The Zika Virus (ZIKV) has been slowly becoming an epidemic in different parts of the world. Since its discovery in 1947, there have been numerous outbreaks affecting many different populations. Currently, there is an ongoing threat of ZIKV in Latin America and the United States of America. ZIKV is mainly spread by the Aedes aegypti mosquito and causes non-specific symptoms such as fever, myalgia, and generalized weakness. In addition to these symptoms, it has been noted the ZIKV is capable of causing associated conditions in adults, particularly in pregnant women as well as in newborns via vertical transmission. These manifestations include microcephaly, lissencephaly, ventriculomegaly, optic neuropathy, and congenital glaucoma, arthralgia, maculopapular rash, and cardiovascular anomalies such as atrial fibrillation. It is important to understand the reason for this specific set of associated conditions that emerge with ZIKV. This paper aims to identify the manifestations of ZIKV in adults and neonates in detail and attempts to understand the pathophysiology behind each one.

BackgroundStudies have linked vitamin D deficiency with the risk of type 2 diabetes mellitus (T2DM) and to the development of chronic complication of diabetes. Vitamin D receptors (VDR) have been found in many tissues in the body including the pancreas, a finding that indicates its role in insulin secretion. In addition, many studies have demonstrated the role of vitamin D and its receptor in insulin sensitivity and signal transduction. Vitamin D deficiency is common throughout the world, but not all vitamin D deficiencies are accompanied by a rise in parathyroid hormone (PTH). The present study was conducted to assess vitamin D deficiency in type 2 diabetic patients in comparison to healthy control and to determine parathyroid gland response to vitamin D deficiency in both groups.MethodsThis observational study was performed during a period from January to October 2018. The study included 151 type 2 diabetic patients selected from three diabetes clinics and 43 age and sex-matched healthy subjects. Informed consent and clinical information were obtained from all participants before the study. Results of the laboratory analysis for serum 25-hydroxyvitamin D (25-OHD), PTH, calcium, and phosphorous were recorded. The data was analyzed using the statistical package for the social sciences (SPSS) Statistics 17.ResultsThe results showed low vitamin D concentration in both groups; however, there was no significant difference in vitamin D concentration between diabetic patients and the control patients. A high percentage of PTH level was found in severe vitamin D deficient diabetic patients and healthy controls. The higher percentage of diabetic and normal subjects with mild vitamin D deficiency had a normal PTH level. All healthy subjects with vitamin D insufficiency showed normal PTH concentration. About 10% of diabetic patients with severe vitamin D deficiency had a low PTH level.ConclusionThe population in our study was generally deficient in 25-OHD irrespective of diabetes mellitus, indicating a greater need for vitamin D supplementation. Not all vitamin D deficient patients have high PTH levels, a finding that supports the emergence of new criteria for vitamin D deficiency, diagnosis and treatment, and highlights the importance of testing PTH in this regard.

BackgroundPlasma uric acid has been shown to be associated with an increased risk of hypertension, cardiovascular disease, chronic kidney disease, insulin resistance, and metabolic syndrome. Conflicting data regarding plasma uric acid levels in type 2 diabetes mellitus and their role in the development and progression of diabetic complications have been observed by many studies. The present study aimed to evaluate plasma uric acid levels in type 2 diabetic patients and to determine the effects of hypoglycemic drugs and pharmacologic insulin on plasma uric acid concentration.Subjects and methodsThe study included 162 type 2 diabetic patients divided into three groups (insulin taking group (N=58), glibenclamide taking group (N=40), and metformin taking group (N=64), and 47 normal healthy controls. A questionnaire that included variables such as age, sex, duration of disease, and body mass index (BMI) were answered by all the participants. Blood samples were collected and estimated for serum uric acid (SUA), fasting blood sugar (FBS), and glycated hemoglobin (HbA1c) using standard methods and the data were statistically analyzed.ResultsDiabetic patients showed a significant increase in serum uric acid, fasting blood sugar, glycated hemoglobin, and body mass index when compared to control subjects. The serum uric acid levels of metformin and glibenclamide taking groups were significantly higher than the control group. The difference of serum uric concentration between the insulin taking group and both the control and metformin groups was statistically non-significant. On the other hand, obese diabetics showed a significantly higher serum uric acid than overweight and lean diabetics. Furthermore, serum uric acid had a significant strong positive correlation with body mass index.ConclusionType 2 diabetes mellitus (T2DM) is associated with high serum uric acid levels. Hypoglycemic drugs and pharmacologic insulin do not have a large impact on SUA concentration, but obesity seems to be the primary determinant of SUA levels in T2DM patients. The condition of diabetes may have a direct effect on the oxidation of the purine nucleotides resulting in the increased uric acid (UA) levels. In addition, hyperinsulinemia could lead to hyperuricemia by increasing the rate of xanthine oxidase synthesis. There is a strong relationship between T2DM and obesity with high uric acid levels.

