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Efavirenz was associated with severe VDD, a condition associated with multiple adverse health outcomes, and efavirenz and tenofovir with increased ALP. The clinical significance of these findings requires further investigation, given the widespread use of efavirenz and tenofovir in first-line combination antiretroviral therapy.

Objective. MTX is widely used to treat synovitis in PsA without supporting trial evidence. The aim of our study was to test the value of MTX in the first large randomized placebo-controlled trial (RCT) in PsA.Methods. A 6-month double-blind RCT compared MTX (15 mg/week) with placebo in active PsA. The primary outcome was PsA response criteria (PsARC). Other outcomes included ACR20, DAS-28 and their individual components. Missing data were imputed using multiple imputation methods. Treatments were compared using logistic regression analysis (adjusted for age, sex, disease duration and, where appropriate, individual baseline scores).Results. Four hundred and sixty-two patients were screened and 221 recruited. One hundred and nine patients received MTX and 112 received placebo. Forty-four patients were lost to follow-up (21 MTX, 23 placebo). Twenty-six patients discontinued treatment (14 MTX, 12 placebo). Comparing MTX with placebo in all randomized patients at 6 months showed no significant effect on PsARC [odds ratio (OR) 1.77, 95% CI 0.97, 3.23], ACR20 (OR 2.00, 95% CI 0.65, 6.22) or DAS-28 (OR 1.70, 95% CI 0.90, 3.17). There were also no significant treatment effects on tender and swollen joint counts, ESR, CRP, HAQ and pain. The only benefits of MTX were reductions in patient and assessor global scores and skin scores at 6 months (P = 0.03, P < 0.001 and P = 0.02, respectively). There were no unexpected adverse events.Conclusions. This trial of active PsA found no evidence for MTX improving synovitis and consequently raises questions about its classification as a disease-modifying drug in PsA.Trial registration. Current Controlled Trials, www.controlled-trials.com, ISRCTN:54376151.

Objective: To estimate the cumulative incidence of severe complications associated with genital chlamydia infection in the general female population. Methods: The Uppsala Women's Cohort Study was a retrospective population based cohort study in Sweden, linking laboratory, hospital, and population registers. We estimated the cumulative incidence of hospital diagnosed pelvic inflammatory disease, ectopic pregnancy, and infertility, and used multivariable regression models to estimate hazard ratios according to screening status. Results: We analysed complete data from 43 715 women in Uppsala aged 15-24 years between January 1985 and December 1989. Follow up until the end of 1999 included 709 000 woman years and 3025 events. The cumulative incidence of pelvic inflammatory disease by age 35 years was 3.9% (95% CI 3.7% to 4.0%) overall: 5.6% (4.7% to 6.7%) in women who ever tested positive for chlamydia, 4.0% (3.7% to 4.4%) in those with negative tests, and 2.9% (2.7% to 3.2%) in those who were never screened. The corresponding figures were: for ectopic pregnancy, 2.3% (2.2% to 2.5%) overall, 2.7% (2.1% to 3.5%), 2.0% (1.8% to 2.3%), and 1.9% (1.7% to 2.1%); and for infertility, 4.1% (3.9% to 4.3%) overall, 6.7% (5.7% to 7.9%), 4.7% (4.4% to 5.1%), and 3.1% (2.8% to 3.3%). Low educational attainment was strongly associated with the development of all outcomes. Conclusions: The incidence of severe chlamydia associated complications estimated from ours, and other population based studies, was lower than expected. Studies that incorporate data about pelvic inflammatory disease diagnosed in primary care and behavioural risk factors would further improve our understanding of the natural history of chlamydia. Our results provide reassurance for patients, but mean that the benefits of chlamydia screening programmes might have been overestimated.

