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M Irshad

Publications and source records attributed to M Irshad.

At least 19 recordsLinked to original sources
PubMed2006

Transfusion transmitted virus: A review on its molecular characteristics and role in medicine.

The present review gives an updated overview of transfusion transmitted virus (TTV), a novel agent, in relation to its molecular characteristics, epidemiological features, modes of transmission, tissue tropism, pathogenesis, role in various diseases and its eradication from the body. TTV, a DNA virus, is a single stranded, non-enveloped, 3.8 kb long DNA virus with a small and covalently closed circular genome comprising 3852 bases. It was tentatively designated Circinoviridae virus. TTV genome sequence is heterogeneous and reveals the existence of six different genotypes and several subtypes. TTV has been reported to transmit not only via parenteral routes, but also via alternate routes. This virus has been detected in different non-human primates as well. At present, TTV is detected by polymerase chain reaction (PCR) with no other available diagnostic assays. It shows its presence globally and was detected in high percent populations of healthy persons as well as in various disease groups. Initially it was supposed to have strong association with liver disease; however, there is little evidence to show its liver tropism and contribution in causing liver diseases. It shows high prevalence in hemodialysis patients, pointing towards its significance in renal diseases. In addition, TTV is associated with several infectious and non-infectious diseases. Though, its exact pathogenesis is not yet clear, TTV virus possibly resides and multiplies in bone marrow cells and peripheral blood mononuclear cells (PBMCs). Recently, attempts have been made to eradicate this virus with interferon treatment. More information is still needed to extricate various mysteries related to TTV.

Animals↗
PubMed2006

Transfusion-transmitted virus in association with hepatitis A-E viral infections in various forms of liver diseases in India.

AIM: To describe the prevalence of transfusion-transmitted virus (TTV) infection in association with hepatitis A-E viral infections in different forms of liver diseases in North India. METHODS: Sera from a total number of 137 patients, including 37 patients with acute viral hepatitis (AVH), 37 patients with chronic viral hepatitis (CVH), 31 patients with cirrhosis of liver and 32 patients with fulminant hepatic failure (FHF), were analyzed both for TTV-DNA and hepatitis A-E viral markers. Presence of hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis E virus (HEV) infections was detected in different proportions in different groups. Moreover, TTV-DNA was simultaneously tested in 100 healthy blood donors also. RESULTS: None of the patients had hepatitis A virus (HAV) and hepatitis D virus (HDV) infections. Overall prevalence of TTV-DNA was detected in 27.1% cases with AVH, 18.9% cases with CVH, 48.4% cases with cirrhosis and 9.4% cases with FHF. TTV-DNA simultaneously tested in 100 healthy blood donors showed 27% positivity. On establishing a relation between TTV infection with other hepatitis viral infections, TTV demonstrated co-infection with HBV, HCV and HEV in these disease groups. Correlation of TTV with ALT level in sera did not demonstrate high ALT level in TTV-infected patients, suggesting that TTV does not cause severe liver damage. CONCLUSION: TTV infection is prevalent both in patients and healthy individuals in India. However, it does not have any significant correlation with other hepatitis viral infections, nor does it produce an evidence of severe liver damage in patients with liver diseases.

Adult↗
PubMed2006

Arsenic-induced cell death in liver and brain of experimental rats.