Type 2 diabetes mellitus (T2DM) has high morbidity and results in increased risk of mortality mainly due to cardiovascular diseases. Different factors have been found to be responsible for the increased prevalence of coronary artery disease (CAD) in T2DM. One of these factors includes raised serum levels of lipoprotein(a) (Lp(a)). The present study was designed to evaluate the association of Lp(a) levels with T2DM in Libyan patients and find the degree of association between Lp(a), glycemic control, insulin, and lipid profile. The study included 100 T2DM patients, recruited from the Benghazi Center for Diagnosis and Treatment of Diabetes, and 30 apparently healthy age and sex-matched individuals, to serve as controls. All participants completed a questionnaire to obtain clinical information and medical history. Blood samples were collected and analyzed for Lp(a), fasting blood glucose (FBS), HbA1c, insulin, total cholesterol (TC), triglycerides (TAG), low-density lipoprotein c (LDL-c), and high-density lipoprotein c (HDL-c). The results from the comparison between the control and experimental groups showed that Lp(a) was significantly higher in diabetic patients. It showed the positive correlation with TC and LDL-c. On the contrary, it showed no significant correlations with glycemic control parameters nor insulin, TAG, HDL-c, body mass index (BMI), and blood pressor (BP). Cardiovascular disease (CVD) risk in type 2 diabetic patients could be dependent on risk factors other than LDL-c, which may not be an independent risk factor for the development and progression of atherogenesis in T2DM. Lp(a) may be a new metabolic syndrome risk factor, and it may be useful as a cardiovascular risk biomarker in future clinical practice.

Background and objectives Vitamin D deficiency is a global public health issue, which affects people of all ages and ethnicities. However, severe deficiency seems to be more prevalent in the Middle East and South Asia. Evidence suggests that low serum 25-hydroxycholicalciferol [25(OH)D] levels are associated with an increase in parathyroid hormone (PTH). Yet, the 25-OHD levels leading to serum PTH increase are still a matter of debate. The objective of this study is to assess deficiency of vitamin D in otherwise healthy individuals, and to determine the response of the PTH to vitamin D deficiency. Methods This observational study was conducted from January 2018 to May 2018. A total of 43 individuals were selected from three separate clinics in Libya (Alrazy clinic, Alhaya clinic, and Alnukbah clinic). Blood drawn from these individuals was assessed for serum calcium, phosphorus, 25(OH)D, and PTH. These data were collected and analyzed using the Statistical Package for Social Sciences (SPSS) version 17.0 for Windows (SPSS Inc., Chicago, IL). Results The mean age and standard (SD) of the study participants was 47.4 ± 12.4. The age range was 19-67 years. The ratio of male to female was 1:2. The percentage of individuals with vitamin D deficiency in the study group was 95.3%, whereas the percentage of vitamin D insufficiency was 4.7%. These data suggest that individuals with severe deficiency show higher PTH values (75.66 ng/ml), whereas those with insufficiency showed lower PTH values (37.5 ng/ml). Conclusion The population in the present study was overall deficient in 25-OH vitamin D, which indicates a greater need for supplementation with vitamin D. However, not all the individuals with vitamin D deficiency have high levels of PTH, a finding that agrees with the need for new criteria in the management of vitamin D deficiency and the importance of PTH testing.

Pernicious anemia (also known as Biermer’s disease) is an autoimmune atrophic gastritis which predominantly affects the fundus of the stomach. It results in a deficiency of vitamin B12 (cobalamin) as it affects the normal process of absorption in the ileum. The pernicious anemia is characterized by a wide range of hematological and neurological features. Neurological features can present without hematological manifestations. One of the early neurological features of this anemia is nominal dysphasia (word-finding difficulties), which was usually not reported before as an isolated finding. We present a case of pernicious anemia with isolated nominal dysphasia responding dramatically to parenteral vitamin B12 therapy.

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