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James H Lewis

Publications and source records attributed to James H Lewis.

16 recordsLinked to original sources
PubMed2006

Drug-induced liver disease.

PURPOSE OF REVIEW: To summarize the pertinent case reports, case series and clinical studies that described clinical, histological, epidemiological and mechanistic features of drug-induced liver disease in 2005. RECENT FINDINGS: Acetaminophen, highly active antiretroviral therapy and drugs for tuberculosis retained their preeminent position as the most commonly reported agents causing drug-induced liver disease, with acetaminophen continuing to be the leading cause of acute liver failure in the USA. While the frequency of drug-induced liver disease remains low, a large case-series of acute drug-induced liver disease from Spain and Sweden supported the observation that acute hepatocellular jaundice from a drug is associated with death or the need for transplant in at least 10% (known as Hy's Law). With respect to using potentially hepatotoxic medications in patients with underlying liver disease, statins and second-generation thiazolidinediones were shown to be safe when used in patients with elevated baseline alanine aminotransferase or aspartate aminotransferase levels. SUMMARY: Drug-induced liver disease remains an important cause of acute liver failure, and research efforts by the National Institutes of Health and others are underway to better determine the risk factors and other host susceptibilities that will allow for the safer use of drugs in the future.

Acetaminophen↗
PubMed2005

Pancreatic tuberculosis diagnosed with endoscopic ultrasound guided fine needle aspiration.

CONTEXT: Isolated pancreatic tuberculosis is rare in the Western world. Its clinical presentation often mimics pancreatic malignancy and the diagnosis is usually not suspected or confirmed prior to laparotomy. Endoscopic ultrasound guided fine needle aspiration cytology has proved to be an excellent tool for the cytological diagnosis of pancreatic and peripancreatic masses. However, this technique has not been reported for diagnosing pancreatic or peripancreatic tuberculosis. CASE REPORT: We describe a 57-year-old South Asian man with pancreatic tuberculosis who presented with fever of undetermined origin and a pancreatic mass on imaging. He was successfully treated with anti-tuberculosis regimen following confirmation of his diagnosis with endoscopic ultrasound guided fine needle aspiration cytology. CONCLUSIONS: Pancreatic tuberculosis should be suspected in patients having a pancreatic mass, particularly if patient presents with fever and lived in, or traveled to, an area of endemic tuberculosis or exposed to tuberculosis. When the diagnosis is suspected, endoscopic ultrasound guided fine needle aspiration cytology of the pancreatic lesion can confirm the diagnosis and so avoid an unnecessary explorative laparotomy or pancreatic resection.

Adult↗
PubMed2005

Drug-induced liver disease 2004.

PURPOSE OF REVIEW: To summarize the salient reviews, studies and case reports and series that dealt with clinical, pathological, methodological, and epidemiological descriptions of drug-induced liver disease in the calendar year 2004. RECENT FINDINGS: While no new causes of drug-induced liver injury were reported for 2004, several new reports of previously recognized hepatotoxins, including herbal products, were published. These include the antiretroviral drugs for HIV and agents to manage tuberculosis. Acetaminophen (APAP) retained its preeminent position as the leading cause of drug-induced acute liver failure, currently accounting for nearly 50% of cases according to the latest figures from the U.S. Acute Liver Failure Study Group. Not surprisingly, APAP also heads the list of drugs and toxins leading to liver transplantation for acute hepatic failure. Efforts to reduce the number of cases of intentional APAP poisonings by restricting the number of tablets sold at any one time in the UK are ongoing, but the success of the program may be lessening, as was pointed out this year. The use of potentially hepatotoxic medications in patients with underlying liver disease was examined with the statins, and they emerged as a safe class for use in this setting. SUMMARY: Given the apparent increasing incidence of acute liver failure attributable to APAP in the US, additional efforts are still needed to better define the risks associated with its use and to further reduce the incidence of severe liver injury from this widely used agent.

Acetaminophen↗
PubMed2005

Hepatic findings in long-term clinical trials of ximelagatran.

