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Biomedical subjects

S K Acharya

Publications and source records attributed to S K Acharya.

At least 19 recordsLinked to original sources
PubMed2006

Non-alcoholic fatty liver disease may not be a severe disease at presentation among Asian Indians.

AIM: To evaluate the clinical and biochemical profile of patients with non alcoholic fatty liver disease (NAFLD) and to assess their histological severity at presentation. METHODS: Consecutive patients presenting to the liver clinic of All India Institute of Medical Sciences (AIIMS) with raised transaminases to at least 1.5 times upper limit of normal, and histologically confirmed non-alcoholic fatty liver disease were included. Patients who had significant alcohol intake or positive markers of other liver diseases or who were taking drugs known to produce fatty liver were excluded. The clinical, biochemical and histological profile of this group was studied. RESULTS: Fifty-one patients with NAFLD formed the study population. Their median age and BMI were 34(17-58) years and 26.7(21.3-32.5) kg/m(2) respectively and 46 (90.1%) were males. The majority of the patients had mild inflammation, either grade 1 [32 (63%)] or grade 2 [16 (31%)] and only 3 (6%) patients had severe (grade 3) inflammation. Twenty-three (45%), 19 (37%), 8(16%) and 1(2%) patient had stage 0, 1, 2 and 3 fibrosis respectively on index biopsy and none had cirrhosis. On univariate analysis, triglyceride levels more than 150 mg % (OR = 7.1; 95% CI: 1.6-31.5, P = 0.002) and AST/ALT ratio>1 (OR = 14.3; 95% CI: 1.4-678.5, P = 0.008) were associated with high grades of inflammation and none was associated with advanced fibrosis. On multivariate logistic regression analysis, hypertriglyceridemia >150 mg% was the only factor independently associated with presence of high grade of inflammation (OR = 1.6; 95% CI: 1.3-22.7, P = 0.02), while none was associated with advanced fibrosis. Triglyceride levels correlated positively with inflammatory grade (r = 0.412; P = 0.003). CONCLUSION: NAFLD in North Indian patients is a disease of young over-weight males, most of whom are insulin resistant and they tend to have a mild histological disease at presentation.

Adolescent↗
PubMed2005

Bovine tuberculosis in India: potential basis for zoonosis.

Our laboratory has designed a specific nested-PCR (N-PCR) assay, based on the hupB gene of Mycobacterium tuberculosis (Rv2986c) and Mycobacterium bovis (Mb3010c) as a method to differentiate these closely related species. The present paper deciphers the utility of this assay for identification of pathogenic Mycobacteria in clinical samples. Extra-pulmonary clinical samples obtained from cattle and humans were investigated. Pre-dominance of M. tuberculosis (15.7%) and M. bovis (26.8%) was seen in humans and cattle, respectively. However, more importantly, both mycobacterial pathogens (mixed infection) were identified in a number of samples. In humans 8.7% of the samples and 35.7% in cattle were classified as mixed infection. The detection of mixed infection with the mycobacterial pathogenic duo in humans and bovines denotes the prospect of potential transmission of these pathogens from humans to cattle (zoonosis) and vice versa (reverse zoonosis).

Animals↗
PubMed2005

Predictive value of arterial ammonia for complications and outcome in acute liver failure.

BACKGROUND AND AIMS: In acute liver failure (ALF), the brain is exposed to high levels of ammonia. Human studies defining the clinical significance of ammonia in ALF are lacking. This prospective study evaluated the relationship of arterial ammonia levels at admission to complications and survival among patients with ALF. METHODS: Eighty consecutive ALF patients admitted from March 2001 to December 2003 were followed up until death or complete recovery. All had arterial ammonia estimation at admission (enzymatic method). Logistic regression analysis was performed to identify independent predictors of mortality. RESULTS: Forty two (52.5%) patients died. Non-survivors had significantly higher median ammonia levels than survivors (174.7 v 105.0 micromol/l; p<0.001). An arterial ammonia level of > or = 124 micromol/l was found to predict mortality with 78.6% sensitivity and 76.3% specificity, and had 77.5% diagnostic accuracy. Patients with higher ammonia levels also developed more complications, including deeper encephalopathy (p = 0.055), cerebral oedema (p = 0.020), need for ventilation (p<0.001), and seizures (p = 0.006). Logistic regression analysis showed that pH, presence of cerebral oedema, and arterial ammonia at admission were independent predictors of mortality (odds ratios 6.6, 12.6, and 10.9, respectively). Incorporating these variables, a score predicting mortality risk at admission was derived: 2.53 + 2.91 ammonia + 2.41 oedema + 1.40 pH, where ammonia is scored as 0 (if <124 micromol/l) or 1 (if > or =124 micromol/l); oedema is scored as 0 (absent) or 1(present); and pH is scored as 1 (if < or =7.40) or 0 (if >7.40). Levels of partial pressure of ammonia were equally correlated with outcome. CONCLUSION: Arterial ammonia at presentation is predictive of outcome and can be used for risk stratification. Ammonia lowering therapies in patients with ALF should be evaluated.

