Normocalcemic primary hyperparathyroidism is an early stage of primary hyperparathyroidism according to fibroblast growth factor 23 level.

Introduction: Normocalcemic primary hyperparathyroidism is a variant of primary hyperparathyroidism with consistently normal albumin-adjusted or free-ionized calcium levels. It may be an early stage of classic primary hyperparathyroidism or could represent primary kidney or bone disorder characterized by permanent elevation of PTH level. Aim of the study: The study aims to compare the FGF-23 levels in patients with PHPT, NPHPT, and normal calcium and PTH levels. Methods: Our study included patients who were referred to the endocrinology clinic with a presumptive diagnosis of primary hyperparathyroidism, an isolated increased level of PTH, or reduced bone densitometry. For each patient, we performed blood analysis of FGF-23, calcium, phosphate, vitamin D [25(OH)D3], estimated glomerular filtration rate (eGFR), bone turnover markers, and urine analysis for calcium/creatinine ratio. Results: Our study included 105 patients. Thirty patients with hypercalcemic hyperparathyroidism (HPHPT group), thirty patients with elevated PTH and normal calcium levels (NPHPT group), and 45 patients with normal calcium and PTH levels in the control group. FGF 23 level was 59.5± 23 pg/ml in the NPHPT group, 77 ± 33 pg/ml in the HPHPT group, and 49.7 ± 21.7 pg/ml in the control group (p=0.012). The phosphate level was lowest in the HPHPT group: 2.9 ± 0.6 vs 3.5 ± 0.44 in the NPHPT and 3.8 ± 0.5 in the control groups (p=0.001). No differences were found in eGFR, 25(OH)D3, C-terminal telopeptide type I collagen (CTX) and procollagen type 1 N-terminal propeptide (P1NP) levels, and bone densitometry scores between the three study groups. Conclusion: Our findings suggest that NPHPT is an early stage of PHPT. Further studies are needed to determine the role of FGF-23 and its usefulness in NPHPT.

Blood glucose control with different treatment regimens in type 2 diabetes patients hospitalized with COVID-19 infection: A retrospective study.

Coronavirus disease (COVID-19) is closely associated with hyperglycemia and a worse prognosis in patients with a previous diagnosis of type 2 diabetes mellitus. A few studies investigated the effects of diabetes treatment regimens in these patients during hospitalization. Here, we evaluate the impact of insulin and non-insulin therapy on glucose control in patients with type 2 diabetes admitted with COVID-19. This is a retrospective study including 359 COVID-19 patients with type 2 diabetes. Patients were divided into 2 groups according to diabetes treatment during hospitalization. The first group included patients treated with insulin only, and the second group patients treated with other antidiabetic agents with or without insulin. Average blood glucose was higher in the insulin-only treatment group (201 ± 66 mg/dL vs 180 ± 71 mg/dL, P = .004), even after excluding mechanically ventilated patients (192 ± 69 vs 169 ± 59 mg/dL, P = .003). In patients with moderate severity of COVID-19, average blood glucose was also significantly higher in the insulin-only treated group (197 ± 76 vs 168 ± 51 mg/dL, P = .001). Most patients (80%) in the combination treatment group received metformin. Moderately affected COVID-19 patients with type 2 diabetes could safely be treated with antihyperglycemic medications with or without insulin.

Glycemic control with a basal-bolus insulin protocol in hospitalized diabetic patients treated with glucocorticoids: a retrospective cohort study.

BACKGROUND: Improved glycemic control is the desired outcome after the discharge of patients with diabetes. We aimed to determine the efficacy of a basal-bolus insulin protocol in hospitalized patients with diabetes treated with glucocorticoids. METHODS: A retrospective cohort study compared the glycemic control of 150 hospitalized patients with diabetes and elevated inflammatory markers who were either treated with (n = 61) or without glucocorticoids (n = 89). All patients were treated with a basal-bolus regimen. RESULTS: Glycosylated hemoglobin A1C (HbA1C) levels, mode of diabetes treatment before admission, length of hospitalization and inflammatory markers were similar in both groups of patients (treated and untreated with glucocorticoid). There was a trend toward female predominance in the glucocorticoid-treated group. Mean daily glucose levels were higher in patients taking glucocorticoids when compared with untreated patients (12.5 ± 2.7 mmol/l vs. 10.9 ± 2.4 mmol/l, p < .0001), and significantly higher at 5:00 PM (13.1 ± 3.4 vs. 10.2 ± 3 mmol/l, p < .0001), and 8:00 P.M. (13.9 ± 4.1 mmol/l vs. 11 ± 3.1 mmol/l, p < 0.001) . No difference was detected between the two groups in prandial and basal insulin doses during hospitalization. Overall, 64% of patients in the glucocorticoid-treated group versus 39% in the untreated group had inadequate glycemic control during hospitalization (p = 0.003). CONCLUSION: A significantly higher percentage of patients with diabetes who were treated with glucocorticoids during hospitalization did not achieve glycemic control with a basal-bolus insulin protocol. These patients had significantly higher mean blood glucose levels due to elevated levels in the afternoon and evening. New basal-bolus protocols with appropriate adjustments of short acting insulin are needed to treat patients with diabetes on glucocorticoid therapy.