OBJECTIVE: In clinical trials, the efficacy and safety of the oral direct thrombin inhibitor ximelagatran have been evaluated in the prevention or treatment of thromboembolic conditions known to have high morbidity and mortality. In these studies, raised aminotransferase levels were observed during long-term use (>35 days). The aim of this analysis is to review the data regarding these hepatic findings in the long-term trials of ximelagatran. PATIENTS AND METHODS: The prospective analysis included 6948 patients randomised to ximelagatran and 6230 patients randomised to comparator (warfarin, low-molecular weight heparin followed by warfarin or placebo). Of these, 6931 patients received ximelagatran for a mean of 357 days and 6216 patients received comparator for a mean of 389 days. An algorithm was developed for frequent testing of hepatic enzyme levels. A panel of four hepatologists analysed all cases of potential concern with regard to causal relation to ximelagatran treatment using an established evaluation tool (Roussel Uclaf Causality Assessment Method [RUCAM]). RESULTS: An elevated alanine aminotransferase (ALT) level of >3 x the upper limit of normal (ULN) was found in 7.9% of patients in the ximelagatran group versus 1.2% in the comparator group. The increase in ALT level occurred 1-6 months after initiation of therapy and data were available to confirm recovery of the ALT level to <2 x ULN in 96% of patients, whether they continued to receive ximelagatran or not. There was some variability in the incidence of ALT level elevation between indications, those with simultaneous acute illnesses (acute myocardial infarction or venous thromboembolism) having higher incidences. Combined elevations of ALT level of >3 x ULN and total bilirubin level of >2 x ULN (within 1 month of the ALT elevation), regardless of aetiology, were infrequent, occurring in 37 patients (0.5%) treated with ximelagatran, of whom one sustained a severe hepatic illness that appeared to be resolving when the patient died from a gastrointestinal haemorrhage. No death was observed directly related to hepatic failure caused by ximelagatran. CONCLUSION: Treatment with ximelagatran has been associated with mainly asymptomatic elevation of ALT levels in a mean of 7.9% of patients in the long-term clinical trial programme and nearly all of the cases occurred within the first 6 months of therapy. Rare symptomatic cases have been observed. An algorithm has been developed for testing ALT to ensure appropriate management of patients with elevated ALT levels. Regular ALT testing should allow the clinical benefits of ximelagatran to reach the widest population of patients while minimising the risk of hepatic adverse effects.

Adult↗
PubMed2005

Sustained virological response rate to pegylated interferon plus ribavirin for chronic hepatitis C in African Americans: results in treatment-naïve patients in a university liver clinic.

OBJECTIVE: The sustained virological response (SVR) to non-pegylated interferon-based regimens for chronic hepatitis-C virus (HCV) has been lower among African Americans compared to Caucasians, a finding attributed to the high proportion of genotype-1 infections in African Americans. To determine whether such a difference in SVR is still present with pegylated interferon and ribavirin regimens, we analyzed SVR rates among treated racial groups according to genotype. METHODS: Consecutive treatment-naïve patients of multiethnic and racial backgrounds attending a university liver clinic received either Peg alfa-2a or -2b plus ribavirin 1-1.2 g based on body weight for 24-48 weeks, depending on genotype. HCV RNA titers were analyzed at 0, six or 12 months, and six months posttreatment. RESULTS: Among the first 193 patients eligible for treatment, 73 received therapy [24 African Americans (genotype 1 in 88%); 49 non-African Americans (genotype 1 in 59%)]. Of the 120 patients not treated (33% African-American and 67% non-African-American), most either had mild hepatitis on biopsy, normal ALT values, an untreated psychiatric condition or had a low expectation of treatment efficacy. SVR results for the 73 patients who completed treatment indicate that African Americans and non-African Americans with genotype 1 have similarly low rates of SVR (19% in African Americans compared with 24% in non-African Americans, p=NS). CONCLUSION: Sustained viral response rates in our open-access liver clinic are similar for genotype-1 African Americans compared to non-African Americans receiving pegylated interferon and ribavirin. The predominance of genotype 1 among African-American patients likely accounts for the lower response rates, but genotype 1 in other racial groups is associated with a proportionately lower SVR as well as a risk for delayed relapse after SVR.

Adult↗
PubMed2004

The frequency of peptic ulcer as a cause of upper-GI bleeding is exaggerated.