Adolescent↗
PubMed2004

Frequency and role of hepatitis-C virus and type II cryoglobulinemia in membranoproliferative glomerulonephritis.

BACKGROUND: Many studies have claimed a major role of chronic hepatitis-C virus (HCV) infection in immune-mediated diseases such as membranoproliferative glomerulonephritis (MPGN). Chronic HCV infection is also known to produce essential mixed cryoglobulinemia (EMC), which in turn may manifest as vasculitis and cryoglobulinemic MPGN. OBJECTIVE: The aim of the study therefore, was to determine frequency of association and pathogenetic role of HCV infection as well as that of EMC in MPGN patients. METHODS: Fifty-three adult patients of MPGN were studied for HCV, HBsAg, EMC, C3, anti-nuclear antibody (ANA), rheumatoid factor serologically. Histopathology, immunofluorescence (IF) were conducted in all patients and electron microscopy (EM) in those who were found HCV positive. Simultaneously 37 follow-up patients of HCV associated chronic hepatitis were investigated for EMC, renal functions and urinalysis done for evidence of glomerulonephritis (GN). RESULTS: Thirteen percent MPGN patients were HCV positive, however, no viral particle could be seen in electron microscopy in glomeruli of these patients. There was no serologic evidence of HCV induced immune complex GN. None of the MPGN patients showed cryoglobulinaemia. Similarly none from HCV associated chronic hepatitis group had EMC nor showed evidences of glumerulonephritis. CONCLUSION: Thirteen percent of adult MPGN patients in north India were seropositive for HCV, indicating significant association. However, clear evidence in favour of its pathogenetic role was lacking in our study. Secondly, this study reveals that MPGN is non-cryoglobulinemic and HCV is not a major cause in our population compared to what is reported from other countries. These observations need confirmation by a larger study.

Adult↗
PubMed2003

Acute liver failure: prognostic markers.

Acute liver failure (ALF) is defined as liver failure occurring within one month of the occurrence of jaundice. The disease has a grim prognosis, with a mortality of 65% to 85%. The management of ALF has till recently been conservative, and newer therapeutic modalities like bioartificial liver, hepatocyte transplant, and extracorporeal liver assist devices have not yet been proven to be successful. Liver transplant has changed the gloomy outlook of the disease, and post-transplant survival rates of 60%-70% have been reported from most centers. However liver transplant is expensive, necessitates life-long immunosupression, and is limited by a global shortage of available organs. It is thus necessary to select patients who are at greatest risk of death for liver transplantation. Prognostic criteria are based primarily either on clinical and laboratory (coagulation tests, serum bilirubin) parameters, or on other parameters like liver volume. Prognostic criteria have been developed both from the East and the West; these are essentially similar except that the Western criteria take into account etiology (drug overdose being the main cause of ALF there) as well as jaundice-encephalopathy interval as factors for prognostication. The King's College criteria were one of the first prognostic systems; it has two parts for both paracetamol as well as non paracetamol ALF. The criteria from our institute found prothrombin time >25 s, serum bilirubin >15 mg/dL, age >40 years, and cerebral edema to be bad prognostic markers. Criteria from the PGIMER, Chandigarh found age >50 years, raised intracranial pressure, prothrombin time >100 s, and onset of HE more than seven days after the jaundice as poor prognostic markers. All these clinical criteria have similar sensitivity and specificity.

Humans↗
PubMed2002

Etiopathogenesis of acute hepatic failure: Eastern versus Western countries.

Etiopathogenesis of acute hepatic failure (AHF) in Eastern and Western countries is distinct. In the East hepatitis viruses cause AHF in more than 95% of such cases, while causes of AHF in the West are quite heterogenous. Hepatitis E virus is the major etiological agent of AHF in countries like India where the virus is hyperendemic. Occult HBV infection may also be causing AHF in a sizable proportion of cases in areas where chronic HBV infection frequency is high. Paracetamol causes AHF in about 70% cases in the UK and about 20% cases in USA, whereas in France and Denmark, non-steroidal anti-inflammatory drugs are more frequently associated with AHF. Hepatitis B virus causes AHF in about one-third of cases in the latter two countries.

