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Dive into the research topics where Vivek A. Saraswat is active.

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Featured researches published by Vivek A. Saraswat.


Journal of Gastroenterology and Hepatology | 2001

Prevalence and natural history of subclinical hepatic encephalopathy in cirrhosis

Ananya Das; Radha K. Dhiman; Vivek A. Saraswat; Meera Verma; Subhash R. Naik

Background and Aims: The natural history of subclinical hepatic encephalopathy (SHE) is unknown. The present study was conducted to study the prevalence and the natural history of SHE in patients with cirrhosis of the liver.


Hepatology | 2006

Demonstration of interstitial cerebral edema with diffusion tensor MR imaging in type C hepatic encephalopathy

Ravindra Kale; Rakesh K. Gupta; Vivek A. Saraswat; Khader M. Hasan; Richa Trivedi; Asht M. Mishra; Piyush Ranjan; Chandra M. Pandey; Ponnada A. Narayana

Brain water may increase in hepatic encephalopathy (HE). Diffusion tensor imaging was performed in patients with cirrhosis with or without HE to quantify the changes in brain water diffusivity and to correlate it with neuropsychological (NP) tests. Thirty‐nine patients with cirrhosis, with minimal (MHE) or overt HE, were studied and compared to 18 controls. Mean diffusivity (MD) and fractional anisotropy (FA) were calculated in corpus callosum, internal capsule, deep gray matter nuclei, periventricular frontal, and occipital white matter regions in both cerebral hemispheres. The MD and FA values from different regions in different groups were compared using analysis of variance and Spearmans rank correlation test. In 10 patients with MHE, repeat studies were performed after 3 weeks of lactulose therapy to look for any change in MD, FA, and NP scores. Significantly increased MD was found with insignificant changes in FA in various regions of brain in patients with MHE or HE compared with controls, indicating an increase in interstitial water in the brain parenchyma without any microstructural changes. A significant correlation was found between MD values from corpus callosum, internal capsule, and NP test scores. After therapy, MD values decreased significantly and there was a corresponding improvement in NP test scores. Further analysis showed that MD values were different for different grades of minimal or overt HE. In conclusion, the increase in MD with no concomitant changes in FA in cirrhosis with minimal or early HE indicates the presence of reversible interstitial brain edema. (HEPATOLOGY 2006;43:698–706.)


The American Journal of Gastroenterology | 2004

Long-Term Follow-Up after Pneumatic Dilation for Achalasia Cardia: Factors Associated with Treatment Failure and Recurrence

Ujjala Ghoshal; S Kumar; Vivek A. Saraswat; Rakesh Aggarwal; A Misra; Gourdas Choudhuri

BACKGROUND:Though most patients with achalasia cardia (AC) respond to pneumatic dilation (PD), one-third experienced recurrence. Long-term follow-up studies on factors associated with various outcomes are scanty.METHODS:In this retrospective study, 126 patients (36.5 ± 14.6 yr, 76 male) with AC (diagnosed by esophagoscopy, barium esophagogram, and/or manometry) were followed up in person or through mail. The median dysphagia-free duration was calculated by Kaplan–Meier analysis. Factors associated with nonresponse and recurrence after PD were determined using univariate and multivariate analyses.RESULTS:Symptoms were dysphagia (126, 100%), chest pain (21, 17%), regurgitation (61, 48%), weight loss (33, 26%), and pulmonary symptoms (23, 18%); 5 of 126 (4%) had megaesophagus (≥7 cm). The mean lower esophageal sphincter (LES) pressure was 38.7 ± 16.8 mmHg. One hundred and fifteen of 126 (91%) patients responded to PD (90 (71%) to first session); 25 of these had recurrence of dysphagia after 15 ± 17 months. Post-PD chest pain requiring hospitalization occurred in 21 of 126 (17%; one had an esophageal perforation). Post-PD LES pressure, which was assessed in 48 of 126 patients, had decreased by >50% from baseline in 14 of 29 responders, 0 of 11 nonresponders (p= 0.004, χ2 test), and 5 of 8 relapsers. The median dysphagia-free duration by Kaplan–Meier analysis was 60 months (SE 2.7, 95% CI 54.7–65.3). On univariate analysis, male gender, pulmonary symptoms (nocturnal coughing spell, history of respiratory infection), absence of chest pain, and failure to achieve a reduction in LES pressure >50% after PD were associated with poor outcome; whereas age, grade of dysphagia, regurgitation, megaesophagus, and LES pressure before PD were not. Male gender was associated with poor outcome by multivariate-analysis.CONCLUSIONS:PD is an effective and safe treatment for AC. Post-PD LES pressure measurement may be helpful in assessing response. Male patients have poorer outcomes following PD.


