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Hyponatremia is the most common electrolyte abnormality in patients with decompensated cirrhosis on Liver Transplantation (LT) waiting list. Most of these patients have dilutional or hypervolemic hyponatremia secondary to splanchnic vasodilatation. Excessive secretion of the antidiuretic hormone also plays an important role. Hypervolemic hyponatremia is commonly associated with refractory ascites, spontaneous bacterial peritonitis, and hepatic encephalopathy. Although uncommon, the use of diuretics and laxatives can cause hypovolemic hyponatremia that is characterized by the striking absence of ascites or pedal edema. Clinical features are often nonspecific and depend on the acuity of onset rather than the absolute value of serum sodium. Symptoms may be subtle, including nausea, lethargy, weakness, or anorexia. However, rarely patients may present with confusion, seizures, psychosis, or coma. Treatment includes discontinuation of diuretics, beta-blockers, and albumin infusion. Hypertonic saline (3%) infusion may be used in patients with very low serum sodium (

The association between alcohol and liver disease, including alcoholic hepatitis, cirrhosis, acute-on-chronic liver failure, and hepatocellular carcinoma, has been well described, but the same cannot be said for the association between smoking, water pipe or tobacco chewing. A review of cumulative evidence suggests that smoking is independently a risk factor for liver fibrosis and contributes to carcinogenesis in HCC. Smoking-related fibrosis has been reported in patients with nonalcoholic fatty liver disease, primary biliary cholangitis, alcoholic liver disease and chronic viral hepatitis. Heavy smoking leads to systemic inflammation, oxidative stress, insulin resistance, and results in tissue hypoxia, as well as free radical damage. Other than damaging the liver, patients also suffer from the systemic effects of the 4000 chemicals associated with tobacco, which include nitrosamines, aromatic hydrocarbons, nicotine, nornicotine, and other alkaloids. These include respiratory ailments, cancer of the lungs, oral cavity, esophagus, pancreas and colon, atherosclerotic vascular disease, and stroke.

As liver is one of the primary organs involved in glucose homeostasis, it is not surprising that patients with liver dysfunction in chronic liver disease usually develop impaired glucose tolerance and subsequently overt diabetes later in their natural course. Diabetes that develops after the onset of cirrhosis of liver is usually referred to as hepatogenous diabetes (HD). It is an underrecognized and a hallmark endocrinological event in chronic liver disease. HD is associated with a higher risk of developing hepatic decompensations, such as ascites, variceal bleeding, hepatic encephalopathy, renal dysfunction, refractory ascites, and hepatocellular carcinoma along with reduced survival rates than normoglycemic patients with cirrhosis of liver. It is quite different from type 2 diabetes mellitus with the absence of classical risk factors, dissimilar laboratory profiles, and decreased incidence of microvascular complications. Furthermore, the management of patients with HD is challenging because of altered pharmacokinetics of most antidiabetic drugs and increased risk of hypoglycemia and other adverse effects. Hence, a clear understanding of the epidemiology, pathophysiology, clinical implications, laboratory diagnosis, and management of HD is essential for both hepatologists as well as endocrinologists, which is narrated briefly in this review.

Hypereosinophilia is defined as an absolute eosinophil count of ≥1.5 × 109/L, and its presence with involvement of at least one organ system defines the hypereosinophilic syndrome. It may occur with parasitic infestation, connective tissue disorder or rarely in clonal disorders such as eosinophilic leucaemia. Organ systems that may be involved include the cardiovascular, central nervous, respiratory and gastrointestinal systems. In the latter, a wide spectrum of clinical presentation may be seen from trivial, to debilitating or rarely fatal. We report an elderly male with a history of bronchial asthma, obstructive sleep apnoea and food allergy who presented with chronic abdominal pain and weight loss. Abdominal examination and routine evaluation were essentially normal other than a peripheral hyper-eosinophilia. We witnessed a brisk and lasting response to an elimination diet and corticosteroids.