The aim of the study was to investigate the prevalence and aetiology of chronic kidney disease (CKD) and trends in estimated glomerular filtration rate (eGFR) in HIV-infected patients. MethodsAscertainment and review of CKD cases among patients attending King's College and Brighton Hospitals, UK were carried out. CKD was defined as eGFR o60 mL/min for ! 3 months. Longitudinal eGFR slopes were produced to examine trends in renal function before, during and after exposure to indinavir (IDV) or tenofovir (TFV). ResultsCKD prevalence was 2.4%. While HIV-associated nephropathy accounted for 62% of CKD in black patients, 95% of CKD in white/other patients was associated with diabetes mellitus, hypertension, atherosclerosis and/or drug toxicity. Exposure to IDV or TFV was associated with an accelerated decline in renal function (4.6-fold and 3.7-fold, respectively) in patients with CKD. In patients initiating IDV, age ! 50 years increased the odds of CKD [odds ratio (OR) 4.9], while in patients initiating TFV, age ! 50 years (OR 5.4) and eGFR 60-75 mL/min (OR 17.2) were associated with developing CKD. ConclusionThis study highlights the importance of metabolic and vascular disease to the burden of CKD in an ageing HIV-infected cohort. In patients who developed CKD, treatment with IDV or TFV was associated with an accelerated decline in renal function.Keywords: glomerular filtration rate, HIV, indinavir, kidney, tenofovir Accepted 20 November 2008 Introduction Acute renal failure (ARF) and chronic kidney disease (CKD) are important complications of HIV infection [1]. Approximately 6% of HIV-infected patients develop one or multiple episodes of ARF [2], and 15% of patients have evidence of CKD [3,4]. ARF usually occurs in the setting of severe (opportunistic) infections, malignancy or liver disease [2,5], and both ARF and CKD are associated with advanced immunodeficiency [2][3][4][5][6]. Black HIV-infected patients are at risk of developing HIV-associated nephropathy (HIVAN), which is characterized by heavy proteinuria and rapid progression to end-stage renal disease (ESRD) [7][8][9]. HIVAN, idiopathic noncollapsing focal and segmental glomerulonephritis (FSGS), immune complex kidney disease and other glomerulopathies predominate in biopsy series and among black patients with ESRD [7,[10][11][12][13].In the general, HIV-uninfected population, the prevalence of CKD increases dramatically in those aged 50 years and over [14]. CKD in these patients is associated with diabetes mellitus, hypertension and atherosclerosis [15], and is an independent risk factor for coronary heart disease [16]. CKD in this setting is often insidious in onset and may take decades to become clinically manifest. The objectives of this study were to describe the prevalence and aetiology of CKD in HIV-infected patients receiving care in the UK, and to examine trends in renal function before, during and after exposure to IDV or TFV in patients with CKD. Methods Case ascertainmentAll HIV-infected adults with CKD who attended King's College Hospital ...

The case-fatality rate following a diagnosis of prostate cancer is higher for Black men compared to White men. How this elevated rate arises is uncertain, with differences in disease biology, presentation, treatment and comorbidity having been suggested. A systematic search was conducted for articles that reported ethnic differences in overall-survival, prostate cancer specific survival (PSS) or biochemical recurrence. 48 articles met the inclusion criteria. Black men had worse overall survival (risk ratio 1.35, 95% CI 1.23-1.48) but this was not due to comorbidity alone as PSS and risk of biochemical recurrence were also elevated (1.29, 95% CI 1.13-1.47 and 1.34, 95% CI 1.23-1.46, respectively). Studies adjusting for clinical predictors and socioeconomic variables no longer supported a difference in overall survival (1.01, 95% CI 0.88-1.16), but continued to find an increased risk amongst Black men for PSS (1.13, 95% CI 1.00-1.27) and biochemical recurrence (1.25, 95% CI 1.11-1.41). Similar results were seen for studies from the pre-PSA era and free-health care settings. In contrast to others, studies of metastatic cancer did not find evidence of BlackWhite differences (p for interaction 5 0.01). In conclusion, Black men had a poorer prognosis which was not fully explained by comorbidity, PSA screening, or access to free health care, although few studies measure these factors well. Either management differences for local disease and/or biological differences may be behind Black-White differences in prostate cancer prognosis. ' 2008 Wiley-Liss, Inc.Key words: prostate cancer; ethnicity; prognosis; meta-analysis It is relatively uncontroversial to state that Black men have a greater incidence of prostate cancer than white men.1-3 The picture is less clear with regards ethnic differences in case fatality following prostate cancer diagnosis. There are several reasons why Black men may have a worse prognosis than their White counterparts.4,5 Some of these reasons may reflect socio-cultural differences that are amenable to intervention, whilst others may reflect genuine racial differences in cancer biology. These 2 types of explanations are not mutually exclusive and both may operate simultaneously.Possible socio-cultural explanations are: (i) Black men may have worse access to health care and therefore present later in the natural history of the disease at a more advanced stage. 6 (ii) In the US, more White men in the past have been diagnosed through screening.7 This will artefactually increase survival differences due to the phenomena of ''lead-time'' and ''length-time'' biases. (iii) Black men may be subject to differences in clinical management such that they are less aggressively investigated or treated. 8,9 (iv) Black men are more likely to have lower socioeconomic status, increased comorbidity and overall reduced life-expectancy compared to White men.10 These factors will increase the apparent difference in mortality rates even if there were no ethnic differences in the natural history of prostate cancer. How...

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ARF was common and was associated with advanced immunodeficiency. The incidence of ARF decreased >10-fold in patients who had received HIV care for > or =3 months.