Europe↗
PubMed2001

A study of autoimmune markers in hepatitis C infection.

BACKGROUND & OBJECTIVES: Hepatitis C virus (HCV) infection is associated with several autoimmune markers. Despite HCV being common in India, no information on this aspect is available. This study was undertaken to ascertain the frequency and clinical significance of autoimmune markers like rheumatoid factor (RF), antinuclear antibodies (ANA), antibodies to double stranded deoxyribonucleic acid (dsDNA), anti neutrophil cytoplasmic antibody (ANCA), anti smooth muscle antibodies (ASMA), anti liver kidney microsomal 1 antibodies (anti LKM1), anti gastric parietal cell antibodies (anti GPCA), anti mitochondrial antibodies (AMA), anti cardiolipin antibodies (ACL) and cryoglobulins in HCV infection and to determine the effect of treatment on these markers. METHODS: Twenty five patients with chronic hepatitis C and 25 healthy controls were studied. Cryoglobulins were detected by cryoprecipitation, RF by latex agglutination, anti dsDNA and ACL by ELISA while indirect immunofluorescence was used to detect all other autoantibodies. RESULTS: Eighteen patients (72%) demonstrated autoimmune markers. RF, cryoglobulins and anti LKM1 antibodies were the most frequently detected markers (in 32% patients each). ASMA, perinuclear ANCA (pANCA), ANA and anti GPCA were seen in 24, 20, 12 and 4 per cent patients respectively. None of the patients exhibited ACL, AMA or antibodies to dsDNA. No antibodies were detected in healthy controls. Sixty per cent of the patients had rheumatological symptoms. Of the seven patients followed up after treatment with alpha interferon, only two exhibited persistence of RF, while symptoms and other markers disappeared. INTERPRETATION & CONCLUSION: Rheumatological symptoms and autoimmune markers are common in HCV infection and are usually overlooked. Patients with unexplained joint pains and/or palpable purpura should be screened for HCV. Further studies are needed to delineate fully the link between infection and autoimmunity.

Adult↗
PubMed2000

Acute hepatic failure in India: a perspective from the East.

Acute hepatic failure (AHF) in India almost always presents with encephalopathy within 4 weeks of the onset of acute hepatitis. Further subclassification of AHF into hyperacute, acute and subacute forms may not be necessary in this geographical area, where the rapidity of onset of encephalopathy does not seem to influence survival. Viral hepatitis is the cause in approximately 95-100% of patients, who therefore constitute a more homogeneous population than AHF patients in the West. In India, hepatitis E (HEV) and hepatitis B (HBV) viruses are the most important causes of AHF; approximately 60% of cases are caused by to these viruses. Hepatitis B virus core mutants are very important agents in cases where hepatitis B results in AHF in this country. Half of the patients with AHF admitted to our centre are female, one-quarter of whom are pregnant. Therefore, pregnant females who contract viral hepatitis constitute a high-risk group for the development of AHF. However, the outcome of AHF in this group is similar to that in non-pregnant women and men. No association with any particular virus has been identified among sporadic cases of AHF. In our centre, approximately one-third of AHF patients survive with aggressive conservative therapy, whereas two-thirds of deaths occur within 72 h of hospitalization. Cerebral oedema and sepsis are the major fatal complications. Both fungal and gram-negative bacteria are major causes of sepsis. Among patients with AHF, despite the presence of sepsis, its overt clinical features (i.e. fever, leucocytosis) may be absent and objective documentation of the presence of sepsis in such patients is achieved by repeated culture of various body fluids. It should be possible to develop simple, clinical prognostic markers for AHF in this geographical region, in order to identify patients suitable for liver transplantation.

Adult↗
PubMed2000

Renal function and structure in subacute hepatic failure.