NAFLD is hepatic pandemic of the twenty rst century, being leading cause of chronic hepatic disease in western world. We did a cross sectional study to nd out prevalence of NAFLD among prospective healthy liver donors at a tertiary care hospital at New Delhi, India over a period from June 2014 to March 2016. 124 apparently healthy prospective liver donors were selected. Exclusion criteria were set to exclude all those who had signicant history of alcohol intake (dened as greater than 30g/day for men and greater than 20g/day for women over last two years), Hepatitis B or C infection, severe surgical weight loss or emaciation, Obstructive Sleep Apnea, Celiac disease, history of drug intake known to cause hepatic steatosis. Out of 124 prospective liver donors included in this study, 29 (23%) donors were found to have fatty liver on USG abdomen; 38 (31%) donors had fatty liver on unenhanced CTof the abdomen (LAI of ≤ 5 HU); 61 (49%) donors had fatty liver on magnetic resonance.

Gallstones are more common in patients with cirrhosis of the liver, and the incidence increases with severity of liver disease. Pigment stones are the most frequent type of gallstones (GSs) in cirrhotics, and majority remain asymptomatic. Hepatitis C virus infection and nonalcoholic fatty liver disease are the underlying etiologies of liver diseases that most often associated with GSs. Multiple altered mechanisms in cirrhosis such as chronic hemolysis due to hypersplenism, reduced bile acid synthesis and transport, decreased cholesterol secretion, decreased apolipoprotein A-I and A-II secretion, gallbladder hypo-motility, autonomic dysfunction, and portal hypertension collectively lead to increased risk of lithogenesis. Asymptomatic GSs should be followed up closely and offered laparoscopic cholecystectomy once symptomatic in Child-Pugh class A and B patients. The model for the end-stage liver disease score is the best predictor of the outcome after cholecystectomy. In patients of Child-Pugh class C, conservative or minimally invasive approaches should be used to treat complications of GSs.

BACKGROUND: Muscle cramps are witnessed in 22–88% of patients with cirrhosis of liver and frequently lead to sleep disturbance with an appalling impact on quality of life. Despite such a high prevalence, there is lack of evidence-based management protocol due to scarcity of trials on treatment options in the literature. This study aimed to review systematically the available therapeutic options for muscle cramps in patients with cirrhosis of liver. METHODS: A systematic review of the relevant databases (PubMed, Scopus, Embase, and Web of Science) to identify treatments for muscle cramps in patients with hepatic cirrhosis was performed. Studies meeting the selection criteria were reviewed and assessed for risk of bias and analyzed. RESULTS: Twenty-four publications were identified as eligible for inclusion in this systematic review. Seven randomized controlled trials (RCTs) and 17 prospective studies were included. Taurine, methocarbamol, baclofen, and orphenadrine are relatively safer and effective treatment option for muscle cramps in cirrhosis on the basis of recently conducted RCTs. Moreover, l-carnitine, branched-chain amino acids (BCAAs), pregabalin, zinc, and vitamin D are also safe and showed beneficial effects on muscle cramps. However, studies on vitamin E revealed contradictory results. CONCLUSION: Taurine, BCAAs, orphenadrine, and baclofen are safe and well-tolerated treatment options for muscle cramps in cirrhosis. However, well-designed randomized controlled clinical trials are the need of the hour to determine the most suitable treatment options for skeletal muscle cramps in patients with cirrhosis of liver.

Renal dysfunction is very common among patients with chronic liver disease, and concomitant liver disease can occur among patients with chronic kidney disease. The spectrum of clinical presentation and underlying etiology is wide when concomitant kidney and liver disease occur in the same patient. Management of these patients with dual onslaught is challenging and requires a team approach of hepatologists and nephrologists. No recent guidelines exist on algorithmic approach toward diagnosis and management of these challenging patients. The Indian National Association for Study of Liver (INASL) in association with Indian Society of Nephrology (ISN) endeavored to develop joint guidelines on diagnosis and management of patients who have simultaneous liver and kidney disease. For generating these guidelines, an INASL-ISN Taskforce was constituted, which had members from both the societies. The taskforce first identified contentious issues on various aspects of simultaneous liver and kidney diseases, which were allotted to individual members of the taskforce who reviewed them in detail. A round-table meeting of the Taskforce was held on 20–21 October 2018 at New Delhi to discuss, debate, and finalize the consensus statements. The evidence and recommendations in these guidelines have been graded according to the Grading of Recommendations Assessment Development and Evaluation (GRADE) system with minor modifications. The strength of recommendations (strong and weak) thus reflects the quality (grade) of underlying evidence (I, II, III). We present here the INASL-ISN Joint Position Statements on Management of Patients with Simultaneous Liver and Kidney Disease.