BACKGROUND: Peptic ulcer disease is considered the cause of upper-GI bleeding in 50% of cases. A recent decline in the proportion of cases of upper-GI bleeding because of a peptic ulcer was noted by us. The objectives of this study were to evaluate the frequency of peptic ulcer in patients with upper-GI bleeding and the proportion of bleeding peptic ulcers with a non-bleeding visible vessel. METHODS: Patients with upper-GI bleeding seen from December 1999 until April 2001 at a tertiary, university-affiliated medical center were studied prospectively. The Clinical Outcome Research Initiative (CORI) database was used to correlate the single institution data with nationwide data. Endoscopic data in the CORI database for patients who had endoscopy for upper-GI bleeding between December 1999 and July 2001 were retrieved and analyzed. RESULTS: A total of 126 patients were included in the prospective study. The endoscopic findings were: peptic ulcer in 31.8%: 95% confidence interval (CI) [23.7%, 40.6%] of patients; a non-bleeding visible vessel was present in 10%: 95% CI[2.8%, 23.7%] of these peptic ulcers. From the nationwide CORI database, data for 7822 patients with upper-GI bleeding were obtained. The endoscopic findings were: peptic ulcer in 20.6%:95% CI[19.7%, 21.5%] of patients with upper-GI bleeding; a non-bleeding visible vessel was present in 7.3%: 95% CI[6.1%, 8.6%] of the ulcers. CONCLUSIONS: The frequency of peptic ulcer in patients with upper-GI bleeding and the proportion of bleeding ulcers with a non-bleeding visible vessel are less than previously reported.

Adult↗
PubMed2004

Drug- and chemical-induced cholestasis.

Cholestasis caused by medicinal and chemical agents is an increasingly well-recognized cause of liver disease. Clinical drug-induced cholestatic syndromes producing jaundice and bile duct injury can mimic extrahepatic biliary obstruction, primary biliary cirrhosis, and sclerosing cholangitis, among others. This article updates the various forms of drug-induced cholestasis, focusing on the clinicopathologic features of this form of hepatic injury and on the known or putative mechanisms by which drugs and chemicals lead to cholestasis.

Cholestasis↗
PubMed2004

Drug-induced liver disease in 2003.

Drug-induced liver disease remains an important topic of concern for all prescribers as well as drug manufacturers. The withdrawal of troglitazone (Rezulin) and bromfenac (Duract) a few years ago remains fresh in the minds of regulatory authorities as well as clinicians and researchers who are focusing renewed attention on ways to better understand mechanisms of injury to predict and avert serious drug-induced liver disease in the future from drugs under development as well as existing agents known to cause liver injury. As in past years, this review describes new and first-time reports of various aspects of drug-induced liver disease for several classes of compounds, including herbal products (such as kava kava), reviews the risk factors seen with antiretroviral and antituberculosis agents among others. It provides a sampling of experimental hepatoprotection studies that may hold the key to treatment and prevention of drug-induced liver disease in the future and discusses the ongoing approaches to be taken to restrict the availability of acetaminophen that have proved successful in reducing the number of overdoses, deaths, and liver transplantations from this drug in the United Kingdom. Given the fact that acetaminophen is the single most important cause of acute liver failure here and abroad, such efforts to limit its use seem appropriate for other nations as well.

Journal Article↗
PubMed2003

Drug-induced liver disease.

The year 2002 saw a warning from the US Food and Drug Administration not to use the diet agent, Lipokinetix, and brought to light a few new agents as potential hepatotoxins. Numerous other reports confirmed the hepatotoxicity of several previously described agents. Refinements in causality assessment remain an important aspect in defining drug-induced liver disease and proposed new upper limits of normal for alanine aminotransferase that are lower than most laboratories currently report may require rethinking our definition of "normal liver function tests." Chronic viral hepatitis B and C remain important risk factors for antiretroviral-induced liver injury in patients co-infected with the human immunodeficiency virus and in patients receiving antituberculosis therapy. Acetaminophen retains its status as the most common cause of acute drug-induced liver failure in the United States and in many other countries. Several papers addressed the issue of accidental versus intentional overdoses, the role of alcohol consumption as a risk factor, and newer aspects of treating and preventing acetaminophen injury to the liver. Finally, the use of potentially hepatotoxic medications in patients with underlying liver disease continues to be a controversial topic and a rational approach to the use of such drugs in this setting is provided.