Arsenic is a well established human carcinogen and is ubiquitous in the environment. The present study demonstrates the effect of acute arsenic administration at three different doses in liver and brain of Wistar rats. Sodium arsenite was administered orally at doses of 6.3 mg/kg, 10.5 mg/kg and 12.6 mg/kg of body weight on the basis of a lethal dose 50% (LD50) for 24 hr. After administration of arsenites, liver and brain were analyzed for various parameters of oxidative stress, histopathological changes and caspase-3 activity. Glutathione levels were decreased significantly in the liver at all doses. In liver the following biochemical changes were observed, a significant lipid peroxidation and cytochrome-P450 induction along with significant decrease in catalase and superoxide dismutase was observed at 10.5 mg/kg and 12.6 mg/kg. The activity of glutathione peroxidase was increased significantly at all doses. In brain, no significant change was observed at 6.3 mg/kg. However, a significant increase in lipid peroxidation and glutathione peroxidase activity along with significant decrease in the activity of glutathione, catalase and superoxide dismutase was observed at 10.5 mg/kg and 12.6 mg/kg. The activity of glutathione-S-transferase was decreased significantly in both liver and brain at 10.5 and 12.6 mg/kg. No significant alteration in the activity of glucose-6-phosphate dehydrogenase and glutathione reductase was observed in either liver or brain at any dose. Dose-dependent histopathological changes, observed in both liver and brain are also described. A significant increase in caspase-3 activity was observed at all doses in liver and at 10.5 and 12.6 mg/kg in brain. Sodium arsenite caused DNA cleavage into fragments and manifested as "DNA laddering", a hallmark of apoptosis.

Animals↗
PubMed2006

Comparison of nebulised magnesium sulphate and salbutamol combined with salbutamol alone in the treatment of acute bronchial asthma: a randomised study.

OBJECTIVE: To test the hypothesis that combined administration of multiple doses of nebulised salbutamol and magnesium sulphate provides additional benefit compared with salbutamol alone in adult patients with acute asthma. DESIGN: Randomised, double blind, prospective study. METHODS: A total of 100 patients presenting to an emergency department with an acute attack of bronchial asthma were randomised to two groups: nebulisation with a combination of salbutamol and magnesium sulphate (group A) and nebulisation with salbutamol only (group B). Both groups received nebulisation thrice at intervals of 20 minutes. Salbutamol and magnesium sulphate were administered in doses of 0.5 mg and 500 mg, respectively, and the solutions were made isotonic to plasma osmolality. Pulse rate, blood pressure, and peak expiratory flow rate (PEFR) were measured at baseline and at 15, 60, 75, and 120 minutes. Serum magnesium levels and blood gases were measured at 0 and 120 minutes in both groups. RESULTS: All patients had either acute severe or life threatening asthma. The baseline characteristics were comparable in the two groups. Both groups showed significant rise in PEFR at all time intervals, however, there was no significant difference between the groups in rise in PEFR at any time point. Serum magnesium levels remained within normal limits, and there was no difference in requirement of additional medication during the study or hospital admission rates in both groups. No significant side effects were noted. CONCLUSION: This study suggests that there is no therapeutic benefit of adding magnesium sulphate to salbutamol nebulisation in the treatment of patients with acute severe or life threatening asthma.

Acute Disease↗
PubMed2006

Hepatitis C virus core protein: an update on its molecular biology, cellular functions and clinical implications.

The present review article is an update on various features of hepatitis C virus (HCV) core protein including its molecular biology, role in HCV replication, involvement in HCV pathogenesis, etiological role in hepatocellular carcinogenesis, significance in diagnosis and vaccination against HCV infection. Core protein is a structural protein of HCV virus and has only recently been characterized. It was found to play a major role in HCV-induced viral hepatitis. Although published information shows a lot about the clinical significance of HCV core protein, several studies are still needed to demonstrate its exact significance in viral biology and underlying HCV pathogenesis.

Apoptosis↗
PubMed2005

Arsenic induced apoptosis in rat liver following repeated 60 days exposure.

BACKGROUND: Accumulation of the wide spread environmental toxin arsenic in liver results in hepatotoxcity. Exposure to arsenite and other arsenicals has been previously shown to induce apoptosis in certain tumor cell lines at low (1-3 microM) concentration. AIM: The present study was focused to elucidate the role of free radicals in arsenic toxicity and to investigate the nature of in vivo sodium arsenite induced cell death in liver. METHODS: Male wistar rats were exposed to arsenite at three different doses of 0.05, 2.5 and 5mg/l for 60 days. Oxidative stress in liver was measured by estimating pro-oxidant and antioxidant activity in liver. Histopathological examination of liver was carried out by light and transmission electron microscopy. Analysis of DNA fragmentation by gel electrophoresis was used to identify apoptosis after the exposure. Terminal deoxy-nucleotidyl transferase mediated dUTP Nick end-labeling (TUNEL) assay was used to qualify and quantify apoptosis. RESULTS: A significant increase in cytochrome-P450 and lipid peroxidation accompanied with a significant alteration in the activity of many of the antioxidants was observed, all suggestive of arsenic induced oxidative stress. Histopathological examination under light and transmission electron microscope suggested a combination of ongoing necrosis and apoptosis. DNA-TUNEL showed an increase in apoptotic cells in liver. Agarose gel electrophoresis of DNA of hepatocytes resulted in a characteristic ladder pattern. CONCLUSION: Chronic arsenic administration induces a specific pattern of apoptosis called post-mitotic apoptosis.