The spectrum of microorganisms causing splenic abscess is large, and commonly involved organisms include Enterobacteriaceae, gram-positive cocci and anaerobes. Group B Streptococcus (GBS) commonly causes infection in newborns and pregnant women, but there is increasing incidence of GBS causing invasive infection among nonpregnant adults, particularly among diabetics. Common presentations of GBS infection in adults include bacteremia, soft-tissue and skin infection, pneumonia, urinary tract infection, meningitis and endocarditis. We report a case of splenic abscess due to Streptococcus agalactiae infection without endocarditis in a diabetic patient.

As the cirrhosis progresses, development of complication like ascites, hepatic encephalopathy, variceal bleeding, kidney dysfunction, and hepatocellular carcinoma signify increasing risk of short term mortality. Malnutrition and muscle wasting (sarcopenia) is yet other complications that negatively impact survival, quality of life, and response to stressors, such as infection and surgery in patients with cirrhosis. Conventionally, these are not routinely looked for, because nutritional assessment can be a difficult especially if there is associated fluid retention and/or obesity. Patients with cirrhosis may have a combination of loss of skeletal muscle and gain of adipose tissue, culminating in the condition of "sarcopenic obesity." Sarcopenia in cirrhotic patients has been associated with increased mortality, sepsis complications, hyperammonemia, overt hepatic encephalopathy, and increased length of stay after liver transplantation. Assessment of muscles with cross-sectional imaging studies has become an attractive index of nutritional status evaluation in cirrhosis, as sarcopenia, the major component of malnutrition, is primarily responsible for the adverse clinical consequences seen in patients with liver disease. Cirrhosis is a state of accelerated starvation, with increased gluconeogenesis that requires amino acid diversion from other metabolic functions. Protein homeostasis is disturbed in cirrhosis due to several factors such as hyperammonemia, hormonal, and cytokine abnormalities, physical inactivity and direct effects of ethanol and its metabolites. New approaches to manage sarcopenia are being evolved. Branched chain amino acid supplementation, Myostatin inhibitors, and mitochondrial protective agents are currently in various stages of evaluation in preclinical studies to prevent and reverse sarcopenia, in cirrhosis.

Background Recurrent hepatitis C virus (HCV) has been a serious problem after liver transplantation (LT). We report our experience of 24-week therapy with sofosbuvir (SOF) and ribavirin (RBV) in post-LT recurrent HCV in living donor liver transplantation (LDLT) setting in South Asia. Methods Data from all patients treated for post-transplantation HCV recurrence in a single center were analyzed. Treatment regimen was 24 weeks of SOF 400 mg daily and RBV (starting at 800 mg daily, increased as tolerated). Sustained virological response (SVR) was assessed 12 weeks and 24 weeks after completion of treatment. Results 63 patients (median age 52 [range 30–69] years; 80% males) were treated. Most (76.2%) were treatment experienced and predominant HCV genotype was 3 (77.7%) followed by 1 (20.6%). Median transient elastography (Fibroscan) score was 7 (range 3–11) kPa and none of the patients had cirrhosis. SVR12 was achieved in 60 of 63 patients (95.2%) while SVR24 was noted in 59 (93.7%). SVR12 rates were as good in genotype-3 as in genotype-1. Older age, longer period after transplantation, higher Fibroscan value and higher need for erythropoietin were likely to be associated with relapse. Adverse effects were noted in 34 patients and weakness and fatigue were the commonest side effects. Significant drop in hemoglobin ( Conclusions SOF + RBV combination therapy for 24 weeks was safe and effective in treatment of for post-LT recurrent HCV in a single LT center and remains relevant due to its low cost and lack of drug interactions.

Treatment of hepatitis C virus (HCV) with newer directly acting antivirals (DAAs) and lead to sustained viral response (SVR) in majority of patients and SVR has been documented to be associated with reversal of liver cirrhosis. The improved SVR rates and safety profiles of DAAs have led to the treatment of patients with decompensated cirrhosis awaiting liver transplantation (LT). Several clinical trials of DAAs in decompensated HCV patients have recently demonstrated SVR rates above 80%, which have been associated with significant improvements, in the Child–Pugh–Turcotte scores/or model for end-stage liver disease scores in a proportion of patients. Moreover, it has been shown that HCV RNA becomes negative after 2–4 weeks of treatment, and those who are transplanted after becoming HCV RNA negative will be have very low the risk of HCV recurrence after transplantation. Some of the patients may have reached the “point of no return” and may proceed to worsening of decomposition over time. To avoid the risk of worsening, there is an additional option of treating these patients after LT should they develop recurrent HCV infection. Currently there are no guidelines as to select patients who would benefit from treatment prior to LT as opposed to those who will be better off being treated after the transplant surgery. The article discusses a possible approach for such selection.

