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Biomedical subjects

S Dasarathy

Publications and source records attributed to S Dasarathy.

At least 19 recordsLinked to original sources
PubMed1997

Magnitude of hepatitis C virus infection in India: prevalence in healthy blood donors, acute and chronic liver diseases.

An enzyme immunoassay (EIA) was developed in-house for the detection of anti-hepatitis C virus (HCV) antibody against the prevailing genotypes in India. The specific reactivity of the test was compared with commercial second and third-generation EIAs and reverse transcription nested polymerase chain reaction (RT-nested PCR). Fifteen thousand nine hundred twenty-two healthy blood donors at the All India Institute of Medical Sciences (AIIMS), New Delhi, India, were screened for anti-HCV antibody. Two hundred ninety-five (1.85%) of these donors were positive. The screening was also used to determine how many patients with acute hepatitis and chronic liver diseases were positive for anti-HCV antibody. Five hundred sixty-four chronic liver disease patients were screened for anti-HCV antibody and 78 (13.83%) were found positive. Two hundred forty-seven sporadic acute viral hepatitis patients were screened for viral infection markers. Hepatitis B and E viruses (HBV and HEV) were the major etiologic agents. HCV was associated with 9% of the acute cases. Anti-HCV core IgM with HCV RNA detection were found to be helpful for the diagnosis of acute HCV infection.

Acute Disease↗
PubMed1996

Fulminant hepatitis in a tropical population: clinical course, cause, and early predictors of outcome.

The profiles of patients with fulminant hepatic failure (FHF) from developing countries have not been reported earlier. The current study was conducted prospectively, at a single tertiary care center in India, to document the demographic and clinical characteristics, natural course, and causative profile of patients with FHF as well as to define simple prognostic markers in these patients. Four hundred twenty-three consecutive patients with FHF admitted from January 1987 to June 1993 were included in the study. Each patient's serum was tested for various hepatotropic viruses. Univariate Cox's regression for 28 variables, multivariate Cox's proportional hazard regression, stepwise logistic regression, and Kaplan-Meier survival analysis were done to identify independent predictors of outcome at admission. All patients presented with encephalopathy within 4 weeks of onset of symptoms. Hepatotropic viruses were the likely cause in most of these patients. Hepatitis A (HAV), hepatitis B (HBV), hepatitis D (HDV) viruses, and antitubercular drugs could be implicated as the cause of FHF in 1.7% (n= 7), 28% (n= 117), 3.8% (n= 16), and 4.5% (n= 19) patients, respectively. In the remaining 62% (n= 264) of patients the serological evidence of HAV, HBV, or HDV infection was lacking, and none of them had ingested hepatotoxins. FHF was presumed to be caused by non-A, non-B virus(es) infection. Sera of 50 patients from the latter group were tested for hepatitis E virus (HEV) RNA and HCV RNA. In 31 (62%), HEV could be implicated as the causative agent, and isolated HCV RNA could be detected in 7 (19%). Two hundred eighty eight (66%) patients died. Approximately 75% of those who died did so within 72 hours of hospitalisation. One quarter of the female patients with FHF were pregnant. Mortality among pregnant females, nonpregnant females, and male patients with FHF was similar (P > .1). Univariate analysis showed that age, size of the liver assessed by percussion, grade of coma, presence of clinical features of cerebral edema, presence of infection, serum bilirubin, and prothrombin time prolongation over controls at admission were related to survival (P < .01). The rapidity of onset of encephalopathy and cause of FHF did not influence the outcome. Cox's proportional hazard regression showed age > or = 40 years, presence of cerebral edema, serum bilirubin > or = 15 mg/dL, and prothrombin time prolongation of 25 seconds or more over controls were independent predictors of outcome. Ninety-three percent of the patients with three or more of the above prognostic markers died. The sensitivity, specificity, positive predictive value, and the negative predictive value of the presence of three or more of these prognostic factors for mortality was 93%, 80%, 86%, and 89.5%, respectively, with a diagnostic accuracy of 87.3%. We conclude that most of our patients with FHF might have been caused by hepatotropic viral infection, and non-A, non-B virus(es) seems to be the dominant hepatotropic viral infection among these patients. They presented with encephalopathy within 4 weeks of the onset of symptoms. Pregnancy, cause, and rapidity of onset of encephalopathy did not influence survival. The prognostic model developed in the current study is simple and can be performed at admission.

