Heart failure is a leading cause of death and disability. Galectin-3 expression is associated with myocardial fibrosis; recombinant galectin-3 can induce myocardial fibrosis in experimental animals. However, the fact that endogenous galectin-3 is causative of myocardial fibrosis is yet to be firmly established. Nevertheless, the important discovery that N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a naturally occurring anti-inflammatory and antifibrotic peptide, inhibits galectin-3 expression, which prevents cardiac remodeling and dysfunction, provides impetus for translational research into anti-galectin therapy. The lack of a close relationship between galectin-3 and brain natriuretic peptide creates the possibility of a complimentary role. Thus, whilst brain natriuretic peptide is a useful biomarker for diagnosing heart failure, galectin-3 appears to be a culprit biomarker that mediates the development of heart failure, raising the possibility that specific anti-galectin therapy may halt the development of heart failure. Furthermore, data are beginning to emerge supporting the hypothesis that galectin-3 is crucial in the angiotensin-aldosterone pathway leading to salt and water retention, a key mechanism which can result in the development of heart failure. Thus, one might expect patients with heart failure and raised levels of galectin-3 to benefit from aldosterone antagonist therapy. Numerous clinical trials have already established the role of galectin-3 in predicting response to heart failure management, in particular how high levels of galectin-3 predicts mortality. A recent post hoc analysis of the Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA) suggested that patients with relatively low galectin-3 levels (<19 ng/ml) are most likely to benefit from statin therapy. This generated an important hypothesis that deserves further study.

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IntroductionGuidelines recommend epidemiological treatment of patients presenting as a contact of infection. This potentially reduces the prevalence of infection, reducing infectivity and reduces patient visits. Over prescription of antibiotics poses a threat of future resistance development and exposes the patient to unnecessary treatment. An audit was carried out to determine if any themes could be identified to indicate a likely positive result in contacts.MethodsWe audited asymptomatic contacts of chlamydia and gonorrhoea (PNC/PNG) attending GU services at BartsHealth (February 2016 for 3 months). Data on gender, sexual orientation, contacts (regular or casual), infection site, time since sex with contact, HIV status, STI in previous year were collected. Testing by Aptima NAATS for chlamydia/gonorrhoea and gonorrhoea culture.ResultsChlamydia75 asymptomatic contacts (55 male/20 female). All treated as contacts. 25 had a positive result (34%). No factors could be associated with predicting a positive result, except a suggestion that a regular partner v casual partner. Gonorrhoea: 85 asymptomatic contacts (76 male/9 female). All treated as contacts. 27 had a positive result (32%). Being male >24years old/MSM/>5 partners (in 3m) and contact being a regular partner were suggestive of predicting a positive result.DiscussionThe audit reinforces epidemiological treatment. Drawbacks of not treating include failure to return, onward STI transmission and inconvenience of re-attending. However, over 60% had potentially unnecessary treatment and with rapid turnaround of results (<2d), future universal treatment may need to be revised.