Coffee is the most popular beverage in the world. Consumption of coffee has been shown to benefit health in general, and liver health in particular. This article reviews the effects of coffee intake on development and progression of liver disease due to various causes. We also describe the putative mechanisms by which coffee exerts the protective effect. The clinical evidence of benefit of coffee consumption in Hepatitis B and C, as well as nonalcoholic fatty liver disease and alcoholic liver disease, has also been presented. Coffee consumption is associated with improvement in liver enzymes (ALT, AST, and GGTP), especially in individuals with risk for liver disease. Coffee intake more than 2 cups per day in patients with preexisting liver disease has been shown to be associated with lower incidence of fibrosis and cirrhosis, lower hepatocellular carcinoma rates, as well as decreased mortality.

Hepatitis B Virus (HBV) reactivation in patients receiving chemotherapy, biologicals, immunosupressants, or corticosteroids is emerging to be an important cause of morbidity and mortality in patients with current or prior exposure to HBV infection. These patients suffer a dual onslaught of illness: one from the primary disease for which they are receiving the culprit drug that led to HBV reactivation, and the other from HBV reactivation itself. The HBV reactivation not only leads to a compromised liver function, which may culminate into hepatic failure; it also adversely impacts the treatment outcome of the primary illness. Hence, identification of patients at risk of reactivation before starting these drugs, and starting treatment aimed at prevention of HBV reactivation is the best strategy of managing these patients. There are no Indian guidelines on management of HBV infection in patients receiving chemotherapy, biologicals, immunosupressants, or corticosteroids for the treatment of rheumatologic conditions, malignancies, inflammatory bowel disease, dermatologic conditions, or solid-organ or bone marrow transplantation. The Indian National Association for Study of the Liver (INASL) had set up a taskforce on HBV in 2016, with a mandate to develop consensus guidelines for management of various aspects of HBV infection, relevant to India. In 2017 the taskforce had published the first INASL guidelines on management of HBV infection in India. In the present guidelines, which are in continuation with the previous guidelines, the issues on management of HBV infection in patients receiving chemotherapy, biologicals, immunosupressants, or corticosteroids are addressed.

The irritable bowel syndrome is the commonest gastrointestinal disorder seen in practice but its exact prevalence in India is not known. This study was carried out to determine the prevalence of symptoms compatible with this diagnosis in general population. A cross sectional random sample survey was conducted in various strata of urban population in Wanoworie area of Pune. Survey utilized personal interviews based on a questionnaire. Symptoms were evaluated as per Manning criteria and the diagnosis of irritable bowel syndrome was defined by Kruis diagnostic index. Of the 1010 subjects interviewed, 370 (37%) reported more than 6 episodes of abdominal pain in previous 6 months, with 333 reporting symptoms consistent with the the diagnosis of irritable bowel syndrome. At least one of the Manning's symptoms was present in 307 out of 370 subjects (83%). The male female ratio was 5.3:1. Among males, 288 (35%) and among females 82 (53.2%) persons had at least some degree of abdominal discomfort. Other common symptoms were: excessive passage of wind (42.2%), irregular bowel habits (33%), excessive belching (30.8%), constipation (27.5) and feeling of incomplete evacuation(28.1%). About one third of the symptomatic subjects (134 or 36.2%) had seen a doctor or wanted to be seen by a specialist. Overall prevalence of the symptoms consistent with irritable bowel syndrome thus, is 33 per cent though only about a third of these may possibly consult a doctor. Follow up of all these patients for a mean duration of 8.3 months showed that no case of organic disease was picked up either by the scoring system or by the gastroenterologist. Symptoms consistent with the diagnosis of irritable bowel syndrome are see in almost one third of the study population residing in Wanoworie area of Pune.

