A Comparison of Emergency First Presentations of Colorectal Cancer in Under-50 and Over-50 Year-Old Patients.

Introduction: Colorectal cancer (CRC) is the second commonest malignancy related death in Western Europe with incidence increasing in young adults. 31% of UK patients with CRC present as emergencies. We compare the incidence, characteristics, management and outcomes in two cohorts presenting as CRC emergencies; under-50 and over-50 years old. Materials and Methods: Retrospective analysis was performed on 322 patients with emergency presentations of CRC over a 9-year period (January 2005-December 2013, West Suffolk Hospital, UK). Data were analyzed for demographics, symptoms, investigations, stage, grade, genetics, tumor location, management, and mortality. Results: 300 patients over 50 years old presented with CRC emergencies; 153 women (51%):147 men (49%); median age 77 years (interquartile range: 67-84). 22 patients under 50-years-old; 12 women (55%):10 men (45%); median age 43 years ([Interquartile Range (IQR)]: 35-46 years). Bowel obstruction was less common in under-50s (18.2% vs. 40.7%; p = 0.04). No over-50s had a positive family history for CRC; 7 under-50s did. A higher proportion of under-50s presented with Dukes A carcinomas (14.3% vs. 0.4%; p = 0.002), but no difference in other Dukes stages. Surgery was performed in a higher proportion of under-50s (95.5% vs. 77.0%; p = 0.04) and a higher proportion had same day surgery (71.4% vs. 28.1%; p = 0.01). Overall mortality was lower in under-50s (36.4% vs. 64.0%; p = 0.02). No significant differences occurred in in-hospital mortality (4.7% vs. 8.0%; p = 0.55), overall one-year survival (31.8% vs. 41.7%; p = 0.36), or median survival to death or study conclusion (27.1 vs. 19.6 months; p = 0.13). Conclusion: Emergency CRC had comparable outcomes between young and old cohorts, during the study time period. Younger patients were more likely to undergo operative interventions but overall survival was comparable.Our study was limited by the reporting biases intrinsic to retrospective analyses and by a small under-50 sample size. Further large-scale studies are warranted to support observations.

Primary hyperparathyroidism presenting as acute psychosis secondary to hypercalcaemia requiring curative parathyroidectomy.

Primary hyperparathyroidism (PHPT) can cause hypercalcaemia secondary to a pathologically high secretion of parathyroid hormone. Rarely this can first manifest as acute psychosis. It is imperative to exclude organic causes of psychosis before labelling the psychosis as primarily psychological. If hypercalcaemia is revealed, investigation is required to elucidate the underlying cause whilst instigating treatment to lower serum calcium levels. If PHPT is the underlying pathology, subsequent treatment involves surgical exploration and resection of the parathyroid adenoma or hyperplasia.

The contribution of the endogenous TRPV1 ligands 9-HODE and 13-HODE to nociceptive processing and their role in peripheral inflammatory pain mechanisms.

BACKGROUND AND PURPOSE: The transient receptor potential vanilloid type 1 (TRPV1) plays a fundamental role in the detection of heat and inflammatory pain responses. Here we investigated the contribution of two potential endogenous ligands [9- and 13- hydroxyoctadecadienoic acid (HODE)] to TRPV1-mediated noxious responses and inflammatory pain responses. EXPERIMENTAL APPROACH: 9- and 13-HODE, and their precursor, linoleic acid, were measured in dorsal root ganglion (DRG) neurons and in the hindpaws of control and carrageenan-inflamed rats by liquid chromatography/tandem electrospray mass spectrometry. Calcium imaging studies of DRG neurons were employed to determine the role of TRPV1 in mediating linoleic acid, 9-HODE- and 13-HODE-evoked responses, and the contribution of 15-lipoxygenase to the generation of the HODEs. Behavioural studies investigated the contribution of 9- and 13-HODE and 15-lipoxygenase to inflammatory pain behaviour. KEY RESULTS: 9-HODE (35 ± 7 pmol g(-1)) and 13-HODE (32 ± 6 pmol g(-1)) were detected in hindpaw tissue, but were below the limits of detection in DRGs. Following exposure to linoleic acid, 9- and 13-HODE were detected in DRGs and TRPV1 antagonist-sensitive calcium responses evoked, which were blocked by the 15-lipoxygenase inhibitor PD146176 and an anti-13-HODE antibody. Levels of linoleic acid were significantly increased in the carrageenan-inflamed hindpaw (P < 0.05), whereas levels of 9- and 13-HODE were, however, decreased. Intraplantar co-administration of anti-9- and 13-HODE antibodies and treatment with PD146176 significantly (P < 0.01) attenuated carrageenan-induced hyperalgesia. CONCLUSIONS AND IMPLICATIONS: This study demonstrates that, although 9- and 13-HODE can activate TRPV1 in DRG cell bodies, the evidence for a role of these lipids as endogenous peripheral TRPV1 ligands in a model of inflammatory pain is at best equivocal.

Lung cancer risk and solid fuel smoke exposure: a systematic review and meta-analysis.

The aim of this systematic review was to quantify the impact of biomass fuel and coal use on lung cancer and to explore reasons for heterogeneity in the reported effect sizes. A systematic review of primary studies reporting the relationship between solid fuel use and lung cancer was carried out, based on pre-defined criteria. Studies that dealt with confounding factors were used in the meta-analysis. Fuel types, smoking, country, cancer cell type and sex were considered in sub-group analyses. Publication bias and heterogeneity were estimated. The pooled effect estimate for coal smoke as a lung carcinogen (OR 1.82, 95% CI 1.60-2.06) was greater than that from biomass smoke (OR 1.50, 95% CI 1.17-1.94). The risk of lung cancer from solid fuel use was greater in females (OR 1.81, 95% CI 1.54-2.12) compared to males (OR 1.16, 95% CI 0.79-1.69). The pooled effect estimates were 2.33 (95% CI 1.72-3.17) for adenocarcinoma, 3.58 (1.58-8.12) for squamous cell carcinoma and 1.57 (1.38-1.80) for tumours of unspecified cell type. These findings suggest that in-home burning of both coal and biomass is consistently associated with an increased risk of lung cancer.