Journal Article↗
PubMed2002

High-resolution chromoendoscopy for classifying colonic polyps: a multicenter study.

BACKGROUND: Chromoendoscopy may reliably separate adenomatous from nonadenomatous polyps. The aim of this multicenter trial was to determine the accuracy of high-resolution chromoendoscopy for the determination of colonic polyp histology. METHODS: This multicenter trial included 4 academic centers and a primary care practice. In 299 patients referred for routine colonoscopy or sigmoidoscopy, 520 polyps 10 mm in size were sprayed with indigo carmine dye. Using a high-resolution endoscope, the endoscopist predicted the histology of each polyp based on its surface characteristics. Hyperplastic polyps had a "pitted" surface pattern of orderly arranged "dots" that resembled surrounding normal mucosa. Adenomatous polyps had at least one surface "groove" or "sulcus." Each polyp was subsequently resected for histopathologic evaluation. RESULTS: The resected polyps were comprised by 193 adenomas (37%), 225 hyperplastic polyps (43%), and 102 "other" types (20%). Forty polyps (7.7%) could not be classified by high resolution chromoendoscopy with indigo carmine dye. For the remaining polyps, the sensitivity, specificity, and negative predictive value of indigo carmine dye staining for adenomatous polyps were, respectively, 82%, 82%, and 88%. The results were consistent among the academic centers and the primary care practice. CONCLUSIONS: High-resolution chromoendoscopy with indigo carmine dye demonstrates morphologic detail of diminutive colorectal polyps that can reliably be used to separate adenomatous from nonadenomatous polyps.

Adenoma↗
PubMed2002

Drug-induced liver disease.

Although the year 2001 did not see any prescription drugs withdrawn because of drug-induced liver disease, the US Food and Drug Administration requested that dietary supplements containing comfrey be taken off the market because of the danger of hepatic injury. The Food and Drug Administration remains very involved in the process by which drug-induced liver disease can be detected early in drug development and in the determination of how best to prevent hepatotoxicity after drug approval. A workshop on drug-induced liver disease cosponsored by the Food and Drug Administration, the Pharmaceutical Research and Manufacturers Association, and the American Association for the Study of Liver Diseases was held in Washington, DC, in February 2001, and the resulting white paper outlined several areas for research. A number of agents were newly described as causing various forms of liver injury, and several others had drug-induced liver disease confirmed by additional reports. Several investigators dealt with the difficulties inherent in establishing causality of drug-induced liver disease and the potential negative consequences of wrongly attributing hepatotoxicity to a particular agent. In one recent series, more than half the instances of alleged drug-induced liver disease were found to have other causes, often leading to a delay in the actual diagnosis and appropriate management. Case reports in particular were often misleading. Although several drug assessment scales have been developed, none appears to be foolproof.

Journal Article↗
PubMed2002

The rational use of potentially hepatotoxic medications in patients with underlying liver disease.

Given the fact that as many as 9% of all adverse drug reactions involve toxic effects on the liver and with upwards of 50% of all cases of fulminant hepatic failure being ascribed to acetaminophen and other agents, the safe use of medications takes on an even greater importance whenever the prescription of potentially hepatotoxic drugs to patients with underlying liver disease is considered. In general, it is thought that most drugs can be safely administered in the setting of liver disease without an increased risk of hepatotoxicity, although the evidence on which this statement is based often relies more on clinical judgement than on clinical studies. Several drugs appear to have an increased risk of hepatotoxicity in patients with underlying liver disease based on either clinical reports or extrapolated pharmacological data. These agents, including methotrexate, niacin and the antiretroviral and antituberculosis drugs, carry warnings about their use in patients with a variety of liver conditions. The data supporting the hepatotoxic risk of scores of additional drugs, such as the 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors ("statins"), the newer thiazolidinediones (rosiglitazone, pioglitazone), and tamoxifen, among others, in patients with liver disease are generally lacking by evidence-based studies. However, clinical and biochemical monitoring is routinely recommended or required, often to make up for the lack of information on the true risk of clinically significant liver toxicity of these agents in individuals both with and without underlying liver disease. This article will review what is and what is not known about prescribing in the setting of acute and chronic liver disease and offers recommendations to help promote the safe and rational use of potentially hepatotoxic medications in these patients.

Chemical and Drug Induced Liver Injury↗