Pulmonary embolism is considered a rare disease in India. The diagnosis is likely to be missed as its presentation is often enigmatic. Ten cases of pulmonary embolism are presented. Nine patients presented with acute pulmonary embolism, while one had chronic pulmonary emboli with cor pulmonale. The diagnosis was based on pulmonary angiography (1 case), lung perfusion/ventilation scan (2 cases), autopsy (2 cases) and characteristic ECG, X-ray chest and clinical features (5 cases). The initial diagnosis was often incorrect (7/10 cases). Common presenting clinical features were: sudden breathlessness (10/10), tachypnoea (10/10) and tachycardia (8/10); chest pain (3/10) was uncommon and hemoptysis was not seen in any patient. ECG revealed isolated sinus tachycardia in 2 cases, S 1 Q 3 T 3 pattern in 2, and right axis with ST-T wave changes in 5 patients. X-ray chest showed either an area of oligemia or non-specific opacities in 7 patients and was normal in three cases. Advances in specific diagnostic modalities coupled with heightened awareness should contribute to an early detection of pulmonary embolism, rarity of which may be more apparent than real.

A 35-year-old healthy male with no history of any past medical illness developed severe headache, vomiting and drowsiness while at high altitude (4,572 m) in the eastern Himalayan ranges. He was evacuated to a tertiary-care hospital where he was diagnosed to have cerebral sinus venous thrombosis (CSVT) on magnetic resonance imaging, with deep vein thrombosis (DVT) of his right popliteo-femoral vein on color Doppler study. Investigation for thrombophilia revealed protein S (PS) deficiency in this patient. Family screening revealed low levels of PS in two elder brothers. One brother had a history of ‘stroke in young’ at the age of 20 years with the other being asymptomatic. This established the hereditary nature of PS deficiency. We are not aware of any previously published report on hereditary PS deficiency combined with CSVT and DVT occurring at high altitude. However, 1 case of protein C deficiency with CSVT has been reported previously.

Background Antituberculosis treatment (ATT) induced hepato-toxicity is common, but risk factors predicting its development are poorly understood. The present study evaluates the clinical risk factors predicting the development of hepatotoxicity in Indian patients with tuberculosis on antituberculosis treatment. Methods Three groups of patients were studied at three service hospitals over a 3 year period from 2000-2002. Patients given ATT were followed up with monthly LFTs. Consecutive patients who developed Liver dysfunction (rise in SGPT > 5 times upper limit of normal) were studied, along with matched controls who did not. Markers for hepatitis B were also noted in these patients once in 6 months. A third group of patients who did not receive ATT but were HBsAg positive, were also similarly followed up. The possible association of age and sex of the patient, alcoholism, unrecognized chronic liver disease, hepatitis B virus carrier status and nutritional status with ATT-induced hepatitis was assessed. Statistical analysis was carried out by Chi square test/Fisher's exact test using WHO provided software Epi Info 6. Sixty-nine patients with ATT-induced hepatotoxicity were prospectively studied. In addition 128 patients on anti-tuberculosis drugs without hepatotoxicity and 39 HBsAg carriers not on ATT were followed up for 1 year. Results Age, Sex, history of alcohol intake and BMI were not found to be related to development of hepatotoxicity. Presence of HBV infection or an underlying silent chronic liver disease were found to significantly increase the risk of development of ATT-induced hepatotoxicity. Continuation of ATT after development of jaundice was associated with a high fatality rate. It was possible to re-introduce isoniazid in 96% and rifampicin in 88% of patients with ATT induced hepatotoxicity. Conclusion ATT-induced hepatitis is common and is potentially fatal. It is likely to occur in those with underlying silent chronic liver disease, HBV infection and have been given ATT without a definite evidence of tuberculosis. Discontinuation of ATT leads to rapid recovery in most cases and drugs can safely be introduced after recovery in a majority of cases.

Jaundice is not an unusual accompaniment of malaria. It can occur due to intravascular hemolysis, disseminated intravascular coagulation, and, rarely, 'malarial hepatitis'. Although the primary schizogony of the malarial parasite always leads to the rupture of the infected hepatocyte, alteration of the hepatic functions is uncommonly recorded due to this event. Histologically, the hepatitis or the actual inflammation in the liver has never been demonstrated. Nonetheless, the term 'malarial hepatitis' (MH) has been used in the literature to describe the occurrence of hepatocellular jaundice in patients with Plasmodium falciparum infection. The authors' own data and review of the literature indicate that it is not an uncommon entity. In endemic areas, jaundice is seen in approximately 2.5% of patients with falciparum malaria. It also appears to be a heterogeneous syndrome and one can recognize two clinical subsets. In one group there was an acute, virulent presentation with coma, renal failure and in some cases even hemorrhagic manifestations. It is only in this setting that jaundice signified a 'severe' disease as noted by the World Health Organization action program. This presentation is often confused with acute viral hepatitis and acute hepatic failure in non-endemic areas, but can be clinically differentiated.

