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Biomedical subjects

S K Sarin

Publications and source records attributed to S K Sarin.

At least 91 records · Page 5Linked to original sources
PubMed1994

Hepatic manifestations in typhoid fever.

Thirty one children with typhoid fever aged 2 months to 12 years and blood culture positive for multidrug resistant S. typhi were prospectively studied for their hepatic functions at the time of hospitalization and 2-3 weeks after completion of antibiotic therapy. Hepatic manifestations included hepatomegaly (51.6%); jaundice (16.1%); raised levels of serum glutamic oxaloacetic transaminase (SGOT) (61.3%), serum glutamic pyruvic transaminase (SGPT) (48.4%), alkaline phosphatase (AP) (22.6%) and serum bilirubin (SB) (6.1%); reduced levels of serum albumin (SA) (41.9%); prolonged prothrombin time (PT) (9.7%) and abnormal ultrasound abdomen (19.3%). Hepatic dysfunction was a notable feature even in those cases without hepatomegaly, with raised levels of SGOT (60%), SGPT (40%), AP (20%), SB (6.7%), decreased SA (53.3%) and prolonged PT (6.7%). There was no correlation between the degree of hepatic enlargement or hyperbilirubinemia with abnormalities in liver functions. Hepatic dysfunction was noticed to be transient, as all these parameters returned to normal within 2-3 weeks after successful antibiotic therapy.

Child↗
PubMed1994

Hepatic visceral larva migrans: evolution of the lesion, diagnosis, and role of high-dose albendazole therapy.

An unusual presentation of hepatic involvement of visceral larva migrans is described. A 45-yr-old male presented with fever, pain in the right upper quadrant, and persistent eosinophilia. Ultrasound initially detected a solitary hypoechoic area in the right lobe of the liver which rapidly progressed to multiple lesions with peripheral hyperechoic lesions. Aspiration from the lesion revealed Charcot-Leyden crystals and sheets of eosinophils. Serology for Toxocara canis was strongly positive. Prolonged and high-dose albendazole therapy, in combination with antibiotics, was required to treat the patient effectively.

Albendazole↗
PubMed1993

Do umbilical vein catheterization and sepsis lead to portal vein thrombosis? A prospective, clinical, and sonographic evaluation.

Extrahepatic portal vein obstruction (EHPVO) affects 20-30% of all patients with portal hypertension in India. The etiopathogenesis of this disease is unknown. In retrospective studies, umbilical vein cannulation and sepsis have been alleged to cause portal thrombosis. This prospective study was undertaken to detect clinically and by serial sonography whether thrombosis and consequent obstruction of the splenoportal venous system develops after umbilical vein catheterization and sepsis. Forty-seven children who had undergone exchange transfusion for hyperbilirubinemia, belonging to two different age groups, were studied. Twenty-two new-borns (Group A) were studied within 4 weeks of birth and later at 3-month intervals until the age of 12 months and subsequently at 24 months. Another group of 25 children (Group B), 1- to 5-year-olds who had earlier undergone exchange transfusion and 15 healthy newborns (Group C) were also screened. In Group A, seven (29%) neonates had septicemia, and in five, the splenic vein could not be initially visualized. The splenic vein was not seen in five of the 15 newborns in Group A who had no umbilical sepsis. Twenty-one of the 22 neonates in Group A were followed-up, and the splenic vein was well visualized and found patent on subsequent ultrasound in all of them. In Group B, four (16%) children had umbilical sepsis. None of these or the other Group B children showed any thrombosis or obstruction of the splenoportal system. The portal vein and its branches and the splenic vein were visualized in all healthy (Group C) neonates.(ABSTRACT TRUNCATED AT 250 WORDS)

Catheterization, Peripheral↗
PubMed1993

Effects of intravenous nitroglycerin and metoclopramide on intravariceal pressure: a double-blind, randomized study.

In search of an effective agent for decreasing intravariceal pressure, 27 patients with portal hypertension and large esophageal varices were studied. Thirteen patients received iv nitroglycerin (150-micrograms bolus), and 14 received iv metoclopramide (20-mg bolus). Continuous measurement of variceal pressure and systemic hemodynamics was carried out. Compared with the baseline, the variceal pressure was significantly reduced 10 min after nitroglycerin injection (20.23 +/- 3.1 vs. 14.6 +/- 4.8 mm Hg, p < 0.05): the percentage reduction was 27 +/- 25.4%. With metoclopramide, variceal pressure decreased by 12.7 +/- 22%; from 21.9 +/- 5.6 to 19.1 +/- 7.7 mmHg (p = NS). There was no significant alteration in the heart rate and mean arterial pressure with either drug. Our results thus suggest that in the dosages used, intravenous nitroglycerin effectively and safely reduces the variceal pressure. Further studies using a combination of nitroglycerin and metoclopramide need to be considered.

