Tramadol is a synthetic, centrally acting analgesic. It is the most consumed narcotic drug that is prescribed in the world. Tramadol abuse has dramatically increased in Egypt. Long term use of tramadol can induce endocrinopathy. So, the aim of this study was to analyze the adrenal insufficiency induced by long term use of tramadol in experimental animals and also to assess its withdrawal effects through histopathological and biochemical genetic study. Forty male albino rats were used in this study. The rats were divided into 4 groups (control group, tramadol-treated group, and withdrawal groups). Tramadol was given to albino rats at a dose of 80 mg/kg body weight for 3 months and after withdrawal periods (7–15 days) rats were sacrificed. Long term use of tramadol induced severe histopathological changes in adrenal glands. Tramadol decreased the levels of serum cortisol and DHEAS hormones. In addition, it increased the level of adrenal MDA and decreased the genetic expression of glutathione peroxidase and thioredoxin reductase in adrenal gland tissues. All these changes started to return to normal after withdrawal of tramadol. Thus, it was confirmed that long term use of tramadol can induce severe adrenal insufficiency.

The landscape of chronic liver disease in Egypt has drastically changed over the past few decades. The prevalence of metabolic-associated fatty liver disease (MAFLD) has risen to alarming levels. Despite the magnitude of the problem, no regional guidelines have been developed to tackle this disease. This document provides the clinical practice guidelines of the key Egyptian opinion leaders on MAFLD screening, diagnosis, and management, and covers various aspects in the management of MAFLD. The document considers our local situations and the burden of clinical management for the healthcare sector and is proposed for daily clinical practical use. Particular reference to special groups was done whenever necessary.

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Carbon monoxide poisoning (CO) is a major public health problem. Brain is the most sensitive organ to hypoxia induced by CO poisoning. Delayed Neurological Sequelae (DNS) is considered to be a delayed onset of neuropsychiatric symptoms after apparent recovery from acute CO poisoning. Therefore, this study was aimed to make a prospective comparative study between three markers (serum glutathione reductase, S100b protein and serum neurone-specific enolase) to predict the occurrence of DNS. This study was performed on 57 adult patients with acute CO poisoning. The markers were measured after arrival and the patients were divided into two groups: the DNS group (8 patients) & the non-DNS group (49 patients). There was a statistical difference between the two groups in terms of significant increase in loss of consciousness, syncope, dizziness, ECG changes, pneumonia, carboxyhemoglobin level, creatine phosphokinase, creatine phosphokinase-MB, troponin I, S100b protein, neurone-specific enolase in DNS grouped patiens and significant decrease in glasgow coma scale and glutathione reductase in DNS group. The cut off value of glutathione reductase was ≤ 30 U/L with a percentage of accuracy 94. 74. The cut off value of S100b protein was > 18.94 Pg/ L with 98.25 % percentage of accuracy, while, the cut off value of neurone-specific enolase was > 30.49 ng/ml and its accuracy was 96.49 %. All these cut off values predicted the occurrence of DNS. SO, it is concluded that serum S100b protein may represent the most reliable chemical marker for the prediction of DNS after acute CO poisoning by logistic regression analysis.