Background HBV DNA quantitation is used extensively world wide for the diagnosis and monitoring of treatment of Hepatitis B virus (HBV) infection. However, it has still to be popular in India. The aim of this study was to quantitate HBV – DNA by Real time – PCR method in Hepatitis B and in immuno-compromised patients, to compare the results with HBeAg detection and to monitor the response to therapy of chronic Hepatitis B patients to antivirals. Methods Ninety one serum samples of Hepatitis group of patients (all HBsAg positive), 41 samples from immuno-compromised patients (all HBsAg negative) and 49 patients of Chronic Hepatitis B group (all HBsAg positive) were the subjects of this first ever study in Armed Forces. Twenty serum samples from healthy volunteers and non-hepatitis B patients served as negative controls. The amplification detection was carried out in a Rotor-Gene 2000-sequence detector Results Amongst Hepatitis B group, 33% (30/91) of the samples were positive for HBV-DNA and 26% (24/91) of samples were positive for HBeAg. In the immuno-compromised group of patients 14.6% (6/11) of samples were positive for HIV-DNA and 9.7% (4/41) were positive for HBeAg. Of the Chronic Hepatitis B patients on treatment, all (100%) were positive by HBV-DNA, whereas 29/49 (59.2%) were positive by HBeAg before treatment. After treatment with antivirals, 06/49 (12.2%) were positive by both tests and 11/49 (22.5%) were positive only by HBV-DNA. 32/49 (65.3%) patients became negative serologically after therapy. Conclusion HBeAg status did not necessarily reflect HBV-DNA level in the serum, as 10/91 (11%) in the Hepatitis B group, 2/41 (4.9%) in the immuno compromised group and 20/49 (40.8%) patients in the Chronic Hepatitis B group were positive for HBV-DNA but negative for HBeAg. HBV-DNA was not found to be positive amongst any of the negative controls. Real time – PCR is a sensitive and reproducible assay for HBV-DNA quantitation and may be started in Armed Forces referral centers in the near future.

Summary Background Chronic abdominal pain and frequent bowel disturbance are common symptoms experienced by more than 15% of apparently healthy people. In areas endemic for Entamoeba histolytica infection, these symptoms are often diagnosed as non-dysenteric intestinal amoebiasis even though no causal relation between such symptoms and E histolytica has been established and clinical presentation of non-dysenteric intestinal amoebiasis and irritable bowel syndrome (IBS) is not distinct. This study was done to assess the clinical significance of E histolytica infection in causation of such symptoms. Methods Patients with symptoms suggestive of nondysentericintestinal amoebiasis were recruited from a survey to assess the prevalence of abdominal symptoms in the general population (group A; n=78) and from medical outpatient clinics (group B; n=66). Participants who had symptoms as well as symptom-free controls (group C; n=100) were clinically examined and underwent stool examination, amoebic serology, colonoscopic examination, histopathological examination of colonoscopic biopsy samples, and a trial of antiamoebic therapy (only for participants with symptoms) with metronidazole and mebendazole. Findings There were no significant differences between the 144 patients with symptoms and the 100 symptom-free controls in the proportion with E histolytica in stools (26 [18%] vs 18 [18%]), serological evidence of E histolytica infection (61 [42%] vs 41 [41%]), colonoscopic abnormalities (five of 66 vs one of 33), or histopathological abnormalities (36 [49%] of 73 vs ten [30%] of 33). Cystpositive and cyst-negative individuals showed no significant difference in serological evidence of E histolytic infection, histological abnormalities, or response to therapeutic trial with metronidazole. A diagnosis of IBS was suggested on the basis of consensus criteria and Kruis diagnostic index in 127 of 144 patients with symptoms. The diagnosis of nondysenteric intestinal amoebiasis could be made in only one patient, who had relapse of symptoms within 6 weeks of antiamoebic therapy and therefore the relapse did not meet criteria for the diagnosis of non-dysenteric intestinal amoebiasis. More than 60% of cyst-positive as well as cystnegative patients with symptoms showed either complete or partial response to treatment strategy for IBS. Interpretation Chronic bowel symptoms, such as pain in abdomen and frequent bowel disturbance, have no association with either past or present infection with E histolytica . Most patients with such symptoms are likely to have IBS. The clinical entity of non-dysenteric intestinal amoebiasis, if it exists, must be extremely rare.