Administration, Oral↗
PubMed2005

Dimethoate-induced effects on antioxidant status of liver and brain of rats following subchronic exposure.

Dimethoate, an organophosphate pesticide, is used in controlling the pests of a variety of crops. The study was carried out to understand the role of dimethoate in inducing oxidative stress leading to generation of free radicals and alterations in antioxidant enzymes and scavengers of oxygen free radicals. The effects of subchronic exposure of dimethoate in the production of oxidative stress were evaluated in male Wistar rats in the present study. Dimethoate was administered orally at doses 0.6, 6, and 30 mg/kg for 30 days in these rats. The results indicated an increase in levels of hepatic Cytochrome P450, lipid peroxidation, catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase in liver and brain at doses 6 and 30 mg/kg. There were no significant changes in the level of glucose-6-phosphate dehydrogenase activity except in liver at 30 mg/kg. A decrease in glutathione was observed at 30 and 6 mg/kg in both liver and brain. Glutathione-S-transferase increased at 30 and 6 mg/kg in liver and 30 mg/kg in brain. Erythrocyte acetylcholinesterase was inhibited at 30 and 6 mg/kg doses. Dose-dependent histopathological changes were seen in both liver and brain. This study concludes that oxidative stress due to dimethoate may be ascribed to induction of Cytochrome P450, inhibition of AChE and disturbance in activities of GSH and GST enzymes causing lipid peroxidation and histological and electron microscopic changes in liver and brain.

Administration, Oral↗
PubMed2005

Effects of acute dimethoate administration on antioxidant status of liver and brain of experimental rats.

Organophosphorus compounds may induce oxidative stress leading to generation of free radicals and alterations in antioxidant and scavengers of oxygen free radicals. The present study demonstrates effect of acute exposure of dimethoate in causation of oxidative stress in male Wistar rats. Dimethoate was administered orally at doses 45, 75 and 90 mg/kg of body weight on the basis of LD(50) for 24 h. After administration of doses, the liver and brain homogenates were analyzed for various parameters of oxidative stress. The results indicated an increase in hepatic cytochrome P450, lipid peroxidation, catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase in liver and brain at 90 and 75 mg/kg doses. There were no significant changes in the levels of glucose-6-phosphate dehydrogenase activity in both liver and brain. Similarly, there were no significant changes in hepatic glutathione and glutathione-S-transferase activities. However, there was a significant increase in glutathione and glutathione-S-transferase in brain at 90 mg/kg dose only. Erythrocyte acetylcholinesterase was inhibited at all doses used. Dose-dependent histopathological changes, observed in both liver and brain, are also described.

Administration, Oral↗
PubMed2004

Serum lipoprotein (a) levels in liver diseases caused by hepatitis.

Lipoprotein (a) [LP(a)] is a genetic variant of low density lipoprotein (LDL) and is mainly synthesized in liver. We conducted a study to evaluate the association of serum [Lp(a)] level with hepatitis viral infections. A total of 130 patients including 50 patients with acute viral hepatitis (AVH), 30 with chronic active hepatitis (CAH), 30 with cirrhosis of liver and 20 patients with fulminant hepatic failure (FHF) were analysed for different hepatitis viral markers and Lp(a) level in their serum samples. For comparison, 50 healthy persons were also tested for Lp(a) level. Serum Lp(a) level in patients in all the disease groups was significantly reduced compared to that observed in controls. Lp(a) level could not be detected in 40 per cent cases with AVH, 46.6 per cent with CAH, 70 per cent with cirrhosis and 80 per cent of FHF patients. On correlating Lp(a) level to viral etiology in these patients, it was found that the extent of diminution in Lp(a) level did not follow any trend with some particular viral infection and was recorded nearly same in all the infections. The findings of this study suggested that serum Lp(a) level was significantly (P<0.001) reduced in patients with liver diseases irrespective of the viral etiology.

