Objective To evaluate the association between pioglitazone use and bladder cancer risk in patients with type 2 diabetes.Design Retrospective cohort study using propensity score matched cohorts.Settings Healthcare databases from Finland, the Netherlands, Sweden, and the United Kingdom. Data comprised country specific datasets of linked records on prescriptions, hospitals, general practitioners, cancer, and deaths.Participants Patients with type 2 diabetes who initiated pioglitazone (n=56 337) matched with patients with type 2 diabetes in the same country exposed to diabetes drug treatments other than pioglitazone (n=317 109). Two matched cohorts were created, using a 1:1 fixed ratio (nearest match cohort) and a 1:10 variable ratio (multiple match cohort). Patients were matched on treatment history and propensity scores accounting for several variables associated with pioglitazone initiation.Main outcome measures Hazard ratios and 95% confidence intervals were estimated by Cox’s proportional hazards model with adjustments for relevant confounders. To assess the robustness of the findings, several sensitivity and stratified analyses were performed.Results In the cohort exposed to pioglitazone treatment, 130 bladder cancers occurred over a mean follow-up time of 2.9 years. In the nearest match and multiple match cohorts not exposed to pioglitazone treatment, 153 and 970 bladder cancers were recorded, with a mean follow‑up time of 2.8 and 2.9 years, respectively. With regards to bladder cancer risk, the adjusted hazard ratio for patients ever exposed versus never exposed to pioglitazone was 0.99 (95% confidence interval 0.75 to 1.30) and 1.00 (0.83 to 1.21) in the nearest and multiple match cohorts, respectively. Increasing duration of pioglitazone use and increasing cumulative dose were not associated with risk of bladder cancer (>48 months of pioglitazone use, adjusted hazard ratio 0.86 (0.44 to 1.66); >40 000 mg cumulative dose, 0.65 (0.33 to 1.26) in the nearest match cohort).Conclusions This study shows no evidence of an association between ever use of pioglitzone and risk of bladder cancer compared with never use, which is consistent with results from other recent studies that also included a long follow-up period.Trial registration Registered to the European Union electronic register of post-authorisation studies (EU PAS register no EUPAS3626).

Right antecubital PICCs are more likely to be placed in the central location in relation to the carina. PICCs inserted through the left antecubital veins need to be pushed further down to aim for a central location. Inter-observer variability in identifying the tip of PICCs is least with the introduction of digital imaging.

Objective: Low birth weight (LBW) is common in the Indian population and may represent an important predisposing factor for type 2 diabetes (T2D) and the metabolic syndrome. Intensive metabolic examinations in ethnic LBW Asian Indians have been almost exclusively performed in immigrants living outside India. Therefore, we aimed to study the metabolic impact of being born with LBW in a rural non-migrant Indian population. Subjects and methods: One hundred and seventeen non-migrant, young healthy men were recruited from a birth cohort in a rural part of south India. The subjects comprised 61 LBW and 56 normal birth weight (NBW) men, with NBW men acting as controls. Subjects underwent a hyperinsulinaemic euglycaemic clamp, i.v. and oral glucose tolerance tests and a dual-energy X-ray absorptiometry scan. The parents' anthropometric status and metabolic parameters were assessed. Results: Men with LBW were shorter (167G6.4 vs 172G6.0 cm, P!0.0001), lighter (51.9G9 vs 55.4G7 kg, PZ0.02) and had a reduced lean body mass (42.1G5.4 vs 45.0G4.5 kg, PZ0.002) compared with NBW controls. After adjustment for height and weight, the LBW subjects had increased diastolic blood pressure (77G6 vs 75G6 mmHg, PZ0.01). Five LBW subjects had impaired glucose tolerance. In vivo insulin secretion and peripheral insulin action were similar in both the groups. Mothers of the LBW subjects were 3 cm shorter than the control mothers. Conclusion: Only subtle features of the metabolic syndrome and changes in body composition among LBW rural Indians were found. Whether other factors such as urbanisation and ageing may unmask more severe metabolic abnormalities may require a long-term follow-up.

Snake bite incidence is highest in Asia and sub-Saharan Africa. This retrospective audit of 533 adult patients, who had presented to the Emergency Department, collates clinical features, effect of pharmacologic interventions and the risk factors that influence morbidity and mortality. Dual toxicity, neurological and haematological, was observed in 30.4% of patients. Laboratory evidence of haematotoxicity was demonstrated in 314 (58.9%) and 40% demonstrated clinical evidence of bleeding. However, 7.3% of these patients did not have laboratory evidence of bleeding disorder (p < 0.001). Conversely, 60% did not have clinical evidence of bleeding, but demonstrated laboratory evidence of abnormal parameters. Acute kidney injury (AKI) was evident in 28% of patients and 15.3% required haemodialysis. About 25% with no haematotoxicity showed evidence of AKI. The majority received 6-12 vials of poly-valent anti-snake venom. Hypersensitivity reaction rate was 8% and predominantly anaphylactoid in nature. The length of hospital stay ranged from 2 to 28 days and 20% required mechanical ventilation. Overall mortality rate was 7.5% with significant association to AKI, haematotoxicity and assisted ventilation. The mortality rate was 18% in patients with pre-hospital delay more than 24 h, as against 5% when admitted within the above specified period (p = <0.001). The strength of this study is the accrued information of over a period of 10 years of snake-bite management through the Emergency Department of a university hospital setting. The limitations are the retrospective study design and the rejection percentage of 15.5% due to insufficient information from the total chart pool.

(65 ± 17.9, P < 0.001). These improvements continued up to the time of weaning (pH 7.38 ± 0.08, PaCO 2 54.7 ± 20) and maintained (within 12 h) postweaning from the ventilator (pH 7.39 ± 0.08, PaCO 2 51.9 ± 12.4). No significant change in the PaO 2 was observed during NIPPV; PaO 2 after 1 h, prior to weaning and after weaning was 90.53 ± 42.85, 84.80 ± 33.76, 78.71 ± 43.81