Liver allograft rejection is usually divided into acute (cellular) rejection and chronic (ductopenic) rejection. Most cases of acute rejection occur within four weeks of transplantation. There is a paucity of published literature on late acute rejection (LAR) in liver allografts and little is known about factors affecting its occurrence and outcome. To study the predisposing factors, clinical presentation, and prognosis of LAR, data prospectively collected on consecutive adult patients who underwent liver transplantation between 1982 and 1994, were analyzed. LAR was defined as histologically confirmed acute cellular rejection occurring 30 or more days after liver transplantation. Of the 717 patients, 59 (7.5%) had 71 episodes of LAR. Fifty-seven episodes were seen during the first year after transplantation, the remaining occurring between 1 and 6 years. Age, sex, pretransplant diagnosis, donor match of HLA, and blood groups was not associated with risk of LAR. Twenty-seven (38%) episodes were preceded by subtherapeutic blood levels of cyclosporine/FK506 (< 100 ng/ml and < 5 ng/ml, respectively) while an additional 6 (8%) had marginally low blood levels (< 150 ng/ml and < 10 ng/ml, respectively). Treatment with high-dose prednisolone resulted in complete resolution of rejection in 36 (51%) episodes, partial response in 21, and no response in 14 patients. Sixteen patients (27%) developed chronic rejection and graft loss. Development of chronic rejection was not affected by age or sex of the patient, timing of LAR, or histological severity of AR. Delayed response to therapy during an earlier episode of AR, and histological findings of centrilobular necrosis or bile duct loss at the time of diagnosis of LAR were associated with high risk of progression to chronic rejection and graft loss.

Eighty patients with various thyroid disorders and 20 controls were investigated to determine antibodies against thyroglobulin and microsomal antigens by haemagglutination and immunofluorescent techniques. They were also tested for immunoglobulin profile by radial immunodiffusion methods. Patients with Hashimoto's disease, idiopathic hypothyroidism, and Grave's disease showed significant elevations of IgG. None of the patients with toxic nodular goitre or thyroid adenoma showed any thyroid antibodies while 69.2% patients with Grave's disease, 16% with euthyroid goitre, 58.3% with hypothyroidism and all the patients with Hashimoto's disease had microsomal antibodies by immunofluorescent test. Similarly, all the cases of Hashimoto's disease, 41.6% of those with hypothyroidism, 30% of Grave's disease patients and none of the patients with toxic nodule or thyroid adenoma had thyroglobulin antibodies by haemaglutination test. Evaluation for auto-antibodies may aid the clinician in the overall assessment of various thyroid disorders.

A few months back the Editor-in-Chief of this journal asked me to write a contemporary piece on ‘the future of hepatology in India’. He said, “You have touched some of these issues as an outgoing president, just put it in writing”. I was very reluctant to take up this task in the beginning. My lack of enthusiasm stemmed from two main reasons. Firstly, I was aware that three doyens of Hepatology in India namely Dr. Subrat K. Acharya, Dr. Yogesh K. Chawla and Dr. Shiv K. Sarin, (in alphabetical order), had delivered exquisite discourses on this issue some time back. And then, given my service background, I was insulated from the forces that have led to chaotic development of this specialty in India. But possibly what I did have was the best ringside view, to be able to introspect and comment on the development of Hepatology in India during the last few decades. In the Armed Forces, we often spend considerable time in planning and in trying to ensure careful execution of the agreed plan. I am still not clear if such an exercise was ever done in India for Hepatology. We are far from having a clear plan as to how many Hepatologists does our country need? How are we going to get so many doctors to specialize in Hepatology? If we do manage the required numbers, how would we employ them to have best results for our people?

To derermine if early ambulation was safe in acute viral hepatitis (AVH), 202 patients of uncomplicated AVH were prospectively randomised into two group. Group A (n=100) received conventional treatment with bed rest while group B (n=102) patients were ambulated as soon as their clinical symptoms abated and progressive clinical and biochemical recovery was noted. While mean recovery time in two groups was not significantlly different (28.8 vs 29.7 days), bed rest period in group B was significantly less (28.8 vs 8.6 days). Natural history of the AVH, clinical and biochemical findings and relapse rate over a follow up period of 14 to 16 months, were no different in the two groups. None of the patients developed chronic hepatitis. Early ambulation is there fore safe in uncomplicated AVH and can lead to enormous saving of manhours and hospital resources.