Adult↗
PubMed1992

Portal-vein obstruction in children leads to growth retardation.

The portal vein is the main source of blood and hepatotrophic factors to the liver. Partial portal-vein ligation in rats results in reduced growth compared with that in control rats. To investigate whether extrahepatic portal vein obstruction occurring in early childhood influences growth in humans, anthropometric and nutritional assessments were prospectively carried out in 61 patients with extrahepatic portal vein obstruction. Comparisons were made with 183 matched healthy controls using National Center of Health Statistics reference. Fifty-one percent of children with extrahepatic portal vein obstruction had stunted growth (height for age less than 90% of normal), compared with 16% of controls (p less than 0.01). Growth retardation was severe in patients with longer (greater than 5 yr) than with shorter (less than 2.5 yr) duration of clinical portal hypertension (height for age, 88.0 +/- 3.2 vs. 95.1 +/- 3.0; p less than 0.01). Little difference was seen in the energy intake (1,302 +/- 463 kcal/day vs. 1,335 +/- 449 kcal/day; p = not significant) and weight for height index (83.6 +/- 9.3 vs. 88.0 +/- 7.9; p = not significant) between extrahepatic portal vein obstruction patients and controls. This suggested that despite comparable nutrition, marked growth retardation occurred in extrahepatic portal vein obstruction patients. Incremental growth velocity was studied in 31 patients; in 24 (73%) the baseline Z score (-2.1 +/- 0.2) had decreased further (-2.4 +/- 0.2) at the end of follow-up (15.5 +/- 1.6 mo). Although the incremental height velocity was only 56% of the expected height, incremental weight gain was 98% of the expected weight for the attained height.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Prevalence, classification and natural history of gastric varices: a long-term follow-up study in 568 portal hypertension patients.

To determine the prevalence and natural history of gastric varices, we prospectively studied 568 patients (393 bleeders and 175 nonbleeders) with portal hypertension (cirrhosis in 301 patients, noncirrhotic portal fibrosis in 115 patients, extrahepatic portal vein obstruction in 117 patients and hepatic venous outflow obstruction in 35 patients). Primary (present at initial examination) gastric varices were seen in 114 (20%) patients; more were present in bleeders than in non-bleeders (27% vs. 4%, respectively; p < 0.001). Secondary (occurring after obliteration of esophageal varices) gastric varices developed in 33 (9%) patients during follow-up of 24.6 +/- 5.3 mo. Gastric varices (compared with esophageal varices) bled in significantly fewer patients (25% vs. 64%, respectively). Gastric varices had a lower bleeding risk factor than did esophageal varices (2.0 +/- 0.5 vs. 4.3 +/- 0.4, respectively) but bled more severely (4.8 +/- 0.6 vs. 2.9 +/- 0.3 transfusion units per patient, respectively). Once a varix bled, mortality was more likely (45%) in gastric varix patients. Gastric varices were classified as gastroesophageal or isolated gastric varices. Type 1 gastroesophageal varices (lesser curve varices) were the most common (75%). After obliteration of esophageal varices, type 1 gastroesophageal varices disappeared in 59% of patients and persisted in the remainder; bleeding from persistent gastroesophageal varices was more common than it was from gastroesophageal varices that were obliterated (28% vs. 2%, respectively; p < 0.001). Type 2 gastroesophageal varices, which extend to greater curvature, bled often (55%) and were associated with high mortality. Type 1 isolated gastric varices patients had only fundal varices, with a high (78%) incidence of bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

Factors influencing development of portal hypertensive gastropathy in patients with portal hypertension.