Adult↗
PubMed2002

Superoxide dismutase and total anti-oxidant levels in various forms of liver diseases.

In order to understand the impact of viral hepatitis on anti-oxidant defence system of the body, blood levels of superoxide dismutase (SOD), an enzymatic anti-oxidant, and total anti-oxidant (TAO) were evaluated and co-related to etiological viral hepatitis in various forms of liver diseases. A total number of 110 patients including 50 patients with acute viral hepatitis (AVH), 30 patients with chronic active hepatitis (CAH) and 30 patients with cirrhosis of liver were analysed for different hepatitis viral markers and the anti-oxidant levels in their blood. For comparison, blood from 100 healthy persons were also simultaneously tested for anti-oxidant levels. Analysis of results indicated that none of the patients belonging to these three liver diseases had hepatitis A viral (HAV) and hepatitis D viral (HDV) infections. AVH group had mainly hepatitis B viral (HBV), hepatitis C viral (HCV) and hepatitis E viral (HEV) infections, CAH group had B and C infections and cirrhosis group had B, C and E infections. A sizeable number of patients in each group had no markers and were labelled as non-BCE group. On co-relating anti-oxidant levels to viral etiology in these patients, it was observed that in comparison to healthy control group, SOD level was significantly reduced in all the patients irrespective of the viral etiology (P<0.05-0.001). The impact of different viruses on reduction in SOD level was recorded to be the same with no significant difference in SOD level between any two viral infections. On the contrary, TAO level in the majority of patients was found to be comparable with that observed in healthy persons. An appreciable change in SOD level but little impact on TAO level during viral hepatitis may be explained by the possible adaptive rise of some other anti-oxidant level in the blood of these patients.

Journal Article↗
PubMed2002

Hepatitis B immunization in low birthweight infants: do they need an additional dose?

AIM: To determine the influence of gestation and weight on the development of protective anti-HB levels and geometric mean titres after three doses of HBV vaccine and to ascertain the need for a fourth dose in low birthweight infants. METHODS: Hepatitis B vaccine (Enivac HB, Panacea Biotec Ltd., India) was given to 82 preterm (PT) and 60 term intrauterine growth-retarded (T-IUGR) infants at birth and at 6, 10 and 14wk of life. RESULTS: Protective anti-HB levels (>10 mIU/ml) were reached in 86.6% (71/82) of PT infants and 96.7% (58/60) of T-IUGR infants after three doses of HBV vaccine (p = 0.044). The odds of having a protective response after the third dose of HBV vaccine was 1.25 (95% CI 1.02-1.53) with every one-week increase in gestation (p = 0.032). Birthweight was not associated with the development of a protective immune response. After the third dose, only 66.7% (8/12) of the PT infants whose mothers had anti-HB antibodies, developed protective anti-HB levels compared with 90% (63/70) of those with no maternal antibodies (p = 0.028). In PT infants after the fourth dose, there was a significant increase in the proportion of infants with protective antibody levels (8.6%, 95% CI 0.6-16.6%) among those with no maternal antibodies and 12.2% overall (95% CI 6.0-21.3) (p = 0.031 to 0.002) over that reached with the third dose. Administration of the fourth dose to T-IUGR infants did not confer such a benefit. CONCLUSION: In HBV-endemic areas, PT infants, irrespective of their birthweights, may benefit from an additional dose of hepatitis B vaccine in a schedule starting at birth. This approach will prevent vertical transmission and bring their immune response up to par with term infants. Term intrauterine growth-retarded infants should be vaccinated as per the schedule recommended for normal term infants. However, studies in other settings with different vaccine formulations and a longer follow-up period will be required before this strategy can be practised more widely.

