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Dive into the research topics where Jaya Benjamin is active.

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Featured researches published by Jaya Benjamin.


Hepatology Research | 2013

Intestinal permeability and complications in liver cirrhosis: A prospective cohort study

Jaya Benjamin; Vikas Singla; Indu Arora; Seema Sood; Y. K. Joshi

Aim:  Increased intestinal permeability (IP) has been implicated as an important factor for bacterial translocation (BT), leading to bacteremia and endotoxemia, resulting in various septic complications, variceal bleeding (VB), hepatic encephalopathy (HE), hepatorenal syndrome (HRS) and death in patients with liver cirrhosis (LC). This study was planned to assess IP in patients with LC and follow them for the occurrence of complications.


Hepatology Research | 2015

Effect of probiotic VSL#3 in the treatment of minimal hepatic encephalopathy: A non-inferiority randomized controlled trial.

Venigalla Pratap Mouli; Jaya Benjamin; Mamta Bhushan Singh; Kalaivani Mani; Sushil Kumar Garg; Anoop Saraya; Y. K. Joshi

Minimal hepatic encephalopathy (MHE) impairs daily functioning and health‐related quality of life in chronic liver disease (CLD). Lactulose is the standard treatment but has side‐effects. Probiotics have an encouraging role in MHE. The aim of the present study was to test whether probiotics are non‐inferior to lactulose in improving MHE.


Alimentary Pharmacology & Therapeutics | 2017

Endoscopic and clinical responses to anti-tubercular therapy can differentiate intestinal tuberculosis from Crohn's disease

V. Pratap Mouli; K. Munot; Ashwin N. Ananthakrishnan; Saurabh Kedia; S. Addagalla; Sushil Kumar Garg; Jaya Benjamin; Vikas Singla; Rajan Dhingra; Veena Tiwari; Sawan Bopanna; Susan Hutfless; Govind K. Makharia; Vineet Ahuja

Differentiation between intestinal tuberculosis and Crohns disease is difficult and may require therapeutic trial with anti‐tubercular therapy in tuberculosis‐endemic regions.


Nutrition | 2010

Enteral nutrition for severe malnutrition in chronic intestinal pseudo-obstruction

Jaya Benjamin; Namrata Singh; Govind K. Makharia

OBJECTIVE Chronic intestinal pseudo-obstruction (CIPO) is a rare intestinal motility disorder. A prolonged avoidance of food due to fear of aggravation of postprandial symptoms leads to severe malnutrition. We report a case of a 21 y old man who was diagnosed as CIPO with a history of recurrent intestinal colic and obstructive symptoms, slow transit type of constipation, bilateral hydronephrosis (non-obstructive), motor dysphagia without any evidence of demonstrable mechanical obstruction. Our aim was to keep his post prandial symptoms to a minimum and nutritionally build him up with enteral nutrition (EN). METHODS He had life threatening malnutrition (BMI of 11 kg/m(2)) and significant postprandial distension with an intake more than 100 ml, compromising the quality of life. In view of a normal absorptive function of the gut, TPN was ruled out and the patient was treated with enteral nutrition (oral & tube) only. The EN regimen followed was ad libitum oral intake along with nocturnal NG tube feeding. Initially a full strength semi-elemental formula at 50 ml/hour was given, later shifted to polymeric formula at 100 ml/hour. Serum levels of magnesium, phosphate and potassium were regularly monitored to prevent refeeding syndrome. He ws constantly motivated, counseled and monitored. RESULT With a gradual increase in the intake from 300 Kcal to 1400 Kcal he was discharged. Eight months from discharge he had a weight of 58 kg (BMI = 22.3 kg/m(2)), with resumption of normal activities and marked improvement in the quality of life. CONCLUSION Carefully planned EN along with motivation, psychological support and regular monitoring are the keys to nutritional management in CIPO.


