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Background: Sickle cell anaemia (SCA) is an inherited hemoglobinopathy resulting in sickling of erythrocytes that cause micro-vascular obstruction leading to acute complications and chronic organ damage. Adults with SCA have endocrine complications and metabolic alterations. The aim of this study was to assess the association between gonadal and thyroid hormones with iron indices and to explore the potential association between serum ferritin levels and sex hormones in adult males with sickle cell disease in New Prince Saud Bin Jalawy Hospital (NPSBJH) in Hofuf city (Eastern region of Saudi Arabia) where there are many patients with SCA. Methods: A cross-sectional analytical study was carried out in the Haematology Clinic at NPSBJH in 2018. A total of eighty (80) male patients with sickle cell anaemia were included in this study and were divided into two groups according to serum ferritin level. Group I (G-I): Included 40 male patients with high serum ferritin level and group II (G-II): included 40 male patients with normal serum ferritin level. Results: There was a significant difference in height/cm between GI and Gil, P value= 0.006. Serum ferritin was significantly higher in GI (P value= 0.000), and serum TIBC was significantly higher in G-II. (P value= 0.022). Testosterone level was significantly higher in G-II (P value= 0.018). Luteinizing hormone (LH) was significantly higher in group I (P-value 0.019). There was a significant relation between serum ferritin level in G-I and the following: serum iron, TIBC, serum testosterone, LH, prolactin, free T3 and free T4. Conclusion: Adult males with SCD with high serum ferritin level were shorter than adult males with SCD who had normal serum ferritin level and had a significant lower level of serum testosterone and significant high level of LH and this was most likely due to endocrine dysfunction secondary to high ferritin level and iron overload.

Introduction Coronary artery disease (CAD) remains the main cause of death in patients with type 2 diabetes mellitus (T2DM). It is more extensive and diffuse in diabetics in spite of antiplatelet therapy. Hence, the prevention and the early diagnosis of CAD among patients with T2DM are very important. There is a variety of hemostasis abnormalities in T2DM. Therefore, fibrinogen and plasminogen activator inhibitor-1 (PAI-1) may have a link between T2DM and CAD. Aim The aim was to evaluate the plasma fibrinogen and PAI-1 levels in some Egyptian patients with T2DM with and without CAD. Patients and methods A total of 30 Egyptian patients with T2DM attending the Internal Medicine Department of Al Zahraa Hospital were included in this study. Their ages ranged between 31 and 54 years. Based on ECG changes and echocardiography, the patients were divided into the following: 15 who had CAD and 15 without. Another 15 apparently healthy participants were enrolled as a control group. Blood samples were analyzed for routine blood tests, fasting lipid profile, renal function, liver function, glycosylated hemoglobin, plasma fibrinogen, and PAI-1, which was measured by enzyme-linked immunosorbent assay. Results Plasma fibrinogen and PAI-1 were significantly higher in Egyptian patients with T2DM with CAD than those who had only T2DM, and both markers were higher in Egyptian patients with T2DM than healthy controls. Fibrinogen and PAI-1 levels were positively correlated with glycosylated hemoglobin in Egyptian patients with T2DM. Conclusion Egyptian type 2 diabetic patients with T2DM are prone to develop CAD more often than not owing to increase in plasma fibrinogen and PAI-1 levels; therefore, we can give a small dose of anticoagulant for all patients with T2DM.

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patients were malnourished. Plasma copeptin, proadrenomedullin, myeloperoxidase, protein, albumin, sodium and systemic blood pressure were not significantly different in each groups. Degrees of over-hydration were not different however, extracellular and intracellular fluid ratio (EI) were different in PD (p ¼ 0.03) and CKD-ND (p ¼ 0.12). EI were 1.08 vs. 0.94 for PD and 1.13 vs. 0.82 for CKD-ND. In pooled analysis, copeptin (0.44 6 0.28 vs 0.35 6 0.19, p ¼ 0.07) and EI (1.04 6 0.23 vs. 0.89 60.15, p ¼ 0.001) were different between malnutrition and normal group. CONCLUSIONS: Malnutrition CKD patients showed higher EI ratio. Even though the overall degree of over-hydration was not different, malnourished CKD patient showed more extracellular fluid accumulation despite similar oncotic pressure (albumin, protein) and plasma osmolality (sodium). This study showed the possibility of causal rela