Stroke is a common medical emergency. There is limited knowledge about stroke at high altitude. We present the clinical profile of 30 cases of stroke at high altitude seen at our center between November 1998 to July 2000. A detailed neurological and systemic examination was carried out. Cases were investigated with blood counts, lipid profile, cardiac evaluation, and CT scan/MRI. Coagulation parameters were studied in some cases. Strokes formed 13.7/1000 of hospital admissions from high altitude area, compared to 1.05/1000 in nonhigh altitude area. All our cases from high altitude area were males (serving soldiers of armed forces). Their mean high altitude stay was 10.2 months, and they were all located at heights greater than 4270 m. Age ranged from 22 to 48 years (mean 33.4 yr). Except for smoking (in four cases), they had no preexisting risk factors. Twenty-two cases were of ischemic stroke, 2 of intracerebral hemorrhage, 4 of TIA/RIND (transient ischemic attack/reversible ischemic neurological deficit), and 2 had cerebral venous thrombosis. Out of 30 cases, 28 were of "stroke in young" (45 yr) and were compared with cases in the same age group from nonhigh altitude areas. Polycythemia with Hb ranging from 16.2 to 22 g.dL(-1) was seen in 21 of these 28 cases (75%). Protein C and S deficiency was found in 1 case in each group. CT scan showed massive infarcts involving at least 50% of one cerebral hemisphere in 12 cases. Multiple infarcts were seen in one case.Long-term stay at high altitude is associated with higher risk of stroke. Although all types of stroke were seen, ischemic stroke was the commonest. Massive infarcts were common. Polycythemia was an important risk factor.

Background/Aims: An accurate and early assessment of the individual patient is critical in deciding whether liver transplantation is indicated in the treatment of fulmitant hepatic failure. Based on analysis of patients treated between 1973 and 1985, the Liver Unit at King's College Hospital, London, developed a prognostic model to identify patients with a poor prognosis. The present study was done to determine the applicability of this model in fulminant hepatic failure patients seen at our center in the 1990s. Methods: The records of 145 patients with fulmitant hepatic failure, treated conservatively at Queen Elizabeth Hospital, Birmingham between 1990 and 1994, were analyzed. An additional 81 patients who were transplanted for fulmitant hepatic failure during the same period were excluded from the study. Results: Application of King's College Hospital criteria at the time of admission to this hospital in the acetaminophen group, had a positive predictive value of 88%, negative predictive value of 65% and predictive accuracy of 71%. The positive predictive value, negative predictive value and predictive accuracy of these criteria for non-acetaminophen-induced fulminant hepatic failure, were 79%, 50% and 68%. Multivariate analysis identified prothrombin time, serum creatinine, white cell count and abnormal potassium levels as independent predictors of mortality in acetaminophen-induced fulmitant hepatic failure; and prothrombin time alone in fulmitant hepatic failure induced by other etiologies. Conclusions: The King's College Hospital criteria for predicting outcome of fulmitant hepatic failure were found to have a slightly lower predictive accuracy than shown in the original study.

To find out the efficacy of sucralfate in preventing gastrointestinal side effects of non-steroidal anti-inflammatory drugs (NSAIDs) a prospective, randomised single blind study was conducted from 1989 to 1992. Patients with osteoarthritis, rheumatoid arthritis and other long standing painful conditions, who were expected to receive NSAIDs for over three months, were recruited into the study. All medicines were discontinued for a period of 10-15 days prior to initial endoscopic assessment. NSAID therapy was started and the patients were randomised to receive either placebo (group A) or sucralfate (group B) in addition. Patient were reassessed clinically every week and an endoscopic examination was repeated after 6-8 weeks of follow-up. A total of 176 patients were studied in group A (n=91) and group B (n=85). At the end of 8 weeks gastrointestinal symptoms were present in 30.6% and 26.4% patients of group A and B respectively. Endoscopic assessment showed superficial lesions in 36.5% and 18.7% while endoscopic ulcer in 2.4% and 1.1% patients of groups A and B respectively. Thus in patients receiving chronic NSAID therapy, simultaneous administration of sucralfate reduces the incidence of superficial gastric lesions but has no significant effect on symptoms or ulcer formation.