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Chronic obstructive pulmonary disease (COPD) is one of the most frequent pathologies among patients hospitalized in Internal Medicine (IM) Departments. COPD is frequently associated with concomitant diseases, which represent major causes of death, and affect disease management. Objectives of our study are to assess the prevalence of COPD patients in IM, to evaluate their comorbidity status, and to describe their complexity, by means of the validated multidimensional prognostic index (MPI) score. COMPLEXICO is an observational, prospective, multicenter study, enrolling consecutive patients hospitalized for any cause in IM, with diagnosis of COPD documented by spirometry. A total of 1002 patients in 43 IM Units in Italy were enrolled. The prevalence of COPD in IM was found to be 18.1%, and 72.8% of patients had at least three chronic diseases other than COPD. The mean MPI was 0.43±0.15, and according to a stratification algorithm 31.8% of patients were classified as having low-risk, 58.9% moderate-risk and 9.3% severe-risk of adverse outcome. More than two-thirds of COPD patients in our study present moderate to severe risk of poor outcome according to the MPI stratification.

Introduction Cholestatic hepatitis is frequently a drug-related syndrome. We describe the case of a 57-year-old man who developed cholestatic hepatitis two months after starting therapy with ticlopidine following a carotid endarterectomy.Materials and methods The patient presented with anorexia, nausea, and dark-colored urine. The work-up included laboratory tests and imaging studies of the liver (ultrasound and magnetic resonance imaging). The authors analyze the case using the scale developed by Maria and Victorino for the diagnosis of drug-induced hepatitis, the Naranjo algorithm for adverse drug reactions, and the RUCAM algorithm for causality assessment of hepatotoxicity. They also review data from the MedLine database on cases of ticlopidine-induced cholestatic hepatitis reported during the period 1982–2011.Results Bilirubin, aminotransferases, alkaline phosphatases, and gamma glutamyl transpeptidase levels were elevated at admission and progressively declined after ticlopidine was discontinued. The absence of biliary obstruction at ultrasonography and magnetic resonance cholangiography, the negative results of viral and immunologic tests, and the resolution of the syndrome after discontinuation of the drug all suggested ticlopidine-induced hepatotoxicity. The assessment of this case with toxicity algorithms confirmed that a causal link to ticlopidine was “probable” or “highly probable.” The patient was treated with ursodesoxycholic acid, clopidogrel (75 mg/day), and (after the laboratory parameters had normalized) rosuvastatin (10 mg/day). No further clinical and laboratory abnormalities have been observed during two month follow-up.Discussion The toxicity of ticlopidine is well established: our review revealed reports of 57 cases of ticlopidine-induced cholestatic hepatitis during the period 1982–2011. The mechanisms underlying the toxic effects of this drug are not clear, but they are probably related to the chemical structure of the drug. The syndrome is usually completely reversible with discontinuation of the drug. We stress the importance for the appropriate use of this drug and the need for adequate follow-up of patients.