Portal hypertensive gastropathy (PGP) is an important cause of bleeding in portal hypertension patients. Although hyperdynamic congestion seems to be the underlying mechanism, the factors that influence the development of PGP are not understood. To investigate these, 107 patients [cirrhosis, 35; noncirrhotic portal fibrosis (NCPF), 24; extrahepatic portal vein obstruction (EHPVO), 46; Budd-Chiari syndrome, 2] were prospectively studied. Eighty-three patients had Child's A, 17 had Child's B, and 7 had Child's C liver disease. Before sclerotherapy, although intravariceal pressure was similar, 4 cirrhosis patients (3.7%) but no NCPF or EHPVO patients had PGP. After sclerotherapy, 21 additional patients (20.3%) developed PGP during a follow-up of 23.2 +/- 3.4 months (range, 1-52). The incidence of PGP was higher in cirrhotic patients (37.1%) than in NCPF (16.7%; P less than 0.05) or EHPVO (8.7%; P less than 0.01) patients. The probability of developing PGP among all patients at the end of 52 months of follow-up was 30%, more in cirrhosis than in EHPVO (55% vs. 15%; P less than 0.005). Only 2 patients bled from PGP during follow-up. Development of PGP correlated with severity of liver disease, being more common in Child's C than Child's A patients (87% vs. 13%; P less than 0.001). PGP was seen more often in patients with gastroesophageal varices than in patients with esophageal varices alone (42% vs. 11%; P less than 0.01). In conclusion, the results show that development of PGP is significantly influenced by sclerotherapy, severity of liver disease, etiology of portal hypertension, coexisting gastric varices and is not directly correlated with intravariceal pressure.

Adult↗
PubMed1992

Management of gastric varices.

Gastric varices (GV) are a common (20%) accompaniment of portal hypertension; they are more often seen in those patients who bleed than in those who do not (27% versus 4%, p < 0.01). They can develop in both segmental and generalized portal hypertension. Depending on their location and relation with oesophageal varices, GVs can be classified as gastrooesophageal varices (GOV) and isolated gastric varices (IGV); each of these can be further subdivided as follows: GOV1 (extension of oesophageal varices along lesser curve) and GOV2 (extension of oesophageal varices towards fundus); and IGV1 (varices in the fundus) and IGV2 (isolated varices anywhere in the stomach). The common presentation of GVs is variceal bleeding and encephalopathy. In comparison with oesophageal varices, GVs bleed significantly less often (64% versus 25%, p < 0.01) but more severely (2.9 +/- 0.3 versus 4.8 +/- 0.6 transfusion units, p < 0.01). Patients with GOV2 and IGV1 bleed more often than patients with other types of GVs. Sclerotherapy for oesophageal varices can significantly influence the natural history of GVs. GOV1, or lesser curve varices, disappear in the majority of cases (59%) after obliteration of oesophageal varices. In those with persisting GOV1, the incidence of bleeding and mortality is high and these patients require gastric variceal sclerotherapy (GVS). During oesophageal variceal sclerotherapy, bleeding can occasionally be induced from GVs. After obliteration of oesophageal varices, recurrence as GVs (secondary GVs) can occur in about 9% of patients. Emergency GVS is quite effective in controlling acute bleeding from GVs, more so than balloon tamponade. Potent sclerosants like tetradecyl sulphate and alcohol and a glue, bucrylate, have been quite effective. Elective GVS can achieve obliteration of GVs in nearly 70% of patients. Rebleeding and ulceration are common complications of GVS; probably related to incomplete obliteration and mucosal injury respectively. Splenectomy is quite effective in treating GVs due to segmental protal hypertension. For GV bleeding due to generalized portal hypertension, a shunt operation is often effective. TIPS procedure appear to be a very promising therapy for GV bleeding. Liver transplantation may be a superior alternative to sclerotherapy and shunt surgery for gastric varices.

Balloon Occlusion↗
PubMed1992

Long term management of oesophageal varices.

Effective control of variceal rebleeding (secondary prophylaxis) or prevention of the initial bleeding (primary prophylaxis) are the main objectives of the treatment of portal hypertension. Endoscopic sclerotherapy is the treatment of choice for secondary prophylaxis, since it significantly decreases rebleeding and, to some extent, mortality. A combination of propranolol and sclerotherapy may be of benefit by decreasing postsclerotherapy rebleeding. Endoscopic variceal band ligation and transjugular intrahepatic shunt are emerging as useful alternative techniques. Devascularisation and preferably selective shunts should be reserved for use as salvage of sclerotherapy failures. Liver transplantation, if feasible, could become the ultimate therapy by controlling variceal bleeding and improving hepatic function. Pharmacotherapy, while not very successful for secondary prophylaxis, has shown promise for primary prophylaxis of variceal bleeding. Nonselective beta-blockers significantly decrease the rebleeding rates but are associated with only marginal survival benefits. beta-Blockers alone cannot decrease the hepatic venous pressure gradient adequately (to less than 12mm Hg). Combination with nitrates and other drugs may prove beneficial and requires clinical evaluation. Endoscopic sclerotherapy and surgery have little role in primary prevention of variceal bleeding in patients with cirrhosis but need evaluation in noncirrhotic patients.

Adrenergic beta-Antagonists↗
PubMed1992

Polymerase chain reaction based diagnostic assay for identification of hepatitis B virus.