Adolescent↗
PubMed1996

Gastroduodenal manifestations in patients with skeletal fluorosis.

A prospective case-controlled study was performed to evaluate the gastrointestinal symptoms and mucosal abnormalities occurring in patients with osteofluorosis. Ten patients with documented osteofluorosis and ten age- and sex-matched healthy volunteers were included in the study. Clinical evaluation, real-time ultrasound, and upper gastrointestinal endoscopy and biopsy from the gastric antrum and duodenum were performed in all subjects. The biopsies were subjected to a rapid urease test and light and electron microscopic examinations. Ionic fluoride levels were estimated in the drinking water, serum, and urine using an ION 85 ion analyzer. All patients with osteofluorosis had gastrointestinal symptoms, the most common being abdominal pain. Endoscopic abnormalities were found in seven patients with osteofluorosis. In all 7 of these patients, chronic atrophic gastritis was seen on histology. Electron microscopic abnormalities were observed in all 10 patients with osteofluorosis. These included loss of microvilli, cracked-clay appearance, and the presence of surface abrasions on the mucosal cells. None of the control subjects had any clinical symptoms or mucosal abnormalities. It was concluded that gastrointestinal symptoms as well as mucosal abnormalities are common in patients with osteofluorosis.

Abdominal Pain↗
PubMed1996

Prognostic markers in amebic liver abscess: a prospective study.

OBJECTIVES: Amebic liver abscess (ALA) is being increasingly recognized with the progressive spread of AIDS. The prognosis of ALA needs to be determined to decide whether aggressive intervention therapy should be used. A prospective study was conducted to determine the factors that predicted mortality in patients with ALA. METHODS: The study population consisted of 135 consecutive patients with ALA who were treated with 80 mg/kg/day of metronidazole for 10 days if they survived. Needle aspiration or open surgical drainage was performed in patients who deteriorated despite drug therapy or had an abscess that clinically appeared to be at risk of impending rupture. Survivors and nonsurvivors were compared by univariate and multivariate analysis to identify predictors of outcome. These predictors were then prospectively evaluated in a subsequent cohort of patients with ALA. RESULTS: Twenty-four patients died during the acute phase. Significant differences between survivors and nonsurvivors were observed. A stepwise logistic regression suggested that a bilirubin level >3.5 mg/dl, encephalopathy, volume of abscess cavity, hypoalbuminemia (serum albumin level <2.0 g/dl), and the number of abscesses were independent risk factors for mortality. The duration of symptoms and type of treatment did not influence mortality. The regression equation derived was then applied prospectively to 64 subsequent patients with ALA, and the validity of the prediction rule was confirmed. The qualities of simplicity, availability, low cost of derivation, and good discriminating power suggest that this index would be useful in assessing prognosis in patients with ALA.

Adult↗
PubMed1995

Prospective study of plasma fibronectin in fulminant hepatitis: association with infection and mortality.

BACKGROUND/AIMS: Plasma fibronectin is an opsonic glycoprotein, normally synthesized by the liver, which decreases subsequent to severe liver damage and low levels of which may contribute to reticuloendothelial system dysfunction by compromising opsonic activity. This may result in an increased frequency of infection and death. The present study was conducted to evaluate the association of plasma fibronectin activity with infection and mortality in patients with fulminant hepatic failure. METHODS: Plasma fibronectin was estimated serially in 69 consecutive patients with fulminant hepatic failure, nine patients with uncomplicated acute viral hepatitis and 32 normal volunteers. RESULTS: Plasma fibronectin levels in patients with fulminant hepatic failure (85.6 +/- 75.8 micrograms/ml) were significantly lower than in patients with uncomplicated acute viral hepatitis (295.5 +/- 88.5 micrograms/ml) and healthy volunteers (362.6 +/- 69.2 micrograms/ml). Forty-nine (72%) patients with fulminant hepatic failure died. The initial values of fibronectin in fulminant hepatic failure did not correlate with mortality. Patients with fulminant hepatic failure who survived showed a progressive rise in the fibronectin levels compared to the absence of an increase in fibronectin levels in the non-survivors. The mortality in patients with fulminant hepatic failure with infection (24/27) was significantly higher (p < 0.05) compared to those without infection (25/42). Initial fibronectin levels in patients with infection (70.3 +/- 54.2 micrograms/ml) were significantly lower (p < 0.05) than in those without infection (92.3 +/- 64.4 micrograms/ml). We conclude that plasma fibronectin levels in patients with fulminant hepatic failure are decreased compared to healthy subjects and the absence of an increase in levels indicates a poor prognosis. Low levels of fibronectin are associated with an increased incidence of infection, which increases the mortality in these patients.

