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Biomedical subjects

Rahul A Nathwani

Publications and source records attributed to Rahul A Nathwani.

6 recordsLinked to original sources
PubMed2006

Drug hepatotoxicity.

Drug-induced liver injury is a common but underdiagnosed cause of liver disease with an incidence that is rapidly increasing. The authors address some of the more controversial aspects in relation to drug-induced liver injury: recommendations on the use of anti-tuberculosis therapy in the presence of underlying cirrhosis, the role of periodic liver test monitoring and steroid therapy in relation to drug-induced liver injury, the presence of class effects associated with certain drugs, and the potential use of ursodeoxycholic acid in prolonged cholestasis.

Anti-Inflammatory Agents↗
PubMed2005

Serum alanine aminotransferase in skeletal muscle diseases.

Although elevation of the levels of serum alanine aminotransferase (ALT) following liver injury is well known, confusion exists concerning skeletal muscle injury as the cause of this rise. We reviewed the records of 16 patients who had muscle necrosis without evidence of liver disease. The patients were divided into three groups: extreme exercise, polymyositis, and seizures. All patients exhibited markedly elevated creatine kinase and lactate dehydrogenase levels consistent with muscle injury. In acute cases, aspartate aminotransferase (AST) and ALT were both elevated, and the AST/ALT ratio was greater than 3, but this ratio approached 1 after a few days because of a faster decline in AST. In conclusion, this difference in half-life accounts for the comparable AST and ALT levels in our cases with chronic muscle injury.

Adult↗
PubMed2005

The effect of GI bleeding on Helicobacter pylori diagnostic testing: a prospective study at the time of bleeding and 1 month later.

BACKGROUND: Some case series and cohort studies suggest that acute GI bleeding decreases the sensitivity of Helicobacter pylori diagnostic testing. OBJECTIVE: To assess H pylori biopsy testing in patients with acute upper-GI bleeding and 1 month later. DESIGN: Prospective cohort study using patients as their own controls. SETTING: Urban county hospital. PATIENTS: Sixty-one patients with acute variceal bleeding. INTERVENTIONS: Antral and body endoscopic biopsies at admission and 1 month later. MAIN OUTCOME MEASUREMENTS: CLOtest and histologic examinations were performed and biopsy specimens were coded and mixed for blinded histologic examination for H pylori density and inflammation. RESULTS: CLOtest results changed from H pylori negative at baseline to H pylori positive at 1 month in two patients (3%), from H pylori positive to H pylori negative in 6 patients (10%), and remained the same in 53 (87%). Histologic results changed from H pylori negative at baseline to H pylori positive at 1 month in two patients (3%), from H pylori positive to H pylori negative in 5 patients (8%), and remained the same in 54 (89%). Changes occurred only in patients with low H pylori density. No significant increase in H pylori density or change in inflammatory cell infiltration was seen. CLOtest sensitivity was 8% higher with bleeding vs. 1 month after bleeding (79% vs. 71%; 95% CI of difference was -11% to 27%; i.e., maximal potential decrease in sensitivity with bleeding is 11%). LIMITATIONS: The population is not one for which H pylori testing is recommended, and biopsy test performance was less consistent than expected. CONCLUSIONS: Acute-GI bleeding did not decrease the sensitivity of rapid urease testing, unless the effect lasts more than 1 month. Furthermore, bleeding did not produce falsely negative histologic examinations for H pylori, decrease H pylori density, or alter inflammatory cell infiltration. However, given the lower than expected overall CLOtest sensitivity and frequent use of proton pump inhibitors for GI bleeding, histology may be preferred in this setting.

Acute Disease↗
PubMed2005

Marked elevation in serum transaminases: an atypical presentation of choledocholithiasis.

BACKGROUND: Choledocholithiasis causes elevations in levels of alkaline phosphatase out of proportion to aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Isolated marked elevation in AST and ALT levels over 1,000 IU/L has been reported infrequently in patients with choledocholithiasis. METHODS: The charts of 18 patients who presented between 1971 and 2002 with documented choledocholithiasis and AST or ALT levels greater than 1,000 IU/L were retrospectively reviewed. An extensive work-up for coexisting disease processes to account for the abnormal AST and ALT levels was negative. RESULTS: Eighteen patients (16 women, 16 Hispanics, age 38 +/- 3 yr) presented with symptoms of choledocholithiasis and marked transaminase elevation. Peak levels of AST and ALT were 1,062 +/- 129 and 1,119 +/- 90, respectively. Following successful management of gallstone disease, AST and ALT levels fell rapidly to 129 +/- 22 and 268 +/- 61, respectively, within 3-14 days. There was also a concomitant improvement in the levels of bilirubin and alkaline phosphatase. CONCLUSIONS: In the absence of other hepatobiliary or pancreatic disease, choledocholithiasis can result in elevations in AST and/or ALT greater than 1,000 IU/L. These levels fall markedly once the gallstone disease is appropriately managed.

Adult↗
PubMed2002

Injury induced neointima formation and its inhibition by retrovirus-mediated transfer of nitride oxide synthase gene in an in-vitro human saphenous vein culture model.

Human saphenous veins were cultured to characterize neointima formation and feasibility of gene transfer to inhibit the intimal proliferative response to injury. Mechanical injury was introduced by abrading the luminal surface of the vein patch with a sterile cotton bud. Both injured and non-injured vein patches were cultured and transduced with retroviral vectors carrying marker or therapeutic genes. After a 14-day culture, the thickness of the intimal layer of non-injured vein patches reached 90+/-28 microm at the edge and 61+/-22 microm at the center (n=29) from the original 22+/-12 microm at harvest (n=6, P=0.02). Mechanical injury to the intimal surface prior to culture resulted in an exaggerated proliferative response. The intimal thickness of injured vein patches increased from 3.4+/-1 microm right after injury to 128+/-23 microm (n=12, P<0.001) at the edge after 14-day culture. Genes were transduced efficiently into a luminal layer of cultured veins using a pseudotyped murine leukemia viral vector. Transduction of gene encoding nitric oxide synthase resulted in reduction of neointima formation to 33+/-7 microm (n=12) at the edge after 14-day culture compared to 90 microm (P<0.01) seen in untransduced non-injured vein patches. Marker gene transduction did not alter intimal proliferative response or its immunohistochemical profile. The data suggest that cultured vein can be used as a model for studying the effects of injury to blood vessels and to evaluate the effects of candidate therapeutic genes.

Cells, Cultured↗