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Hepatitis E virus (HEV) is a member of the genus Hepevirus within the family Hepeviridae. Hepatitis E is recognized as a zoonosis, and swine and wild boars (Sus scrofa) are known reservoirs of HEV infection. The aim of this study was to investigate the presence of HEV in wild boars and hunters exposed to infection in central Italy (Latium region). During the hunting season, blood samples were collected from 228 wild boars and 20 hunters. The seroprevalence of HEV infection was determined using a commercial enzyme-linked immunosorbent assay, previously validated for use in man, pigs and wild boars. The estimated HEV seroprevalence in wild boars and in hunters was 40.7% (93/228; 95% confidence interval [CI] 34.4-47.1%) and 25% (5/20; 95% CI 6.1-43.9%), respectively. Liver samples were collected from the boars and HEV RNA was detected by nested reverse transcriptase polymerase chain reaction. Fifty-five of 164 tested wild boar liver samples (33.5%; 95% CI 26.2-40.7%) and three of 20 (15.0%; 95% CI 1.3-28.7%) tested human serum samples were positive for HEV RNA. Phylogenetic analysis of the nucleotide sequences obtained from PCR products indicated that the HEV strains present in wild boars and the human population all belonged to genotype 3, supporting the zoonotic role of wild boars in the spread of HEV infection., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Unlabelled: The present study was aimed to investigate the variability of cardiac troponin I (cTnI) in the first week of acute myocardial infarction (AMI) course with regard to some epidemiological and clinical parameters and in patients with non-AMI acute coronary ischemic disease. Serum cTnI was assayed in 82 patients, 42 affected with AMI and 40 with non-AMI acute coronary ischemic disease, on admission in coronary care unit, within 6 h after the onset of symptoms, and, in AMI group, on 24 and 48 h and 7th day of illness course. cTnI is increased within the first 6 h, remaining above normal until 7th day. However, some distinctive features in the subgroups scheduled for this study are present. (1) The mean values of cTnI in AMI patients who died, >60 years old and with anterolateral necrosis are constantly higher than in survivors, <60 years old and with inferoposterior necrosis, respectively. (2) The cTnI concentration is already returned in normal range at 7th day of illness course in survivors and in patients with inferoposterior AMI. (3) The 24-h peak level of cTnI is significantly higher in fibrinolysed than in patients who didn't undergo fibrinolysis. (4) A direct correlation between the cTnI value and the Killip class is present either in the whole group or in any subset of patients and the progressive decrease of the cTnI concentration along the AMI course doesn't occur in Killip>2 group. (5) cTnI is higher in unstable than in stable anginous patients and normal subjects but not in stable angina with respect to healthy controls., Conclusions: (1, 2) The less increase and the early return in normal range of cTnI serum levels which occur in AMI subgroups with a better prognosis could be regarded as favourable prognostic signs. (3) The persistent higher values of cTnI in fibrinolysed subjects being associated with the angiographic finding of patent coronary arteries, it can be suggested that the large and persistent relase of cTnI from myocardium represents a reliable biochemical marker following the wash-out associated to a successful reperfusion. (4) The persistent increase of cTnI in AMI patients with advanced Killip class suggests that the high cTnI values are not only a strong index of myocardial necrosis but also of ongoing myocyte injury and hemodynamic impairment predictive of poor outcome. (5) The hypothesis can be reasonably advanced that the higher values of cTnI in unstable angina are due to focal areas of myocardial necrosis undetectable by the conventional serum markers or to a clinically silent AMI occurred in the week or so before in-hospital admission.

A marked discrepancy between mild and late clinical features and a nearly complete absence of erythrocyte uroporphyrinogen decarboxylase activity (Ery-UROD activity) was observed in a case of inherited porphyria cutanea tarda. The entity and time of appearance of clinical features, the onset of clinical symptoms after exposure to contributing factors, the effectiveness of phlebotomies and heterozygosity of the mother alone for uroporphyrinogen decarboxylase (UROD) deficiency were typical for familial porphyria cutanea tarda (F-PCT), whereas the extremely low UROD activity was peculiar to hepatoerythropoietic porphyria (HEP). These observations indicate that: 1) Ery-UROD activity may not always be useful to discriminate between F-PCT and HEP; 2) Ery-UROD activity does not always correlate with clinical symptoms; 3) in inherited UROD deficiency, the genetic defect may be heterogeneous. Finally, the observed discrepancy may provide additional evidence for the existence of tissue-specific isozymes.