Minimally invasive follicular thyroid carcinoma developed in dyshormonogenetic multinodular goiter due to thyroid peroxidase gene mutation.

BACKGROUND: The occurrence of thyroid carcinoma in patients with congenital hypothyroidism (CH) caused by dyshormonogenesis is very rare, and has only been reported in one patient harboring mutations in the thyroid peroxidase (TPO) gene. PATIENT FINDINGS: We report on a 29-year follow-up of two consanguineous siblings with CH due to total iodide organification defect who also had sensorineural hearing loss. Molecular analysis revealed a novel biallelic mutation of the TPO gene in which phenylalanine substitutes serine at codon 292 (c.875C>T, p.S292F) in exon 8. Despite early initiation, adequate doses of levothyroxine treatment and consequently normal thyrotropin (TSH) levels, the proposita developed a huge multinodular goiter (MNG) and underwent total thyroidectomy due to tracheal compression. Pathological examination revealed a unifocal follicular thyroid carcinoma without vascular invasion in the left lobe of the thyroid gland. SUMMARY: Our finding of follicular thyroid carcinoma arising from dyshormonogenetic MNG in a patient without elevated serum TSH levels indicates that genetic and environmental factors other than TSH level might be involved in the development of thyroid carcinoma in dyshormonogenetic MNG. CONCLUSIONS: Despite the rare occurrence of thyroid carcinoma in dyshormonogenetic MNG, we recommend long-term follow-up and regular neck ultrasound imaging to prevent delayed diagnosis of thyroid carcinoma.

Minimal Invasive Follicular Thyroid Carcinoma Developed in Dyshormonogenetic Multinodular Goiter Due to Thyroid Peroxidase Gene Mutation.

Background: The occurrence of thyroid carcinoma in patients with congenital hypothyroidism (CH) caused by dyshormonogenesis is very rare, and has been reported in only one patient harboring mutations in the thyroid peroxidase (TPO) gene. Patient findings: We report on a 29-year follow-up of two consanguineous siblings with CH due to total iodide organification defect who also had sensorineural hearing loss. Molecular analysis revealed a novel biallelic mutation of the TPO gene in which phenylalanine substitutes serine at codon 292 (c.875C>T, p.S292F) in exon 8. Despite early initiation, adequate doses of L-thyroxine treatment and consequently normal TSH levels, the proposita developed a huge multinodular goiter (MNG) and underwent total thyroidectomy due to tracheal compression. Pathological examination revealed a unifocal follicular thyroid carcinoma without vascular invasion in the left lobe of the thyroid gland. Summary: Our finding of follicular thyroid carcinoma arising from dyshormonogenetic MNG in a patient without elevated serum TSH levels indicates that genetic and environmental factors other than TSH level might be involved in the development of thyroid carcinoma in dyshormonogenetic MNG. Conclusions: Despite the rare occurrence of thyroid carcinoma in dyshormonogenetic MNG, we recommend long-term follow-up and regular neck ultrasound imaging to prevent delayed diagnosis of thyroid carcinoma.

Biomarkers of hypercoagulability and inflammation in primary hyperparathyroidism.

BACKGROUND: Severe primary hyperparathyroidism (PHP) has been associated with increased cardiovascular morbidity. Hypertension, dyslipidemia and impaired glucose metabolism were demonstrated in severe PHP, with improvement after surgery in these variables. Such an association in mild PHP is not known. The study was conducted to determine biomarkers of hypercoagulability and inflammation for cardiovascular disease in patients with primary hyperparathyroidism. MATERIAL/METHODS: Patients (n=35) without CVD were evaluated. Patients were subdivided into two groups, severe (n=15) and mild (n=20) hyperparathyroidism, based on disease severity and whether they had indications for surgery. Results were compared with those obtained in 25, age and weight matched controls. Participants were examined in the hospital endocrine clinic and had measurement of fasting blood levels of calcium, phosphate, alkaline phosphatase, PTH, C-reactive protein, Serum IL-6, D-dimers, Fibrinogen, plasminogen activator inhibitor 1 [PAI-1], and white blood cells (WBC) count. RESULTS: PAI-1 was significantly higher in symptomatic patients (41.4 g/L +/-20) vs. controls (32.5 g/L +/-13.0); (p=0.009). Levels of fibrinogen, d-dimers, IL-6, CRP and leukocytes were similar in patients and controls. Across all subjects PAI-1 was significantly correlated with PTH levels (f=8.44;p=0.005). CONCLUSIONS: Patients with severe primary hyperparathyroidism have increased risk for cardiovascular disease, mainly due to the effect of PTH and also the duration and severity of disease. Elevated PAI-1 levels may imply that hypercoagulability may be involved in the pathogenesis of CVD in these patients.