Adolescent↗
PubMed1994

Toxic effects of chronic fluoride ingestion on the upper gastrointestinal tract.

In a prospective case controlled study, we evaluated the adverse effects of long-term fluoride ingestion on the gastrointestinal tract. Ten patients with otosclerosis who were receiving sodium fluoride 30 mg/day for a period of 3-12 months, and 10 age- and sex-matched healthy volunteers were included. They were all evaluated clinically and subjected to a real time ultrasound examination, upper gastrointestinal endoscopy, and biopsies from the gastric antrum and duodenum. The biopsies were subjected to a rapid urease test as well as light and electron microscopic examinations. Ionic fluoride was estimated in the serum, urine, and drinking water using an ION 85 Ion Analyzer. Seven subjects (70%) ingesting fluoride had abdominal pain, vomiting, and nausea. Petechiae, erosions, and erythema were seen on endoscopy in all the subjects, but not in the controls. Histological examination of the gastric antral biopsy showed chronic atrophic gastritis in all the subjects but in only one (10%) healthy volunteer. Scanning electron microscopic examination showed "cracked-clay" appearance, scanty microvilli, surface abrasions, and desquamated epithelium in the subjects ingesting fluoride, but not in the controls. We conclude that long-term fluoride ingestion is associated with a high incidence of dyspeptic symptoms as well as histological and electron microscopic abnormalities.

Adolescent↗
PubMed1993

A prospective randomized study to evaluate propranolol in patients undergoing long-term endoscopic sclerotherapy.

A prospective randomized double-blind study was conducted to evaluate the efficacy of propranolol in patients with portal hypertension undergoing long-term endoscopic sclerotherapy (EST) for recurrent variceal bleeding. Consecutive patients with portal hypertension (Child's class A or B) due to cirrhosis (n = 72), non-cirrhotic portal fibrosis (n = 29) and extrahepatic portal venous obstruction (n = 13) attending the liver clinic of a tertiary care center were included in the study. All patients had had at least one documented episode of variceal bleed in the previous 4 weeks. Fifty-eight patients received propranolol and 56 received placebo in addition to weekly EST. Rebleeding occurred in 12 (21%) patients in the placebo group and 10 (17%) patients in the propranolol group during a mean follow-up period of 24.4 +/- 10.4 months in the former and 23.8 +/- 9.2 months in the latter group (P > 0.1). The number of episodes of rebleeding (14 in the placebo and 12 in the propranolol group) were also similar (P > 0.1). The median bleeding-free period was more than 40 months in both treatment groups (P > 0.1). The mean transfusion requirements and the number of hospital admissions for rebleeding were also similar in the two treatment groups (P > 0.1). Complete obliteration of varices was achieved in 44 (78.9%) patients in the placebo group and 43 (75.5%) patients in the propranolol group (P > 0.1). Recurrence of new varices was seen in two patients in the placebo and in three of those in the propranolol group. Seven patients in the placebo group and five in the propranolol group died (P > 0.1). Complications related to EST were similar in the two treatment groups but additional adverse effects were observed in the propranolol group. The cumulative incidence of rebleeding in the placebo group was 12.7 and in the propranolol group it was 11.2 per 100 patient years of follow-up. It is concluded that the addition of propranolol in patients with portal hypertension and fair hepatic function on long-term EST does not confer any additional benefit.

Administration, Oral↗
PubMed1993

Omeprazole versus famotidine in the healing and relapse of duodenal ulcer.

Sixty patients with symptomatic duodenal ulcer were randomized to receive either omeprazole (20 mg each morning) or famotidine (40 mg at night time) for 2-4 weeks in a double-blind parallel group clinical trial. Healing rates were higher with omeprazole in comparison with famotidine after 2 weeks (77% vs. 40%, P < 0.001) and 4 weeks (93% vs. 80%, P = 0.2) of treatment. Assessment of daily diary cards completed by all patients revealed that omeprazole rapidly relieved ulcer-related day pain and nocturnal pain in comparison to famotidine. Treatment with omeprazole for 2 weeks was also associated with lower cumulative antacid intake (P < 0.05) and reduced absenteeism from work. Helicobacter pylori infection was present in all patients and remained unaffected by treatment with either of the drugs. None of the drugs produced any significant adverse effects. During 6 months follow-up of all the patients after ulcer healing (without maintenance therapy), ulcer relapse was seen in 40% of omeprazole- and 37% of famotidine-treated patients (P > 0.1). The duration of ulcer-free period following initial healing of ulcer was also similar in both the groups (median time: 22 weeks for omeprazole, 21 weeks for famotidine). We conclude that omeprazole is superior to famotidine in rapidly healing duodenal ulcers and achieving more rapid pain relief, but does not influence subsequent ulcer relapse.