A highly sensitive polymerase chain reaction (PCR)-based diagnostic assay was developed to detect the presence of hepatitis B virus (HBV) in human serum. The assay involved amplification of HBV DNA sequences using primers specific to HBV. This in vitro enzymatic amplification technique, when used in combination with molecular hybridization assay can detect HBV genome in the patient's serum, with a higher degree of sensitivity than achieved with dot blot assay. The assay can identify samples containing 3-10 virus particles.

Base Sequence↗
PubMed1991

Caroli disease: computed tomographic diagnosis.

Computed tomographic (CT) scan findings in patients with cavernous ectasia of the biliary tract (Caroli disease) have been described. Our patient had the isolated form of Caroli disease characterized by saccular dilatation of intrahepatic bile ducts and no evidence of portal hypertension. CT scan of the liver showed tiny dots with strong contrast enhancement within dilated intrahepatic bile ducts (the central dot sign). This finding when correlated with sonogram indicated portal radicles surrounded by dilated intrahepatic bile ducts.

Adolescent↗
PubMed1991

Propranolol ameliorates the development of portal-systemic shunting in a chronic murine schistosomiasis model of portal hypertension.

We investigated the role of early portal hypotensive pharmacotherapy in preventing the development of portal-systemic shunting in a portal hypertensive model of chronic murine schistosomiasis induced by infecting C3H mice with 60 cercariae of Schistosoma mansoni. Propranolol was administered in drinking water to 20 animals for a period of 6 wk at a dose of 10 mg.kg-1d-1, starting at 5 wk of schistosomal infection. 32 age-matched mice with chronic schistosomal infection served as controls. All animals were studied 11 wk after the infection. Compared with controls the portal pressure (10.8 +/- 0.40 mmHg) was significantly lower (P less than 0.001) in the propranolol-treated animals (7.9 +/- 0.80 mmHg). Portal-systemic shunting was decreased by 79%, from 12.2 +/- 3.34% in controls to 2.5 +/- 0.99% in the propranolol group (P less than 0.05). Portal venous inflow was reduced by 38% in the propranolol treated animals (2.50 +/- 0.73 ml/min; n = 6) compared with controls (4.00 +/- 0.34 ml/min; n = 8; P less than 0.05). The worm burden, the granulomatous reaction, the collagen content of the liver, and the serum bile acid levels were not significantly different between the two groups of animals. These results demonstrate that in chronic liver disease induced by schistosomiasis, the development of portal-systemic shunting can be decreased or prevented by the reduction of flow and pressure in the portal system.

Animals↗
PubMed1991

Pyoderma gangrenosum in ulcerative colitis.

We present a patient with pyoderma gangrenosum, a rare complication of ulcerative colitis. The patient's disease was limited to the distal colon, was clinically mild and responded quickly to treatment, and yet it was associated with pyoderma gangrenosum and arthritis, complications generally associated with more severe and extensive ulcerative colitis.

Abdominal Muscles↗
PubMed1991

Hyperdynamic circulation in a chronic murine schistosomiasis model of portal hypertension.

Chronic murine schistosomiasis is a natural disease model of portal hypertension closely mimicking the clinical and histological features of human hepatic schistosomiasis. We studied the splanchnic and systemic hemodynamics in the murine model of schistosomiasis by radioactive microsphere technique. Mice infected with 60 cercariae of Schistosoma mansoni (n = 8) were studied hemodynamically 11 wk after the infection and were compared with age-matched healthy controls (n = 11). Mean portal venous inflow in the infected mice (3.82 +/- 0.32 ml/min) was 61% higher than in the healthy animals (2.37 +/- 0.25 ml/min; p less than 0.01). A twofold increase in hepatic arterial flow was also seen in mice with schistosomiasis (0.47 +/- 0.14 ml/min) as compared with controls (0.16 +/- 0.03 ml/min; p less than 0.05), whereas splanchnic arteriolar resistance (60.91 +/- 7.64 vs. 101.21 +/- 11.06 mm Hg.min.ml-1.gm; p less than 0.05) and peripheral vascular resistance (112.05 +/- 14.05 vs 254.53 +/- 29.86 mm Hg.min.ml-1.gm; p less than 0.01) were reduced. There was a significant increase in cardiac index (752 +/- 99 vs. 453 +/- 55 ml.min-1.kg body weight-1; p less than 0.05) and reduction in mean arterial pressure (81.37 +/- 3.09 vs. 101.45 +/- 5.85 mm Hg; p less than 0.05) in the infected animals compared with controls. These observations clearly demonstrate the existence of a hyperdynamic circulatory state in this model of portal hypertension.

Animals↗