Inflammatory Bowel Diseases | 2008

Association between intestinal permeability and anti-Saccharomyces cerevisiae antibodies in patients with Crohn's disease

Jaya Benjamin; Govind K. Makharia; Y. K. Joshi

To the Editor: Recently Janus kinase 2 (JAK2) mutations have been described in several Philadelphia-negative myeloproliferative disorders (MDP) as polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis, conditions complicated by thrombosis.1 The point mutation in JAK2 encodes a valine-tophenylalanine change at position 617 (JAK2 V617F) and confers constitutive tyrosine kinase activity.2 It has been suggested that thrombosis in MPD may be due to JAK2 mutation. Moreover, screening for JAK2 V617F has been carried out in a series of splanchnic, cerebral, and leg deep vein thromboses (DVTs) without overt MDP.3,4 Results from these studies indicate that the JAK2 V617F mutation in the absence of overt MDP is highly associated with splanchnic vein thrombosis and sporadically with cerebral thrombosis. Thromboembolism is a diseasespecific extraintestinal manifestation of inflammatory bowel disease (IBD)5 that develops as the result of multiple interactions between acquired and genetic risk factors. Arterial and venous thromboembolism is the most important complication, representing a significant cause of morbidity and mortality in IBD patients. The most commonly detected risk factors for thrombophilia in this disease are factor V R506Q (Leiden) mutation, plasminogen activator inhibitor gene polymorphism, hyperhomocysteinemia, and antiphospholipid antibodies. However, the prevalence of these factors does not differ between patients with IBD associated with vascular complications and those with thrombosis without IBD.6 Different cytokines stimulate the JAK and signal transducer and activator of transcription (JAK/STAT) pathway. JAK2 is also important in vascular diseases, such as atherosclerosis in which inflammation plays an important role.7 The aim of our study was to investigate the frequency of the JAK2 V617F mutation, which is the most common mutation described in MPD, in a group of 48 thrombotic IBD patients (22 with CD, 26 with UC) from Argentina (n 23) and Crete (n 25). The clinical characteristics of patients included in this study are reported in Table 1. No case had overt MPD, whereas some cases (n 4) had a history of more than 1 thrombotic event. The diagnosis of vascular complications was defined by typical clinical characteristics and diagnostic instrumental investigation (Doppler ultrasonography, computed tomography, magnetic resonance imaging, or angiography). Genomic DNA was isolated from peripheral blood according to an inhouse DNAzol extraction procedure (Invitrogen, Breda, The Netherlands). Forty-eight patients with IBD varying in age of onset of IBD from 2 to 65 years (median 37.5 years) presented with different thrombotic events (Table 1). A semiquantitative Taqman assay was used to determine the percentage of the JAK2 V617F mutation among wild-type DNA. No JAK2 V617F mutation was found in the 48 IBD patients with thrombotic complications. JAK2 V617F mutation has been found associated with elevated hemoglobin levels and leukocytosis, which may be directly associated with the increased thrombotic risk in MPD. On the other hand, thromboembolism in IBD is not associated with elevated hemoglobin levels and leukocytosis. The finding of the absence of the JAK2 V617F mutation in the thrombotic IBD patients suggests that other mechanisms play an important role in the pathogenesis of thrombosis in IBD. The small number of cases with splanchnic vein thrombosis in our series (but also in other IBD series), which is mainly associated JAK2 V617F mutation, could also be an explanation of this finding. Because recent studies in MPD have found other mutations in the gene coding for JAK2 (chromosome 9p24) such as JAK2 exon 12 mutations,8 further study of IBD patients with these serious complications is being undertaken.


Liver International | 2017

Impact of family history of metabolic traits on severity of NASH related cirrhosis: a cross‐sectional study

Ajeet Singh Bhadoria; Chandan Kumar Kedarisetty; Chhagan Bihari; Guresh Kumar; Ankur Kumar Jindal; Ankit Bhardwaj; Varsha Shasthry; Tanmay Vyas; Jaya Benjamin; Shvetank Sharma; Manoj Sharma; Shiv Kumar Sarin

Familial aggregation of metabolic traits with fatty liver disease is well documented. However, there is scarcity of data regarding such association with non‐alcoholic steatohepatitis (NASH)‐related cirrhosis. This study was aimed to explore the association of family history of metabolic traits with severity of cirrhosis.


