ACTA ENDOCRINOLOGICA (BUC)

Background. Primary hyperparathyroidism and vitamin D deficiency are both associated with increased prevalence\r\nof anemia. Relationship of hemoglobin and parathyroid hormone in normal ranges were not investigated appropriately.\r\nMethods. We analysed laboratory data of 476 patients without primary hyperparathyroidism. The patients had concurrent measurements of calcium, phosphorus, alkaline phosphatase, parathyroid hormone, 25-OH vitamin D and hemoglobin.\r\nResults. Parathyroid hormone was negatively correlated with hemoglobin (p=0.01), the correlation persisted after\r\ncorrection for vitamin D levels (p=0.045), and in sub-group of normal (>20 ng/mL) 25-OH vitamin D levels (p=0.005). Parathyroid hormone was also correlated negatively with\r\nferritin (p=0.02), correlation persisted after being adjusted to vitamin D (p=0.021). In anemic patients, these with low ferritin (<12 ng/mL) had higher PTH levels than these with higher ferritin despite having similar calcium\r\nand vitamin D levels (p=0.014).\r\nConclusion. Interaction of parathyroid hormone and erythropoiesis seems to be present in normal ranges where\r\nerythropoietin may mediate key roles regulating both.

COVID-19 is a viral disease that is recognized now as a pandemic by the World Health Organization. It is known that some viral infections may trigger autoimmune diseases. It has been revealed that COVID-19 may also lead to the pathogenesis of some autoimmune diseases, including Type 1 DM (T1DM) and autoimmune thyroid diseases. Here, we aimed to present a young female patient with COVID-19, who we followed up in our clinic, who presented with diabetic ketoacidosis (DKA), and developed Hashimoto’s disease during the treatment process. In order to emphasize that COVID-19 may trigger the emergence of T1DM, that it may mask nonspecific DKA symptoms like nausea and vomiting, that it may cause delay in diagnosis of DKA, and also to emphasize the importance of evaluating other autoimmune diseases accompanying COVID-19, we found it appropriate to present this case.

Background. Iodine deficiency and/or thyroid autoimmunity are the most common causes of hypothyroidism development among pregnant women. In this study, we aimed to investigate the effect of iodine consumption and thyroid autoimmunity on TSH levels and abortus. The study sample consisted of 104 patients, 79 in abortus and 25 in control groups. TSH, free T4, free T3, anti-TPO, anti-Tg, spot urinary iodine concentrations, and thyroid volumes of the cases were measured by ultrasonography. The spot urine concentration was below 100 μg/L in 93% of the cases included in the study. The TSH levels of the abortus group cases were significantly higher than those of the controls (p=0.025). The percentage of subclinical hypothyroid cases were significantly higher among the cases evaluated due to abortus compared to the control group (p<0.001). Abortus and control groups did not differ statistically with respect to the presence of autoimmune thyroid diseases (p=0.424). Spot urine iodine concentrations of abortus cases with subclinical hypothyroid were significantly lower than those with TSH levels below the defined range (p=0.001). Spot urine iodine concentrations of the cases with subclinical abortus with negative thyroid autoantibodies were also significantly lower than those with TSH levels below the defined range (p=0.017). TSH levels above 1 μIU/mL for the first trimester and 2 μIU/mL for the second trimester may be indicators of iodine nutrition in pregnancy losses.