Opioids are mainly used to treat both acute and chronic pain. Several opioids are metabolized to some extent by CYP2D6 (codeine, tramadol, hydrocodone, oxycodone, and methadone). Polymorphisms in CYP2D6 have been studied for an association with the clinical effect and safety of these drugs. Other genes that have been studied for their association with opioid clinical effect or adverse events include OPRM1 (mu receptor) and COMT (catechol‐O‐methyltransferase). This guideline updates and expands the 2014 Clinical Pharmacogenetics Implementation Consortium (CPIC) guideline for CYP2D6 genotype and codeine therapy and includes a summation of the evidence describing the impact of CYP2D6, OPRM1, and COMT on opioid analgesia and adverse events. We provide therapeutic recommendations for the use of CYP2D6 genotype results for prescribing codeine and tramadol and describe the limited and/or weak data for CYP2D6 and hydrocodone, oxycodone, and methadone, and for OPRM1 and COMT for clinical use.

Background: Obesity-associated type 2 diabetes is rapidly increasing throughout the world. It is generally recognized that natural products with a long history of safety can modulate obesity.

Aim: We evaluated healthcare practitioners’ perspectives regarding clinical pharmacogenetics in Cairo, Egypt. Materials & methods: We administered a paper-based survey to pharmacists and physicians practicing at Children’s Cancer Hospital Egypt. The survey assessed practitioners’ knowledge, attitudes, and perspectives about pharmacogenetic testing. Results: The study included 184 respondents (67.9% pharmacists; 32.1% physicians. Overall, the pharmacogenetic knowledge was low (mean = 41.7%) but attitudes toward pharmacogenetic testing and its potential clinical application were generally positive. Pharmacists responded more favorably than physicians to statements attributing the responsibility of applying pharmacogenetics in the clinical setting to their profession. However, several challenges were identified; the most common being: lack of pharmacogenetic knowledge and skill, lack of pharmacogenetic testing devices, and limited funding. Conclusion: Future efforts to promote pharmacogenetic implementation should focus on foundational education, practical training, and exploration of potential funding sources.

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Profenofos as an organophosphorus insecticide has been used in the agricultural countries as Egypt, may find its way to water system and adversely effect on aquatic life particularly fish. Nile tilapia, Oreochromis niloticus as a major fish species in River Nile and one of the major sources of protein for human beings in Egypt, and it can also be a source of threaten to human health. Transport profenofos directly to tilapia fish may affect their physiological status and then fish production. The mortality of profenofos toxicity was estimated on tilapia and LC50 was detected as 0.87 mg/l. Also fish were exposed to 1/2 LC50 for 96 hrs and to 1/10 LC50 for 28 days and lastly were left after the chronic toxicity for another 28 days as recovery period. The increase of blood glucose was accompanied with decrease in liver and muscles glycogen throughout the acute and chronic trail periods. Fish showed also highly significant decrease in serum total protein and globulin with increasing in albumin and A/G ratio. A sharp elevation in serum creatinine, urea and uric acid with decrease in serum total lipid, triglyceride and cholesterol were also recorded. Lastly gradual and sharp elevation in the levels of serum enzymes, S-AST, S-ALT and S-ALP was revealed in profenofos-exposed tilapia. Same behavior as S-AST and S-ALT were in liver transaminases (L-AST & L-ALT). Our study revealed adverse change of metabolism in tilapia due to profenofos exposure. This may inform about the dangerous use of profenofos and limitations should be managed.