Liver International | 2017

Characterization of body composition and definition of sarcopenia in patients with alcoholic cirrhosis: A computed tomography based study

Jaya Benjamin; Varsha Shasthry; Chetan Ramesh Kaal; Lovkesh Anand; Ankit Bhardwaj; Vanshja Pandit; Ankur Arora; Sasidharan Rajesh; Viniyendra Pamecha; Vikas Jain; Guresh Kumar; Anthony Loria; Puneet Puri; Y. K. Joshi; Shiv Kumar Sarin

Alterations in body composition (BC) as loss of fat and muscle mass (sarcopenia) are associated with poor outcome in alcoholic cirrhosis (ALC). Prevalence of sarcopenia depends upon the method of assessment. Computed Tomography (CT) is a gold standard tool for assessing BC.


Liver International | 2018

Positive familial history for metabolic traits predisposes to early and more severe alcoholic cirrhosis: A cross-sectional study

Ajeet Singh Bhadoria; Chandan Kumar Kedarisetty; Chhagan Bihari; Guresh Kumar; Ankur Kumar Jindal; Ankit Bhardwaj; Varsha Shasthry; Jaya Benjamin; Manoj Sharma; Shiv Kumar Sarin

Familial aggregation of metabolic traits in NAFLD is well documented. However, relevance of these traits in alcoholic cirrhosis is not well studied. We aimed to explore the association of family history of metabolic traits with age at diagnosis, severity and complications of alcoholic cirrhosis.


Gastroenterology | 2016

The Intensiveness of Intensive Enteral Nutrition Therapy.

Jaya Benjamin; Y. K. Joshi; Shiv Kumar Sarin

2 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 Dear Editors: With great interest we have read the recent article from Moreno et al, wherein a very vital aspect pertaining to the management of patients with severe alcoholic hepatitis has been addressed. The authors underline the ineffectiveness of “intensive enteral nutrition” in individuals with severe alcoholic hepatitis treated with corticosteroids in their multicenter study. We would like to raise some methodologic issues in the study that limit the interpretation of the findings. The ‘intensive’ nature of the nutrition therapy is reflected in not just the mode of meeting the nutritional needs, but its very essence lies in the overall assertiveness of the approach. Especially when, unlike drug trials, 100% delivery of the recommended nutritional calories is never achieved in the enteral nutrition interventional studies. Furthermore, the difference between the intervention—intensive nutrition—and the control group was only about 4 kcal/kg per day. It would be highly improbable to expect a survival benefit with such a limited caloric intake difference between the 2 groups. At the outset, the very premise of giving an higher amount of calories and proteins to the intervention compared with the control group was not achieved. We would be interested to know if any targets in relation to calories and proteins per kilogram body weight were fixed, and a deliberate plan to meet these targets was developed. There is also no account of the oral and enteral nutritional intake separately. The forte of being the multicenter study, in our opinion, paradoxically turns out to be its limitation as the “conventional local practices” of nutritional management of the 20 “expert” and “non-expert” centers could not have been uniform. Moreover. a blanket order of enteral nutrition in milliliters of a commercial closed circuit enteral nutrition formula vis-a-vis a specified percentage of the requirements being met ends up in supplying calories ranging anywhere from 20 to 35 kcal/kg per day. We also have reservations regarding the methods adopted to assess the nutritional intake. A record of nutritional intake only thrice a week for a total 14-day intervention in a captive patient population in the hospital is a potential source of bias, because there could be an error of missing out a record on good nutritional intake days and conversely recording a low nutrition on other days. A


Digestive Diseases and Sciences | 2009

Crohn's Disease in India: A Multicenter Study from a Country Where Tuberculosis Is Endemic

Kshaunish Das; Uday C. Ghoshal; Gopal K. Dhali; Jaya Benjamin; Vineet Ahuja; Govind K. Makharia

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Govind K. Makharia

All India Institute of Medical Sciences

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Y. K. Joshi

All India Institute of Medical Sciences

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Vineet Ahuja

All India Institute of Medical Sciences

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Shiv Kumar Sarin

Jawaharlal Nehru University

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Anoop Saraya

All India Institute of Medical Sciences

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Mani Kalaivani

All India Institute of Medical Sciences

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Vikas Singla

All India Institute of Medical Sciences

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Ajeet Singh Bhadoria

All India Institute of Medical Sciences

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Ankur Kumar Jindal

Post Graduate Institute of Medical Education and Research

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Indu Arora

All India Institute of Medical Sciences

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