Absenteeism↗
PubMed1993

A preliminary open trial on interferon stimulator (SNMC) derived from Glycyrrhiza glabra in the treatment of subacute hepatic failure.

The efficacy of the interferon stimulator named Stronger Neo Minophagen-C (SNMC) derived form the plant G. glabra was studied at a dose of 40 or 100 ml daily for 30 days followed by thrice weekly intravenously for 8 wk in 18 patients of subacute hepatic failure due to viral hepatitis. The survival rate amongst these patients was 72.2 per cent, as compared to the earlier reported rate of 31.1 per cent in 98 patients who received supportive therapy (P < 0.01). Death in four of the five patients was due to associated infections leading to hepatorenal failure and terminal coma. Further studies are necessary to standardize the dose and duration of therapy with SNMC in subacute hepatic failure.

Adolescent↗
PubMed1992

A prospective randomized trial comparing repeated endoscopic sclerotherapy and propranolol in decompensated (Child class B and C) cirrhotic patients.

A prospective randomized study was conducted to compare the efficacy of long-term endoscopic sclerotherapy vs. propranolol in Child class B and C patients with variceal bleeds within the 30 days before the study. Forty-five and 46 patients were randomized to receive sclerotherapy and propranolol, respectively, after preentry stratification for Child scores. Sclerotherapy was administered with 1% polidocanol at 10-day intervals until obliteration of varices was achieved. Propranolol was administered to achieve a reduction in resting pulse rate of 25%. Rebleeding occurred in 19 patients undergoing sclerotherapy and in 31 receiving propranolol (p less than 0.05). The number of episodes of rebleeding was higher (p less than 0.05) in the propranolol group (n = 64) than in the sclerotherapy group (n = 35). The mean bleeding risk factor, number of hospitalizations for rebleeding and blood transfusion requirement were also significantly higher in the propranolol-treated patients. The median bleed-free period was more than 36 mo in the sclerotherapy group and 2.5 mo in the propranolol group (p less than 0.01). The median survival time was significantly longer in the sclerotherapy group (greater than 36 mo) than in the propranolol group (greater than 24 mo). We conclude that in decompensated cirrhotic patients, long-term endoscopic sclerotherapy is superior to propranolol in preventing rebleeding and improving survival.

Adult↗
PubMed1992

Sodium benzoate in the treatment of acute hepatic encephalopathy: a double-blind randomized trial.

A prospective randomized double-blind study was conducted to evaluate the efficacy of sodium benzoate in the treatment of acute portal-systemic encephalopathy. Seventy-four consecutive patients with cirrhosis or surgical portasystemic anastomosis and hepatic encephalopathy of less than 7 days duration were randomized to receive lactulose (dose adjusted for 2 or 3 semiformed stools/day) or sodium benzoate (5 gm twice daily). Assessment of response included mental status, asterixis, arterial ammonia level, electroencephalogram and number-connection test. Each was given a score between 0 and 4+. A portal-systemic encephalopathy index was calculated with these scores. Visual, auditory and somatosensory evoked potentials and a battery of psychometric tests for intelligence and memory were also performed to assess improvement. Thirty-eight patients received sodium benzoate; 36 took lactulose. Thirty patients (80%) receiving sodium benzoate and 29 (81%) receiving lactulose recovered; the remaining patients died. Improvement in portal-systemic encephalopathy parameters occurred in both treatment groups and was similar (p greater than 0.1). Electroencephalogram and evoked potentials were not as helpful as mental status in assessing of recovery. Psychometric test scores remained abnormal after recovery of mental status (21 to 42 days) and were probably too sensitive for monitoring of these patients. The incidence of side effects was similar in the two treatment groups. The cost of lactulose for one course of therapy was 30 times that of sodium benzoate. We conclude that sodium benzoate is a safe and effective alternative to lactulose in the treatment of acute portasystemic encephalopathy.

Acute Disease↗