Analysis of Variance↗
PubMed2002

Oxidant-antioxidant system: role and significance in human body.

Present article gives a holistic view of the causes, role and conrol of oxidative stress in the development and progression of various human diseases. Several types of reactive species are generated in the body as a result of metabolic reactions in the form of free radicals or non-radicals. These species may be either oxygen derived or nitrogen derived and called prooxidants. They attack macromolecules including protein, DNA and lipid etc. causing cellular/tissue damage. To counter their effect, the body is endowed with another category of compounds called antioxidants. These antioxidants are produced either endogenously or received from exogenous sources and include enzymes like superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, minerals like Se, Mn, Cu and Zn, and vitamins like vitamin A, C and E. Other compounds with antioxidant activity include glutathione, flavonoids, bilirubin and uric acid etc.. In a healthy body, prooxidants and antioxidants maintain a ratio and a shift in this ratio towards prooxidants gives rise to oxidative stress. This oxidative stress may be either mild or severe depending on the extent of shift and remains the cause of several diseases such as cardiovascular diseases, neurological diseases, malignancies, renal diseases, diabetes, inflammatory problems, skin diseases, aging, respiratory diseases, liver diseases and different types of viral infections. As more and more reports are pouring in, a lot of information is being unfolded about oxidative stress in relation to several other diseases.

Antioxidants↗
PubMed2001

Sero-epidemiology of hepatitis E virus (HEV) in urban and rural children of North India.

OBJECTIVE: To estimate the prevalence of anti-HEV IgG and IgM antibodies to ORF3 peptide of Hepatitis E virus genome in an age stratified urban and rural population of children. DESIGN: Cross sectional survey. SETTING: Pediatric out-patient clinics in a tertiary hospital and a rural dispensary. METHODS: Study subjects between 6 months and 10 years with minor, non-hepatic illnesses were recruited for the study from March to December 1996. Baseline demographic details, drinking water source, sewage disposal methods, reasons for attending the hospital, histories of parenteral exposure in the past 12 months and acute hepatitis in the subjects and the family in the previous six months were obtained. Serum anti-HEV IgG antibodies were screened in all subjects, and in those who were positive, anti-HEV IgM antibodies were assayed as an indicator of recent infection. Serum aminotransferase (ALT) was estimated in those who were anti-HEV IgM antibody positive. RESULT: Out of 2160 subjects recruited, 2070 samples could be screened for anti-HEV IgG antibodies. In the urban population (n = 1065) anti-HEV IgG antibodies were detected in 306 subjects (28.7%; 95% CI 26.0-31.6) and of these 131 (42.8%; 95%CI 37.2-48.6) were anti-HEV IgM antibody positive. Amongst 1005 rural children, anti-HEV IgG antibodies were present in 239 (23.8%; 95% CI 21.1-26.4) and IgM antibodies in 113 (47.3%; 95% CI 40.9-53.7) children. The antibodies were present since the first year of age till 10 years of age and, increased with advancing age. Serum transaminases were raised in 7.5% (9/120) and 5.5% (5/88) of subjects with anti-HEV IgM antibodies in urban and rural centers respectively. Overall the seroprevalence of IgG antibodies against HEV were significantly more in urban as compared to that in rural subjects (p = 0.011). However, proportion of children with anti-HEV IgG carrying IgM antibodies was similar in the two study groups (p = 0.298). A model for estimating expected prevalence of anti-HEV IgG antibodies was developed. The observed antibody prevalence in both urban and rural subjects at each age interval after 48 months was less as compared to the expected levels and this gap increased with advancing age categories. It appeared that there was a decay of HEV antibodies with time. CONCLUSIONS: Children are susceptible to HEV infection since early infancy. The probability of exposure to HEV during childhood was higher in urban than rural population. Seropositivity to HEV antibodies increased by over 2 times beyond 4 years of age as compared to younger age. Anti-HEV IgG antibodies appear to wean off with increasing age.