Journal of Gastroenterology and Hepatology | 2010

Minimal hepatic encephalopathy: Consensus statement of a working party of the Indian National Association for Study of the Liver

Radha K. Dhiman; Vivek A. Saraswat; B. K. Sharma; Shiv Kumar Sarin; Yogesh Chawla; Roger F. Butterworth; Ajay Duseja; Rakesh Aggarwal; Deepak Amarapurkar; Praveen Sharma; Kaushal Madan; Samir Shah; Avnish K. Seth; Rakesh K. Gupta; Abraham Koshy; Ramesh R. Rai; J. B. Dilawari; Sri Prakash Mishra; Subrat K. Acharya

Hepatic encephalopathy (HE) is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Overt HE occurs in approximately 30–45% of cirrhotic patients. Minimal HE (MHE), the mildest form of HE, is characterized by subtle motor and cognitive deficits and impairs health‐related quality of life. The Indian National Association for Study of the Liver (INASL) set up a Working Party on MHE in 2008 with a mandate to develop consensus guidelines on various aspects of MHE relevant to clinical practice. Questions related to the definition of MHE, its prevalence, diagnosis, clinical characteristics, pathogenesis, natural history and treatment were addressed by the members of the Working Party.


Liver International | 2009

Clinical features and predictors of outcome in acute hepatitis A and hepatitis E virus hepatitis on cirrhosis.

Yellapu Radha Krishna; Vivek A. Saraswat; Khaunish Das; Goel Himanshu; Surender Kumar Yachha; Rakesh Aggarwal; Gour Choudhuri

Background and Objectives: Acute hepatitis A and E are recognized triggers of hepatic decompensation in patients with cirrhosis, particularly from the Indian subcontinent. However, the resulting acute‐on‐chronic liver failure (ACLF) has not been well characterized and no large studies are available. Our study aimed to evaluate the clinical profile and predictors of 3‐month mortality in patients with this distinctive form of liver failure.


Metabolic Brain Disease | 2005

Cytotoxic Edema Is Responsible for Raised Intracranial Pressure in Fulminant Hepatic Failure: In Vivo Demonstration Using Diffusion-Weighted MRI in Human Subjects

Piyush Ranjan; Asht M. Mishra; Ravindra Kale; Vivek A. Saraswat; Rakesh K. Gupta

It is not clear whether cerebral edema in fulminant hepatic failure is predominantly vasogenic or cytotoxic, though cytotoxic edema due to astrocyte swelling is more likely. Diffusion-weighted magnetic resonance imaging can differentiate vasogenic from cytotoxic edema. We performed diffusion-weighted imaging in patients with fulminant hepatic failure to clarify the issue by measuring apparent diffusion coefficient, which quantifies movement of water molecule across cell membrane. Seven patients with fulminant hepatic failure underwent conventional and diffusion-weighted magnetic resonance imaging. Apparent diffusion coefficient was measured in four cortical areas and 12 deep white and gray matter regions in both cerebral hemispheres. Thirteen healthy subjects served as controls. The apparent diffusion coefficient values in patients and controls were compared using Wilcoxon signed rank test. Two patients who survived underwent repeat imaging using same protocol. Patients with FHF had significantly lower apparent diffusion coefficient in all cortical and deep white and gray matter regions of interest compared to controls (p < 0.001), suggesting cytotoxic cell swelling. In two survivors with repeat imaging, one showed complete resolution while the changes persisted in the other, suggesting ischemic injury. Cerebral edema in fulminant hepatic failure is predominantly due to cytotoxic edema.


Journal of Gastroenterology and Hepatology | 1995

Figure connection test : a universal test for assessment of mental state

Radha Krishan Dhiman; Vivek A. Saraswat; Meera Verma; Subhash R. Naik

Abstract The number connection test (NCT), which assesses the extent of organic brain damage, has been used extensively to evaluate mental state in portasystemic encephalopathy, but has certain inherent limitations. It cannot be performed by illiterates and those unfamiliar with Roman alphanumeric notations. We, therefore, devised a figure connection test (FCT) based on the subjects identification of figures rather than alphabets or numerals. Four variations each of FCT‐A (A1‐A4) and FCT‐B (B1‐B4) employing different motifs were developed and compared with four variations each of NCT‐A (A1‐A4) and NCT‐B (B1‐B4) in groups of healthy volunteers with differing educational status. These volunteer groups were as follows: postgraduates 64; graduates 66; subgraduates 75; and illiterates 45. Significant differences in mean scores of various tests were observed between these normal groups. Control values of the tests for these groups have been standardized and can serve as nomograms. The effect of educational attainments on performance of FCT and other psychometric tests was analysed and trail‐making tests were validated for serial use.


