In this review, I aim to provide a complete overview of recent advances in knowledge regarding severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2)-induced thyroid dysfunction. I discuss the findings regarding the role of SARS-CoV-2 in the development of thyroid dysfunction, including subacute thyroiditis, Graves’ disease, non-thyroidal illness, thyrotoxicosis and Hashimoto’s thyroiditis during and subsequent to coronavirus disease 2019 (COVID-19). The thyroid gland and the entire hypothalamic–pituitary–thyroid (HPT) axis may represent key targets of SARS-CoV-2. Thyroid dysfunction during and subsequent to COVID-19 has been documented in clinical studies and is usually reversible. Most of the thyroid disorders, including Graves’ disease, euthyroid sick syndrome, Hashimoto’s thyroiditis and subacute thyroiditis, have been documented as sequelae to COVID-19, and the SARS-CoV-2 virus has been implicated in the aetiology of each. COVID-19 has been suggested to trigger the activation of pre-existing thyroid disease or autoimmunity. Furthermore, patients with uncontrolled thyrotoxicosis are at risk of SARS-CoV-2 infection-related consequences. Because of the neutropenia caused by antithyroid medications, which may obscure the signs of COVID-19, this group of patients should receive special attention. It is suggested that thyroid dysfunction during COVID-19 is caused by direct infection of the thyroid or “cytokine storm”-mediated autoimmune effects on the thyroid.

Background and Aim: Renal function is noticeably altered in both hypothyroidism and hyperthyroidism. However, clinical studies on thyroid dysfunction and its association with renal function are scarce. The purpose of this study was to evaluate changes in biochemical parameters of renal function in subjects with thyroid dysfunction and to correlate these values with the patient's thyroid profile. The effect of changes in thyroid function during therapy on renal function was also investigated. Methods: A prospective cohort study included 41 patients with untreated primary hypothyroidism and 16 patients with untreated hyperthyroidism. Thyroid-stimulating hormone (TSH), free thyroxine, and free triiodothyronine were assessed using immunoassay. The estimated glomerular filtration rate was calculated by the Modification of Diet in Renal Disease formula. Renal function tests were assessed in all patients at each of the two-time points: during thyroid dysfunction (hypo- or hyperthyroidism) and after attaining euthyroidism. Results: Our study demonstrated a statistically significant reduction in the average serum creatinine level in the hypothyroid patients after treatment compared to before treatment whereas the mean estimated glomerular filtration rate (eGFR) significantly improved after treatment compared to before treatment. Moreover, the average serum creatinine level in the hyperthyroid patients was significantly lower before treatment compared to after treatment, whereas the mean eGFR significantly dropped after treatment. TSH had a significant positive correlation with serum creatinine and a significant negative correlation with eGFR in all patients with thyroid dysfunction. Conclusions: Thyroid dysfunction is associated with deranged kidney function. It is crucial for the clinician to be aware of the link between thyroid disorders and aberrant renal function in order to consider a thyroid function test when treating a patient whose biochemical markers of renal function are only mildly elevated. There is a need for monitoring creatinine in patients with thyroid dysfunction.

Background: The incidence of cognitive impairment (CI) is higher in patients with diabetes mellitus (DM). The association between DM and CI and the risk factors for CI need to be addressed to estimate the prevalence of cognitive impairment in patients with DM and to identify the potential risk factors. The study is a cross-sectional study using a convenient sample of 269 subjects. Sociodemographic diabetes-related variables including biochemical markers were collected. CI and diabetes-related distress (DRD) were assessed using the Arabic version of Montreal Cognitive Assessment scale (MoCA) and the Diabetes Distress Screening Scale respectively. Results: Overall, 80.3% had cognitive impairment while 33.8% had severe impairment. Older age, female gender, low level of education, and low income were associated with CI; duration of diabetes and DRD were associated with CI while ophthalmic complications were associated with severe CI. Duration of diabetes was inversely associated with CI. Level of HbA1c was significantly higher in patients with severe CI, and the probability of CI increased as the level of HbA1c increased. Low level of education was associated with severe CI, and CI was two times more likely among patients with DRD. Conclusion: CI was higher than worldwide figures. Elderly females with low educational level, long duration of DM, and low socioeconomic status are at more risk. The probability of severe CI increased with increased level of HbA1c. Screening for CI in patients with diabetes along with intervention programs while considering the DRD and the level of HbA1c is crucial.

Background. Transforming growth factor-beta (TGF-β) and hepatocyte growth factor (HGF) are inflammatory cytokines which function as key regulators of immunological homeostasis and inflammatory responses. They have been linked to inflammatory bowel diseases (IBD). In this study, we aim to assess the levels of TGF-β and HGF and other inflammatory markers in patients with IBD and correlate them with the disease activity. Study Design. A cross-sectional study involving 100 patients with ulcerative colitis (UC) and 100 patients with Crohn’s disease (CD) and 50 control subjects. TGF-β and HGF levels were measured and correlated with disease activity. Results and Conclusion. Serum levels of TGF-β and HGF were significantly higher in IBD patients compared with the control group. In the UC group, the levels of HGF and TGF-β were significantly higher than in the CD group. Levels of TGF-β and HGF correlate with the activity of IBD.

Objective: This study aimed to estimate the risk of cardiovascular disease (CVD) among patients with and without diabetes mellitus (DM) using the Framingham risk score (FRS) and to investigate the effect of DM control on CVD risk. Methodology: A total of 2432 participants who had their glycosylated hemoglobin (HbA1c) measured within the last three months were included in this study. The study cohort was divided into three categories: non-diabetic, participants with controlled DM (HbA1c< 7%), and uncontrolled DM (HbA1c≥ 7%). The World Health Organization’s stepwise approach to chronic disease risk factor Surveillance-Instrument v2.1 was used in this study to collect the anthropometric and biochemical measurements. The Framingham Coronary Heart Risk Score (FRS) was used to calculate the 10-year cardiovascular risk (CVR). The groups were compared concerning the prevalence of metabolic, socioeconomic, and cardiac risks. Results: Out of 2432 participants, 149 had controlled DM (6.1%), 286 had uncontrolled DM (11.8%), and 1997 participants were normoglycemic (82.1%). Compared to healthy participants, diabetic participants showed more high-risk characteristics across all CVR parameters. Uncontrolled diabetic patients had a graver laboratory and clinical profiles compared to the controlled DM group. As measured by FRS, nearly half of patients with controlled DM (49.9%) and two-thirds of patients with uncontrolled DM (63.3%) were classified as intermediate and high-risk compared to 4.6% of the healthy participants. Compared to healthy participants, patients with controlled DM showed a threefold increased CVR (OR = 3.02, 95% C.I. = 1.41– 7.24) while this risk catapulted to 13 times among those with uncontrolled DM (OR = 13.57, 95% C.I. = 6.99– 26.36). Conclusion: Participants with DM are at moderate to high CVR. Individuals with uncontrolled DM showed higher CVR profiles as measured by FRS and have a higher prevalence of obesity, unhealthy diet, and physical inactivity.