IDDM, and 1 of 29 normal subjects. Similarly, anti-BSA antibodies were not detected significantly more often in patients with new-onset IDDM (3 of 31, 10 percent) than in normal subjects (1 of 37, 3 percent; P = 0.32). However, many patients with autoimmune disease and subjects at increased risk for IDDM had anti-BSA antibodies (frequency, 10 to 31 percent). CONCLUSIONS: Anti-BSA antibodies may reflect a general defect in the process of immunologic tolerance associated with a predisposition to autoimmunity rather than immunity specific to beta cells. The absence of cellular immunity to BSA and ABBOS in IDDM does not support a role for this antigen in the pathogenesis of the disorder.

Adult↗
PubMed1993

Tracheal tear during laryngopharyngectomy with gastric transposition.

Tracheal rupture occurred in 7 of 174 (4%) patients undergoing laryngopharyngectomy with gastric transposition. Tracheal tears were classified as proximal if they involved the upper two-thirds of the trachea (five patients), or distal if they extended into the lower one-third of the trachea (two patients) and their clinical features and management analyzed. Predisposing factors, including prior radiotherapy (three patients) and preoperative tracheostomy (1 patient) did not influence the site or severity of tracheal injury. Proximal tears were detected incidentally in four patients, but in one patient, manifested postoperatively with subcutaneous emphysema and pneumothorax. Distal tears manifested dramatically with a ventilatory leak. Adequate access for repair of distal tears may necessitate a right thoracotomy while proximal tears may be sutured through the cervical incision. Gastric transposition alone did not prevent air leak in two patients. Postoperative complications included prolapse of the stomach and bilateral pneumothoraces in one patient. Close interaction between the surgeon and the anesthesiologist ensured a successful outcome in six patients. There was one mortality.

Anastomosis, Surgical↗
PubMed1992

Response of peripheral-blood mononuclear cells to glutamate decarboxylase in insulin-dependent diabetes.

Insulin-dependent diabetes is characterised by autoantibodies to several pancreatic-islet-cell antigens, including glutamate decarboxylase. We measured the proliferative responses to this antigen of peripheral-blood mononuclear cells from patients with newly diagnosed insulin-dependent diabetes, relatives of diabetic patients, and healthy controls. The likelihood of a positive response was substantially greater among the diabetic patients and relatives positive for islet-cell autoantibodies (ICA) than among subjects at low risk of diabetes (controls and ICA-negative relatives). Glutamate decarboxylase may have a pathogenetic role in insulin-dependent diabetes.

Autoantibodies↗
PubMed1991

Insulin resistance and hyperinsulinemia induce hyperandrogenism in a young type B insulin-resistant female.

An adolescent female with type B insulin resistance and hyperandrogenemia is described. Evidence presented suggests that hyperinsulinemia leads to an increase in serum total and free testosterone. Support for this hypothesis is noted during an in vivo experiment in which large doses of regular insulin (305 U/kg-day) were infused iv, and multiple serum total testosterone measurements obtained. After 35 days of iv insulin therapy, the serum total testosterone values rose from 4.9 nmol/L (142 ng/dL) to 22.8 nmol/L (660 ng/dL), and the ovarian volume increased 2-fold. Basal (9.8 nmol/L; 282 ng/dL) and stimulated (16.8 nmol/L; 481 ng/dL) androstenedione measurements were elevated, and the dehydroepiandrosterone/androstenedione ratio was low, suggesting increased 3 beta-hydroxysteroid dehydrogenase activity. After resolution of the insulin-resistant state and the concomitant hyperinsulinemia, the serum total testosterone values returned to normal. This case illustrates that long term hyperinsulinemia leads to elevation of serum total testosterone.

Adolescent↗
PubMed1989

A randomized trial of intensive insulin therapy in newly diagnosed insulin-dependent diabetes mellitus.

A period of early, intensive insulin treatment is thought to improve subsequent beta-cell function in insulin-dependent diabetes mellitus (IDDM). To study this hypothesis, we randomly assigned adolescents with newly diagnosed IDDM to receive either conventional treatment (n = 14) (NPH insulin, 1 U per kilogram of body weight per day, in two divided doses) or an experimental treatment (n = 12) (a two-week hospitalization with maintenance of blood glucose levels between 3.3 and 4.4 mmol per liter by continuous insulin infusion delivered by an external artificial pancreas [Biostator]). During the two-week intervention, the experimental-therapy group received four times more insulin than the conventionally treated group, and their endogenous insulin secretion was more completely suppressed, as evidenced by a urinary C-peptide excretion rate one seventh that of the conventionally treated group. After the first two weeks, both groups were treated similarly and received similar amounts of insulin. At one year, the mean (+/- SEM) plasma level of C peptide was significantly higher after mixed-meal stimulation in the experimental-therapy group than in the conventionally treated group (0.51 +/- 0.07 vs. 0.27 +/- 0.06; P less than 0.01). The experimental-therapy group also had better metabolic control, as evidenced by lower glycohemoglobin values (7.2 +/- 0.7 vs. 10.8 +/- 1.2 percent; P less than 0.01). We conclude that suppression of endogenous insulin by intensive, continuous insulin treatment during the first two weeks after the diagnosis of IDDM may improve beta-cell function during the subsequent year.

Adolescent↗
PubMed1989

Evaluation of endoscopic variceal sclerotherapy in various grades of liver disease.

Forty four patients with portal hypertension of varying etiology, including 25 patients with an acute episode of variceal bleeding and 19 with past history of hematemesis, were followed up for eighteen months following endoscopic variceal sclerotherapy (EVS). Of 11 patients in Child's A group, two died of acute bleed, three were subjected to shunt surgery and the remaining six survived the follow-up period. Ten of 11 cases in Child's C did not survive more than six months in spite of sclerotherapy. We conclude that rebleed and death due to rebleed following EVS occur more commonly in patients with poor hepatic reserve (Child's C) as compared to patients in Child's A and B.

Child↗