Journal of Gastroenterology and Hepatology | 2008

Cerebral diffusion tensor imaging and in vivo proton magnetic resonance spectroscopy in patients with fulminant hepatic failure

Sona Saksena; Vijan Rai; Vivek A. Saraswat; Ramkishore Rathore; Ankur Purwar; Manoj Kumar; M. Albert Thomas; Rakesh K. Gupta

Background and Aim:  Cerebral edema is a major complication in patients with fulminant hepatic failure (FHF). The aim of this study was to evaluate the metabolite alterations and cerebral edema in patients with FHF using in vivo proton magnetic resonance spectroscopy (MRS) and diffusion tensor imaging, and to look for its reversibility in survivors.


Journal of Gastroenterology and Hepatology | 1996

Frequency and factors influencing portal hypertensive gastropathy and duodenopathy in cirrhotic portal hypertension.

Rakesh K. Gupta; Vivek A. Saraswat; M. Kumar; S. R. Naik; Rakesh Pandey

Portal hypertensive gastropathy and duodenopathy are distinct clinical and endoscopic entities. Data on factors influencing the development of these lesions are still emerging. Data on portal hypertensive duodenopathy are scarce. We prospectively studied 230 patients with liver cirrhosis and oesophageal varices attending the liver clinic of the Sanjay Gandhi Post Graduate Institute of Medical Sciences. One hundred and forty‐two patients had no history of upper gastrointestinal bleeding, while the remainder had bled in the past. Endoscopic appearances were recorded before starting patients on a sclerotherapy programme. Forty‐four patients were re‐evaluated after variceal eradication. The frequency of portal hypertensive gastropathy (PHG) and duodenopathy (PHD) was 61 and 14%, respectively. Mild PHG was present in 85% and was severe in the rest. Portal hypertensive duodenopathy was mild in 50%, while in the other half it was severe. There was no relationship of PHG and PHD to: (i) a history of upper gastrointestinal bleed; (ii) size of oesophageal varices; (iii) aetiology of liver cirrhosis; or (iv) liver function status as assessed by Child Pughs scores (P=NS for all). The prevalence of PHG was higher in those patients with oesophagogastric varices (74 of 107; 69%) compared with patients with oesophageal varices alone (68 of 123; 55%; P<0.05). However, no such increase in frequency of PHD was noted in patients with oesophagogastric varices. Sclerotherapy increased the frequency of PHG. Twenty‐four patients had PHG before starting sclerotherapy, while it was noted in 33 patients 1–3 months after variceal eradication (P< 0.05). In contrast, there was no increase in the prevalence of portal hypertensive duodenopathy after sclerotherapy (P=NS). There was no correlation between endoscopic and histological changes of PHG and PHD. In conclusion, PHG is quite frequent in patients with cirrhosis and its frequency increases with the presence of oesophagogastric varices and after sclerotherapy. However, the frequency of PHD is low and is not affected by the factors studied.


Journal of Gastroenterology and Hepatology | 2004

Biliary microlithiasis in patients with idiopathic acute pancreatitis and unexplained biliary pain: Response to therapy

Vivek A. Saraswat; Barjesh C Sharma; Deepak K. Agarwal; Rakesh Kumar; Tajeshwar Singh Negi; Tandon Rk

Background and Aims:  Microlithiasis has been suspected to cause acute pancreatitis and biliary pain. We studied the frequency of microlithiasis and response to treatment in recurrent idiopathic acute pancreatitis (RIAP) and unexplained biliary pain.

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Samir Mohindra

Sanjay Gandhi Post Graduate Institute of Medical Sciences

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Uday C. Ghoshal

Sanjay Gandhi Post Graduate Institute of Medical Sciences

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Rakesh K. Gupta

Sanjay Gandhi Post Graduate Institute of Medical Sciences

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Gaurav Pandey

Icahn School of Medicine at Mount Sinai

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Gourdas Choudhuri

Sanjay Gandhi Post Graduate Institute of Medical Sciences

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Rakesh Aggarwal

Centers for Disease Control and Prevention

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Ajay Duseja

Post Graduate Institute of Medical Education and Research

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Abhai Verma

Sanjay Gandhi Post Graduate Institute of Medical Sciences

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Anshu Srivastava

Sanjay Gandhi Post Graduate Institute of Medical Sciences

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