Vascular and Chronological Age in Subjects with Erectile Dysfunction: A Cross-Sectional Study

IntroductionVascular age, as derived from the SCORE project algorithm for cardiovascular (CV) risk estimation, is an effective way for communicating CV risk. However, studies on its clinical correlates are scanty.AimTo evaluate if the difference between vascular and chronological age (Δage), in a population of subjects with erectile dysfunction (ED), can identify men with a worse risk profile.MethodsA consecutive series of 2,853 male patients attending the outpatient clinic for erectile dysfunction (ED) for the first time was retrospectively studied. Among them, 85.4% (n = 2,437) were free of previous MACE and were analyzed.Main Outcome MeasuresSeveral clinical, biochemical, and penile color Doppler parameters were studied. Vascular age was derived from the SCORE project algorithm, and the Δage was considered.ResultsHigher Δage is associated with several conventional (family history of CV diseases, hyperglycemia, elevated triglycerides, and increased prevalence of metabolic syndrome) and unconventional (severity of ED, frequency of sexual activity, alcohol abuse, lower education level, fatherhood, extramarital affairs, compensated hypogonadism, and low prolactin levels) risk factors. Δage is inversely related to penile color Doppler parameters, including flaccid and dynamic peak systolic velocity and flaccid acceleration (β = −0.125, −0.113, and −0.134, respectively, all P < 0.0001).ConclusionsIn subjects referring for ED without a personal history of CV events, Δage is associated with an adverse cardio-metabolic profile and worse penile color Doppler ultrasound parameters. Δage provides a simple method for identifying high-risk men that must undergo significant modification in their lifestyle and risk factors. In addition, it can be considered a simple, inexpensive, and safe surrogate marker of penile arterial damage.     

Toxicité des antirétroviraux chez les patients co-infectés par les virus VIH et VHC

The introduction of HAART (Highly Active Antiretroviral Therapy) has deeply modified the epidemiologic data on HIV infection. Consequently, chronic hepatotoxicities, particularly those related to HCV, became a leading cause of morbidity and mortality amongst co-infected HIV-HCV patients. They became a major factor to be considered before starting and conducting a HAART regimen. Due to the epidemiology of these two infections and referring to several huge randomised prospective clinical trials recently reported, understanding the antiretroviral toxicity is a true challenge in the follow-up of co-infected patients. It includes: i) understanding the intrinsec toxicities of each antiretroviral class, particularly drugs-related hepatotoxicities; then ii) the incidences of those treatments in co-infected patients, with or without anti-HCV bitherapy; and iii) the pathogenic reciprocal interactions between HIV and HCV and between anti-HIV and anti-HCV treatments. Four mechanisms of drug-related liver toxicity have been recognized: i) direct drug toxicity; ii) immune reconstitution; iii) hypersensitivity reactions with liver involvement; and iv) mitochondrial toxicity. The benefit-risk ratio notion must be strongly evaluated and the therapeutic strategy must include, for each patient, a strict monitoring of biochemichal (liver parameters, hemogram, amylasemia, lipasemia, evaluation of liver fibrosis index) and clinical (weight, lipodystrophy) parameters. A better pharmacological knowledge, a global view and the development of new drugs with less hepatotoxicity, like fusion inhibitors, would increase the quality of life of co-infected patients. Liver transplantation could be a hope for patients with severe hepatic failure.     

Clinical features of hepatocellular carcinoma that occur after sustained virological response to interferon for chronic hepatitis C

Background and Aim: This study investigated the clinical features of hepatocellular carcinoma in patients with sustained virological response to interferon for hepatitis C viral (HCV) infection. Methods: A total of 7715 patients with HCV infection were treated with interferon and followed up for more than 1 year after withdrawal of interferon in 64 Japanese hospitals and clinics between July 1988 and August 2001. Sustained virological response was obtained in 2515 (32.6%) patients. Of these 2515 patients, clinical data were collected for 38 patients in whom hepatocellular carcinoma developed. Sustained virological response was defined as HCV RNA negativity more than 6 months after the termination of interferon. Results: All patients were HCV RNA negative at the time of diagnosis of hepatocellular carcinoma. The median period until the detection of hepatocellular carcinoma was 4.7 years (range 1.4–9.0 years). There were significant improvements in hepatic function including serum albumin, aspartate aminotransferase, alanine aminotransferase, indocyanine green test, platelet count and histological activity grade in comparison with those before interferon therapy and at the onset of hepatocellular carcinoma. The maximum tumor size in patients without medical follow‐up for 1 year or more (median: 60 mm) was significantly larger than in patients who were periodically followed up for 6 months or less (median: 25 mm) (P = 0.002). Conclusions: The present findings emphasize the importance of regular medical follow up of patients with HCV infection, as even patients showing a sustained virological response to interferon and in whom hepatic function has improved have the potential to develop hepatocellular carcinoma.     

Protontherapy of eye tumours in the UK: A review of treatment at Clatterbridge

The Scanditronix MC-60 PF cyclotron at Clatterbridge was commissioned in 1984 for fast neutrontherapy trials. It also produced a 60.0 MeV clinical beam suitable for treating ocular tumours with a maximum penetration of 31 mm (water) and a 0.9 mm fall-off. An additional treatment room was built with an ocular beamline constructed in-house. The first group of eye patients was treated in June 1989, making this the first hospital-based proton facility. More than 1700 eye patients have been treated by the only UK proton service.     

Roadmap to vasculitis: a rheumatological treasure hunt: Part II. Classification,features of individual vasculitides and differential diagnosis against pseudovasculitis

Since the triggering factors causing primary vasculitides are by definition not (yet) known, we have to classify them to clinical syndromes based on the size, site, type and effect of the blood vessel involvement. ACR classification criteria and Chapel Hill nomenclature are useful tools to familiarize with the primary vasculitides, although a lot of criticism has been voiced in the literature indicating that they only represent the best available consensus. The present text takes advantage of the recent developments such as introduction of the anti-neutrophilic cytoplasmic auto (ANCA) antibodies, and divides the vasculitides to those affecting typically the large, medium and small arteries or only small blood vessels. In addition, some vasculitides, which are still difficult to place to the vasculitis map, like Bürger's disease, Goodpasture's syndrome, primary angiitin of the central nervous system (PACNS) and panniculitis, are dealt with. As it is a long and winding road, attention has to be paid to the clinical details to follow the road sign to “pseudovasculitis”, when that is the right way to go. They represent a bunch of non-vasculitic conditions, which lead to structural or vasospastic impairment of the blood flow, bleeding or thromboembolism and hyperviscosity. These imitators have to some extent, similar clinical symptoms and signs as well as laboratory and radiological findings to those found in true systemic vasculitides. This also emphasizes the importance of internal medicine as the intellectual (albeit not necessarily organizational) home of rheumatology and rheumatologists as we deal with conditions like atherosclerosis, antiphospholipid antibody syndrome, infectious endocarditic, myxoma of the heart and cholesterol embolism.