BACKGROUND AND AIMS: Subacute hepatic failure (SHF) is a fatal complicaton of acute viral hepatitis. Renal failure has been implicated as the main cause of death in this disease. However, renal functional and structural evaluation in such patients have not been performed. The present prospective study evaluated the renal functional and structural abnormalities in patients with subacute hepatic failure. METHODS: Fourteen consecutive patients with SHF, 11 with acute liver failure (ALF) and 15 with cirrhosis of the liver (Child's B or C) were included in the present study. All 40 patients had liver disease caused by hepatitis viruses. The glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) estimations were measured in all patients by the use of technetium-99m diethylenetriaminepentaacetic acid and [131I]-labeled ortho-iodohippuric acid, respectively. Ante-mortem or post-mortem liver biopsies were performed in all patients. In three patients with SHF, post-mortem kidney biopsies were also performed. RESULTS: Thirty six percent (5/14) of patients with SHF, 18% (2/11) of patients with ALF and 20% (3/15) of patients with cirrhosis had renal failure. Seven patients with SHF, seven with ALF and nine with cirrhosis died. All the patients with renal failure in each of the three groups were among the deceased patients. Glomerular function was markedly affected among patients with SHF, which was shown by significantly higher (P < 0.05) proteinuria levels (0.367 +/- 0.38 g/24 h) compared to levels in patients with ALF (0.178 +/- 0.11 g/24 h) and cirrhosis (0.212 +/- 0.133 g/24 h). The GFR in SHF (56 +/- 27 mL/min per 1.73 m2) and cirrhotic patients (58 +/- 36 mL/min per 1.73 m2) was significantly lower compared to those in ALF patients (102 +/- 51 mL/min per 1.73 m2; P < 0.05). A significantly higher proportion (P < 0.05) of patients with SHF and cirrhosis (64 and 73%, respectively) had a GFR below 80 mL/min per 1.73 m2 compared to patients with ALF (18%). The GFR value among the deceased SHF patients (46 +/- 26 mL/min per 1.73 m2) was significantly lower (P < 0.05) than those SHF patients who survived (65 +/- 25 mL/min per 1.73 m2). However, similar features could not be documented among patients with ALF or cirrhosis. Subtle structural changes in the glomerulus were also noted in patients with SHF. These included mesangial proliferation and thickening, basal membrane thickening and increased cellularity with interstitial edema. The ERPF was markedly reduced (P = 0.058) among patients with SHF (347 +/- 131 mL/min per 1.73 m2) and cirrhosis (395 +/- 137 mL/min per 1.73 m2) in comparison to ERPF documented among patients with ALF (436 +/- 217 mL/min per 1.73 m2). Such a reduction in renal tubular blood flow, along with histologic documentation of hyaline presence, bile and grannular cast in the tubule, indicated a possible tubular dysfunction in patients with SHF. CONCLUSION: It is concluded that glomerular and tubular dysfunction with subtle structural abnormalities does occur in patients with SHF. These are similar to renal changes in cirrhosis and may have similar pathogenetic mechanisms that require further evaluation.

Adolescent↗
PubMed1999

2,6-Dichloro-phenol indophenol prevents switch-over of electrons between the cyanide-sensitive and -insensitive pathway of the mitochondrial electron transport chain in the presence of inhibitors.

To evolve a simple oxygen electrode-based method to estimate alternative respiration, one needs to develop a procedure to prevent switch-over of electrons to either pathway upon inhibition by cyanide or salicylhydroxamic acid. It was hypothesized that the inclusion of appropriate electron acceptor, possessing redox potential close to one of the electron transport carriers in between ubiquinone (branch point) and cytochrome a-a3, should be able to stop switch-over of electrons to either pathway by working as an electron sink. To test the hypothesis, 2,6-dichloro-phenol indophenol (DCPIP; redox potential +0.217 V), an artificial electron acceptor having a redox potential quite similar to the site near cytochrome c1 (redox potential +0.22 V) on the cyanide-sensitive pathway, was used with isolated mitochondria and leaf discs in the absence and presence of inhibitors (potassium cyanide, antimycin A, and salicylhydroxamic acid). Polarographic data confirmed electron acceptance by DCPIP only from the inhibited (by cyanide or salicylhydroxamic acid) mitochondrial electron transport chain, hence preventing switch-over of electrons between the cyanide-sensitive and cyanide-insensitive pathway of respiration. Results with antimycin A and reduction status of DCPIP further confirmed electron acceptance by DCPIP from the mitochondrial electron transport chain. Possible implications of the results have been discussed.

2,6-Dichloroindophenol↗
PubMed1999

Is protein-deficient diabetes mellitus a pancreatitis?

BACKGROUND: Malnutrition-related diabetes mellitus is a distinct clinical entity subdivided into protein-deficient diabetes mellitus (PDDM) and fibrocalculus pancreatic diabetes (FCPD). Whereas FCPD has obvious pancreatitis manifested by pancreatic duct calculi, the evidence for involvement of the pancreas in PDDM is limited to the presence of ketosis-resistant hyperglycaemia. METHODS: We studied 10 patients with PDDM biochemically and radiologically. Endoscopic retrograde cholangiopancreatography was performed to determine if they had any evidence of chronic pancreatitis. RESULTS: Their mean faecal chymotrypsin level was low (13.2+/-5.72 microg/g), as was their basal c-peptide value (0.35+/-0.15 mmol/L). Islet cell antibodies were not detected in any of these patients. Ultrasound examination revealed pancreatic atrophy. In two patients, however, the pancreas was bulky. The ERCP showed generalized thinning of the pancreatic duct, measuring 2.4+/-0.06mm in the head, 2.01+/-0.08 mm in the body and 1.02 +/- 0.03 mm in tail region; side branches were seen but they were too sparse and thin. CONCLUSIONS: The significance of these changes is not clear, but they may represent an ongoing pancreatic disease and may, indeed, be the earliest changes of chronic pancreatitis.

