Effects of ventilator vs manual hyperinflation in adults receiving mechanical ventilation: a systematic review of randomised clinical trials.

BACKGROUND: Ventilator hyperinflation (VHI) and manual hyperinflation (MHI) are thought to improve secretion clearance, atelectasis and oxygenation in adults receiving mechanical ventilation. However, to the authors' knowledge, a systematic review of their relative effectiveness has not been undertaken previously. OBJECTIVE: To determine whether VHI is more effective than MHI for the improvement of clinical outcomes in adults receiving mechanical ventilation. DATA SOURCES: The electronic databases PubMed, Cochrane Library, CINHAL Plus, Wiley Online Library, ScienceDirect and PEDro were searched from January 1993 until August 2013. OpenGrey, the metaRegister of Controlled Trials (mRCT) and the reference lists of all potentially relevant studies were also searched. STUDY ELIGIBILITY CRITERIA: Full English reports of randomised clinical trials comparing at least one effect of VHI and MHI in adults receiving mechanical ventilation. STUDY SYNTHESIS AND APPRAISAL: Included studies were appraised using the Cochrane risk of bias tool. The findings were synthesised using a purely qualitative approach. RESULTS: All four included studies reported no significant differences in sputum wet weight, dynamic and static pulmonary compliance, oxygenation and cardiovascular stability between VHI and MHI. LIMITATIONS: All of the included studies had considerable limitations related to the protocols, equipment, participants and outcome measures. Furthermore, the overall risk of bias was judged to be high for three studies and unclear for one study. CONCLUSION: Only four studies, all of which had a high or unclear risk of bias and significant additional limitations, have compared the effects of VHI and MHI in adults receiving mechanical ventilation. As such, further research in this area is clearly warranted.

Changes in epidemiological patterns of HCV infection and their impact on liver disease over the last 20 years in Greece.

SUMMARY: The aim of this study was to investigate the relative frequency of hepatitis C virus (HCV) genotypes in Greek patients with chronic infection as well as possible secular changes in their distribution in relation to modes of transmission, age and time at acquisition of the infection and other variables. We evaluated 434 unselected patients, 241 males and 193 females with a median age of 46.2 years (18-75), with chronic HCV infection presenting during the period 1996-2000. HCV infection was confirmed by the detection of HCV-RNA by polymerase chain reaction (PCR), while HCV genotyping was performed by the Inno-LiPA assay. Liver biopsies were evaluated according to Ishak's scoring system. Of 434 patients, 167 had a history of blood transfusion [post-transfusion hepatitis (PTH)], 80 were i.v. drug users and in 187 the route of infection remained unknown. The overall distribution of HCV genotypes 1, 2, 3 and 4 was 47, 8.3, 27 and 15.2%, respectively. Genotype 3 was common in younger adults and i.v. drug users, whereas genotype 1 predominated in older people and PTH patients (P < 0.001 for both). Infection acquired before 1981 (group A) was related to transfusion and genotype 1, while after 1981 (group B) with i.v. drug use and genotype 3 (P < 0.01). Biopsy was available in 369 (85%) patients, of whom 22.5% had cirrhosis; 29.8% in group A and 9.9% in group B. In a multivariate analysis, cirrhosis was strongly associated with the duration of infection (P = 0.013). Our study revealed a change of HCV genotype distribution in the last 20 years among Greek patients with chronic HCV infection as a result of epidemiological changes in HCV transmission. The presence of cirrhosis was associated only with the duration of infection. These observations have impact both on prevention and treatment.

Gliclazide-induced acute hepatitis.

There are few reports in the literature related to sulfonylurea-induced hepatotoxicity. We describe the case of acute hepatitis induced by gliclazide, a second generation sulfonylurea. A 60-year-old woman with diabetes mellitus (type 2) developed an acute icteric hepatitis-like illness 6 weeks after the initiation of gliclazide therapy. Other causes of acute hepatocellular necrosis were excluded. Liver histology showed marked portal inflammation with lymphocytes, monocytes and eosinophils, associated with lobular inflammation (indicative of a histological pattern consistent with drug-induced hepatitis). The drug was immediately withdrawn and the patient was given glibenclamide. The patient recovered clinically and, in less than 4 weeks, her serum bilirubin and aminotransferases returned to normal levels. We believe that this is the first description of acute hepatitis caused by an idiosyncratic adverse reaction to gliclazide or to one of its metabolites. In conclusion, this case strongly suggests that gliclazide can induce acute icteric liver necro-inflammation which may be misdiagnosed clinically as acute viral hepatitis. In patients who show abnormal liver function tests, the immediate discontinuation of gliclazide is recommended.

Cholestatic jaundice as a paraneoplastic manifestation of renal cell carcinoma.

Malignant diseases may cause cholestatic jaundice through either main bile duct obstruction or widespread hepatic metastasis. Renal cell carcinoma (hypernephroma, RCC) can cause a variety of paraneoplastic manifestations which can be the main presenting symptoms. Cholestasis, as a paraneoplastic syndrome, has been well described in patients with malignant lymphohyperplastic diseases. Non-metastatic nephrogenic hepatic dysfunction syndrome without jaundice has often been described in patients with hypernephroma (Stauffer's syndrome). Paraneoplastic cholestatic jaundice has not yet been described. We report, for the first time, two patients who presented with pruritus and cholestatic jaundice. During the diagnostic work-up, RCC was diagnosed. The renal tumour was an unexpected finding during computed tomographic (CT) scan. No clinical manifestations of hypernephroma, short of microscopic haematuria, were detected. Conjugated bilirubin, alkaline phosphatase and gamma-glutamyltranspeptidase were markedly increased. No hepatic metastasis or main bile duct obstruction were detected by appropriate investigations. After radical nephrectomy, liver abnormalities disappeared rapidly. We conclude that RCC should be included among neoplasms causing not only anicteric intrahepatic cholestasis but also frank jaundice as part of a paraneoplastic syndrome. The differential diagnosis from hepatic metastasis, main bile duct obstruction or other causes of jaundice is of clinical importance and of prognostic value. Patients with unexplained cholestasis should be investigated for malignant diseases including hypernephroma.