Adherence to separate aspects of guidelines for surgical prophylaxis has to be improved. The duration of antibiotic prophylaxis was the main parameter of interest. Interventions have to be made about the development, distribution and adoption of adequate guidelines in collaboration with surgeons.

Although botulinum toxin is generally considered safe, its widespread use and the constantly expanded indications raise safety issues. This study aimed to review the serious and long-term adverse events associated with the therapeutic and cosmetic use of botulinum toxin. Serious adverse events included dysphagia, respiratory compromise, generalized muscle weakness, marked bilateral ptosis, pseudoaneurysm of the frontal branch of the temporal artery, necrotizing fasciitis, sarcoidal granuloma, Fournier gangrene, and cervical kyphosis. Death was attributed to botulism or anaphylactic shock. In conclusion, botulinum toxin may cause serious adverse events, which are more common after its therapeutic use, but can also be noticed after its cosmetic use. Thorough knowledge of the anatomy of the treated muscles and of the pharmacology of the drug is imperative to avoid serious adverse events.

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Compliance is associated with more effective BP control. Physicians can enhance patient compliance and hypertension control by devoting more time to counselling, avoiding unnecessary changes in drug regimens and restricting the tablet numbers.

Background: Sclerotherapy has been extensively used in the treatment of valvular insufficiency of superficial veins. Although sclerotherapy seems safe, reports of serious adverse events (AE) have been published. This paper aims to review AE of sclerosing agents. Methods: Electronical databases were searched for identifying articles on local, serious and long-term AE of sclerotherapy. Results: Hyperpigmentation and matting are the most often local AE of sclerotherapy. Other local AE include superficial thrombophlevitis, pyoderma gangrenosum, pain, ulcer formation, and hypertrichosis. Local AE can be serious, that is, it can include cutaneous necrosis, intra-arterial injection with subsequent acute ischemia that can lead to amputation, and necrotizing fasciitis. Most data on systemic AE of sclerotherapy are extracted from case series and case reports. Systemic AE include neurological complications, such as ischemic stroke, transient ischemic attack, visual disturbances and cardiac toxicity, that is, myocardial infarction, Takotsubo cardiomyopathy, chest tightness, pulmonary embolism, deep vein thrombosis, septicemia, anaphylaxis. It is difficult to estimate the frequency of serious systemic AE of sclerotherapy. Conclusion: Physicians practicing sclerotherapy should be aware of the possible local and systemic AE of sclerotherapy, inform patients accordingly and be prepared for the appropriate management of the rare but possibly lethal serious AE.

So, although the existing evidence is still limited, evidence is accumulating that epigenetic targets may represent nodal targets for the anti-proliferative actions of salicylates and NSAIDs. This, in turn, may have implications for cancer chemoprevention and treatment. Undoubtedly, this notion requires further investigation, but if proved correct, it could lead to the design of less toxic agents that target epigenetic processes as part of existing or novel multi-targeted treatment modalities.

Variation exists in patient response on analgesic treatment in terms of efficacy and safety. This variation may be in part explained by pharmacogenomics. This paper aimed to review data on pharmacogenomics of opioid analgesics focusing on the effect of genetic variation on the efficacy and safety of these agents. Current evidence suggests that pharmacogenomics contribute to variation in efficacy and safety of opioids. However, most data come from case control studies and case reports. In addition, a recognized drawback in the field of pharmacogenomics is the common occurrence of false positive association between polymorphisms and the investigated outcome. Prospective studies are needed to further elucidate the clinical implications of available data as well as to define the guidelines for the clinical application of pharmacogenomic data. Furthermore, basic research should focus on the identification of biologically meaningful polymorphisms enabling a hypothesis with biological plausibility driven research in the field of pharmacogenomics of analgesics. Moreover, the publication of relevant negative results should be favoured.

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