Background and Objective: Thyroid hormones play an important role in intermediate metabolism, and abnormal glucose tolerance is often observed in patients with hyperthyroidism. Several pathogenic mechanisms have been proposed as contributors. However, there is no conclusive evidence in the existing literature regarding the predominant underlying pathophysiology. Our objective was to determine the changes in insulin resistance parameters and beta-cell function in patients with Graves’ disease following restoration of a euthyroid state. Methodology: This was an observational study with a before-after study design. Forty-five treatment-naïve adults with Graves’ diseases were included and 36 completed the study. An oral glucose tolerance test was performed at baseline and after 3 months of achieving a stable euthyroid state to assess glucose tolerance, insulin sensitivity, and beta-cell function. All patients were treated with antithyroid medication. The outcome measures studied were the Homeostasis Model Assessment-2 Insulin Resistance (HOMA2-IR), Matsuda index, and Insulin Secretion-Sensitivity Index (ISSI)-2. Results: Two-thirds of the patients had abnormal glucose tolerance at baseline. Among those with abnormal glucose tolerance at baseline, 34.7% had persistent abnormality during follow-up. During follow-up, no significant change was noted in the indices of insulin resistance. Patients with abnormal glucose tolerance had a significantly lower ISSI-2 index at baseline and it improved after achieving a euthyroid state. Conclusions: Abnormal glucose tolerance is a significant metabolic consequence in patients with Graves’ disease. Decreased beta-cell function was observed among those with abnormal glucose tolerance and it improved during follow-up. In a proportion of patients, abnormal glucose tolerance persisted after 3 months, emphasizing the need for continued follow-up.
Background: Diabetes-related distress (DRD) is the negative emotional and psychological reaction to living with diabetes mellitus (DM). DRD has been reported to affect glycemic control and self-management practices adversely. Limited research is available on the effectiveness of psychological interventions for DRD. We aimed to study the effectiveness of a brief psychological intervention for patients with DRD. Methods: The findings of a targeted brief psychological intervention conducted for patients with DRD, as a part of psycho-endocrinology liaison services in a general hospital, are reported. Details regarding the assessment and intervention given were collected from the patients’ records. Forty-one patients with DRD diagnosed using Diabetes Distress Scale (DDS) were given the single session intervention consisting of brief diabetes education focusing on physical activity and medication adherence, relaxation techniques, and illness-specific problem-solving strategies. Effectiveness was assessed using change in Clinical Global Impression-Severity (CGI-S), patient-rated visual analog scale, brief physical activity questionnaire, and medication adherence at baseline and 2-month follow-up. Results: Analysis using Wilcoxon signed rank test found a significant change in the follow-up scores on all the assessment scales. Conclusions: The study highlights the benefits of brief intervention for reducing DRD, thus reducing the emotional burden of living with DM.
Osteoporosis is the most common metabolic bone disorder worldwide, especially in women. Postmenopausal status is the most common risk factor for osteoporosis in elderly women. The operational diagnosis of osteoporosis is usually made with the help of central dual energy X-ray absorptiometry scan. Clinically, osteoporosis is suspected in the background of one or more fractures of the hip, vertebra, proximal humerus or pelvis in the absence of local disease or high-energy trauma. Serious underlying illness can present with vertebral fractures and can be missed if other clues from clinical examination and investigations are overlooked. We report a case emphasising this aspect.
Context: Thyroid hormones play an important role in reproductive and sexual function in both sexes. Comprehensive information on the ill-effects of hypothyroidism on Leydig cell, Sertoli cell and germ cell function is lacking in the existing literature. Aims: To investigate the effect of primary hypothyroidism and its treatment on testicular function – Sertoli cell, Leydig cells, seminal fluid and spermatozoa. Methods and Material: This study was carried out as a descriptive study with a before-after study design in the endocrine department of a tertiary care hospital in South India. Forty treatment naïve, overtly primary hypothyroid, consenting male patients were included. Hormones assessed were free T3, free T4, thyroid stimulating hormone, follicle stimulating hormone [FSH], luteinizing hormone [LH], prolactin, testosterone, inhibin B[INHB], and insulin like factor 3[INSL3]. Semen analysis was done according to WHO 2010 guidelines in 37 subjects. Sexual function questionnaires like Androgen Deficiency in Aging Male [ADAM], and Arizona Sexual Experience Scale [ASEX] were used. After ensuring euthyroid state for consecutive 6 months with adequate dose of thyroxine sodium, reassessment of all parameters was done. Results: At baseline, 72.5 % had a low serum testosterone value (< 230 ng/dl), 67.56 % had low total sperm motility, 72.97% had low total progressive sperm motility, 80% had low ADAM score and 72.72% had low ASEX score. A raised prolactin level was seen in 32.5% of study subjects. Hypogonadotropic hypogonadism was more common than hypergonadotropic hypogonadism (89.66% vs. 10.34%). On restoration of euthyroidism, all these parameters improved. Serum INSL3 and LH increased significantly after thyroxine replacement, unlike FSH and INHB. Conclusions: Leydig cell function seemed more severely affected by hypothyroidism as compared to Sertoli cell function. Among sperm function parameters, motility was predominantly affected.
Metastatic pulmonary calcification (MPC) is an uncommon entity resulting from abnormalities in calcium-phosphorus homoeostasis. Most cases reported in the literature are among patients with chronic kidney disease receiving haemodialysis. Primary hyperparathyroidism is a relatively common condition affecting calcium homoeostasis, in which MPC can rarely occur. We report the case of one such patient who presented with severe hypercalcaemia and features of interstitial lung disease. Radiographic imaging was normal and the diagnosis was clinched by diffuse pulmonary uptake in 99mTechnetium-methylene diphosphate scan.
Phosphate is indispensable for human life and evolutionary changes over several millions of years have established tightly regulated mechanisms to ensure phosphate homeostasis. In this process, calcium and phosphate metabolism have come to be intricately linked together. Three hormones (PTH, FGF23 and Calcitriol) maintain the fine balance of calcium and phosphate metabolism through their actions at three sites (the gut, the kidneys and the skeleton). Disorders that disrupt this balance can have serious clinical consequences. Acute changes in serum phosphate levels can result in life threatening complications like respiratory failure and cardiac arrythmias. Chronic hypophosphataemia predominantly affects the musculoskeletal system and presents as impaired linear growth, rickets, osteomalacia and dental problems. Hyperphosphataemia is very common in the setting of chronic kidney disease and can be difficult to manage. A thorough understanding of calcium and phosphate homeostasis is essential to diagnose and treat conditions associated with hypo and hyperphosphataemia. In this review, we will discuss the calcium and phosphate metabolism, aetiologies and management of hypo and hyperphosphataemia.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.