Adolescent↗
PubMed1999

Portal systemic shunting of insulin does not lead to insulin resistance in patients with extrahepatic portal vein obstruction.

There is no clear relation between portal systemic shunting, reduced hepatic insulin extraction leading to an increased systemic delivery of insulin, and, resultant peripheral hyperinsulinemia and insulin resistance. Extrahepatic portal vein obstruction is a natural human model of portal systemic shunting with essentially normal liver function. To investigate the role of portal systemic shunting of insulin in creating systemic hyperinsulinemia and insulin resistance, we studied nine subjects with portal systemic shunting and nine controls matched for age (+/- 2 years), body weight (+/- 2 kg) and height (+/- 5 cm). We carried out an oral glucose tolerance test and hyperinsulinemic euglycemic clamp study at insulin infusion rate of 40 mU/m2/ min. Comparable (p = 0.61) basal insulin concentrations in the two groups (Mean (SE): 21.0 (3.98) vs. 24.1 (4.28) mU/L) demonstrated a lack of hyperinsulinemia in the presence of portal systemic shunting. The lower (p = 0.03) insulin area under curve on oral glucose tolerance test in presence of portal systemic shunting (7.40 (0.95) vs. 10.83 (1.15) U/L-min) indicated that lower extraction of insulin by the liver leads to a lower requirements in the periphery. The coefficient of variation for plasma glucose between 60 and 120 min of the clamps was 4.44 (0.55)%. Comparable (p = 0.82) M-values (6.21 (0.67) vs. 6.38 (0.45) mg/kg/min) in the two groups proved a lack of significant insulin resistance in the presence of portal systemic shunting. We conclude that isolated portal systemic shunting leads to neither hyperinsulinemia nor insulin resistance.

Adult↗
PubMed1998

Portal hypertensive gastropathy in noncirrhotic patients. The effect of lienorenal shunts.

We studied 25 consecutive patients with noncirrhotic portal hypertension to determine whether portal hypertensive gastropathy occurred and whether it was related to hypoacidity, hypergastrinemia, or portal venous congestion. Preoperative tests included gastrointestinal endoscopy, gastric mucosal biopsies, gastric acid estimation, and serum gastrin measurements. All patients had a central splenorenal shunt performed during which a full-thickness gastric biopsy was performed. The tests were repeated 3 to 16 months postoperatively. Eight of the 25 patients showed endoscopic evidence of portal hypertensive gastropathy. The shunt procedure reversed the gastropathy in 6 of 7 patients followed up. Mucosal biopsies revealed vascular ectasia in 24 of 25 patients; in 8 of the most severely affected there was partial or complete regression after surgery. The basal and peak acid outputs in the patients were normal for our laboratory at 2.9 +/- 0.25 meq/hour and 16.37 +/- 0.96 meq/hour, respectively. They remained unchanged after surgery. Fasting serum gastrin levels were also normal both before and after surgery. Our findings indicate that venous congestion is the cause of portal hypertensive gastropathy in patients with noncirrhotic portal hypertension and that it can be reversed by a decompressive procedure.

Adolescent↗
PubMed1998

Hepatitis G virus in multitransfused thalassaemics from India.

Hepatitis G virus (HGV)/GB virus-C (GBV-C) has been identified as a blood-borne agent with disputed pathogenicity. This virus belongs to the flaviviridae with a distant relationship to hepatitis C virus (HCV). Genetically divergent HGV isolates have been reported from different parts of the world. This study describes the prevalence of HGV in multitransfused thalassaemic children in India and genomic sequence variations in 11 HGV isolates from the same geographical location. Hepatitis G virus RNA was detected in 39.7% multitransfused thalassaemic children. The seroprevalence of hepatitis B virus (HBV) and HCV was 23.8% and 17.1%, respectively, and 11.4% had dual infection. The nucleotide sequence of a 166 bp HGV genomic segment from the putative capsid-envelope region (nucleotide; nt 578-743) from 11 Indian isolates was compared to the sequences available in the nucleotide databases. The isolates from India were 81.3-94.5% homologous to the isolates from other parts of the world. On phylogenetic analysis, it was observed that HGV isolates from India may belong to two genetically divergent types.

Amino Acid Sequence↗
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↗