Antibodies, Viral↗
PubMed2000

Impact of hepatitis C virus infection on renal transplant outcome in India--a single centre study.

BACKGROUND: Hepatitis C virus (HCV) infection is currently the main cause of hepatotropic viral infection in renal transplant (RT) recipient throughout the world. Contrary reports are available as regard graft and patient survival and liver disease outcome in these patients. From India, outcome of HCV positive patients following RT has not been documented. Herewith, we present results of RT in HCV positive patients at our centre. METHODS: Study design was prospective case control with primary end point being graft and patient survival and the exposure being HCV infection. Between June 1995 till February 1998, 128 patients had RT at our hospital, of which, 37 (28.9%) were anti-HCV positive at the time of RT. All the patients were on triple immunosuppressive therapy. As a policy of unit, none of the donor had HBV and/or HCV infection. Anti-HCV positive patients formed the subjects (Gr. I), while anti-HCV negative patients severed as control (Gr. II). Anti HCV was done using 3rd generation ELISA tests kit. HCV-RNA could not be done due to non-availability. None of the positive patient was treated with anti-viral therapy. Acute rejection, serious infections, patient and graft survival and outcome of liver disease was compared in these patients. RESULTS: Mean age of the patients, number of males, number of pre-RT haemodialysis and blood transfusion, donor age and HLA-mismatch were comparable in both the groups. Mean follow-up in Gr. I was 28 +/- 9.4 months and in Gr. II 31.4 +/- 7.6 months. At the end of this follow-up, acute rejection was seen in 43% and 33.3% patient in Gr. I and II respectively. In Gr. I, serious infections were seen in 30% while the same in Gr. II was 11.8% (p < 0.01). There was no difference in graft survival in Gr. I and II (72% and 66%) and the patient survival were also similar (72% and 66%). Of the deaths in Gr. I, 80% died of sepsis and 20% died of liver cell failure related to one each of hepatitis B and hepatitis E. Of the deaths in Gr. II, 65% died of sepsis and 17% died of hepatic cell failure. But, there was no difference in causes of deaths in these two groups. In both the groups, none of liver related death was due to isolated HCV infection. There was no effect of donor age, HLA mismatch, number of haemodialysis and pre-RT blood transfusion on the survival of graft as well as patient. CONCLUSION: In conclusion, HCV infection is major problem in RT with us. In a short follow-up of nearly 30 months, graft and patient survival is same in HCV positive and negative patients. However, serious infections are significantly more common in HCV positive patients.

Adult↗
PubMed1999

Comparison of two schedules of hepatitis B vaccination in patients with mild, moderate and severe renal failure.

Seroconversion rate following hepatitis B vaccination in patients of chronic renal failure (CRF) has been in the range of 10%-82% in various studies. Different approaches have been tried to improve seroconversion rate. We studied two schedule of hepatitis B vaccination, 0,1,2 (Group A) and 0,1,2,6 (Group B) in mild (creatinine 1.5 to 3.0 mg%), moderate (creatinine 3.0 to 6.0 mg%) and severe CRF (creatinine > 6.0 mg%). Between Oct. 93 to Oct. 95, 117 patients with CRF who were negative for HBsAg and anti-HBs were included in the study. Forty micrograms of recombinant vaccine "ENGIREX" (20 micrograms in each deltoid region) was given in both the groups. Number of cases of mild, moderate and severe CRF were 18, 15 and 42 in group A and 12, 13 and 17 in group B, respectively. One month after the last dose of vaccination, anti-HBs was measured using ELISA kit (Abbot Laboratories, India). Anti-HBs titres of > 10 IU/L were taken as criteria of positive seroconversion. In group A seroconversion rate was 87.5%, 66.6% and 35.7% in mild, moderate and severe CRF respectively while same results in group B were 100%, 77% and 36.36%, respectively. We conclude that patients of chronic renal failure should be vaccinated at very early stage of the disease using 40 micrograms of vaccine. Four doses schedule of 0,1,2,6 give better results than three doses schedule in early CRF.

Adult↗