Wiedza Medyczna

Antipsychotic Drug-Induced Insulin Resistance: A Narrative Literature Review

2025-09-29T08:42:09+00:00

Insulin resistance is a metabolic disorder and a key factor in the pathogenesis of conditions such as type 2 diabetes, metabolic dysfunction-associated steatotic liver disease (MASLD), and atherosclerosis. Risk factors for insulin resistance include genetic and environmental influences, such as overweight/obesity, low physical activity, and the use of certain medications, including glucocorticosteroids or antipsychotics.

Antipsychotics (neuroleptics) are widely used in the treatment of various mental disorders, primarily schizophrenia, and such therapy is often lifelong. Due to the mechanism of action via receptors, including serotonergic, muscarinic, and histaminergic, atypical (second-generation) antipsychotics cause metabolic disorders of varying severity. Clozapine and olanzapine have the worst metabolic profiles and aripiprazole and lurasidone are associated with the mildest profiles. Regardless of the potential for developing metabolic complications from specific antipsychotics, baseline predictors of susceptibility are sought in patients. To date, studies have identified risk factors such as higher body weight, male gender, and non-white ethnicity. In addition, patients with schizophrenia are at greater risk for insulin resistance, as shown in studies involving individuals with a first episode of psychosis. This supports the hypothesis that schizophrenia and diabetes may share a common pathogenesis. Despite clear evidence of an increased risk for insulin resistance and, consequently, metabolic syndrome and high cardiovascular risk, insufficient attention is paid to early diagnosis, prevention, and treatment of carbohydrate and lipid metabolism disorders in patients taking neuroleptics. Improved management in this area could benefit not only physical health but also adherence to medical recommendations and the overall effectiveness of psychiatric treatment.

Factors associated with quality of life in patients with euthyroid lymphocytic thyroiditis-a review of literature

2025-09-29T08:54:44+00:00

Hashimoto's thyroiditis (HT) represents the most common organ-specific autoimmune disorder, characterized by chronic lymphocytic infiltration of the thyroid parenchyma and the presence of circulating antithyroid autoantibodies, predominantly thyroid peroxidase antibodies (TPO Ab) and thyroglobulin antibodies (Tg Ab). The pathogenesis of HT involves a complex interplay between genetic predisposition and environmental factors, culminating in the loss of immune tolerance and progressive destruction of thyroid tissue. Although HT remains the principal etiology of hypothyroidism in developed countries, accumulating evidence indicates that patients may exhibit systemic manifestations and reduced health-related quality of life (HRQoL) even in the euthyroid state. These clinical features are mediated by ongoing autoimmune activity, chronic inflammation, and the pathogenic effects of autoantibodies, contributing to structural and functional alterations within the thyroid gland. Furthermore, HT is frequently associated with a spectrum of comorbidities, including other autoimmune disorders, metabolic syndrome, cardiovascular diseases, psychiatric conditions, and neoplasms, which collectively exacerbate morbidity. Optimal management of HT necessitates a multidisciplinary approach that extends beyond thyroid hormone replacement to include comprehensive evaluation of psychological status and screening for concomitant diseases. This review delineates the multifactorial determinants of HRQoL impairment in HT and underscores the imperative for integrative, patient-centered therapeutic strategies. Continued research into the immunopathogenesis, novel biomarkers, and targeted interventions is essential to improve clinical outcomes and quality of life in affected individuals.

Quality of Life in Adults with Growth Hormone Deficiency: A Comprehensive Review of Clinical Evidence and Psychological Impacts

2025-09-29T08:59:07+00:00

Adult growth hormone deficiency (AGHD) negatively affects quality of life (QoL) through physical, metabolic, and psychological impairments. Growth hormone (GH) replacement therapy may improve QoL, but individual responses vary. This review summarizes current evidence on QoL in untreated and treated AGHD, explores factors influencing outcomes, and highlights gaps in research and clinical practice. Growth hormone therapy improves QoL in most patients, especially those with low baseline well-being. Women and younger patients report greater benefits. Psychological and behavioral factors, including coping strategies and beliefs about treatment, significantly influence outcomes. Improvement in QoL should be a central outcome in AGHD management. Future research must address long-term outcomes, adherence, and patient-centered metrics, especially in underrepresented subgroups such as traumatic brain injury (TBI) survivors and transitioning adolescents.

Why does body weight often increase again after initial loss? The role of metabolic adaptation

2025-10-07T08:24:26+00:00

Obesity, often referred to as the "tsunami of the 21st century", is a chronic, incurable disease prone to relapses. The crucial intervention aimed at reducing body weight for health benefits is lifestyle modification, but unfortunately, in most cases after the initial period of weight loss, a recurrence of overweight or obesity is observed. A similar process occurs in patients after bariatric surgery. It should be understood that the reason for this phenomenon does not necessarily must be associated with the lack of the patient adherence, but is a consequence of the activation of a strong objective mechanism - metabolic adaptation, i.e. changes in energy homeostasis to counteract lossing of energy. The article briefly describes the most important mechanisms of metabolic adaptation and presents the ways to counteract it.

Bone disease in primary hyperparathyroidism

2025-10-07T09:47:55+00:00

Primary hyperparathyroidism is a disorder of calcium-phosphate balance and bone metabolism, characterized by increased bone turnover, reduced bone mineral density—especially in cortical bone—and an elevated risk of fractures. The introduction of automated methods for measuring serum calcium levels, along with the widespread availability of reliable parathyroid hormone (PTH) assays, has changed the clinical presentation of PHPT. The classic form of the disease (osteitis fibrosa cystica), which used to require differentiation from bone malignancies, is now seen much less frequently. Effective surgical treatment of primary hyperparathyroidism leads to skeletal recovery ("self-repair") and an increase in bone mineral density (BMD). With the growing number of patients presenting with subclinical primary hyperparathyroidism, there is an increasing need to explore alternative—pharmacological—treatment options. Anti-resorptive drugs, such as bisphosphonates and denosumab, have attracted particular interest in the context of managing bone loss in patients with PHPT.
This article aims to present the current state of knowledge regarding bone loss in primary hyperparathyroidism.