Polycystic ovary syndrome (PCOS) is one of the most common endocrinopathies in reproductive age women; it is a complex health issue with numerous comorbidities. Attention has recently been drawn to amino acids as they are molecules essential to maintain homeostasis. The aim of the study was to investigate the branch chain amino acid (BCAA) profile in women with PCOS. A total of 326 women, 208 diagnosed with PCOS and 118 healthy controls, participated in the study; all the patients were between 18 and 40 years old. Anthropometrical, biochemical and hormonal parameters were assessed. Gas-liquid chromatography combined with tandem mass spectrometry was used to investigate BCAA levels. Statistical analysis showed significantly higher plasma levels of BCAAs (540.59 ± 97.23 nmol/mL vs. 501.09 ± 85.33 nmol/mL; p < 0.001) in women with PCOS. Significant correlations (p < 0.05) were found between BCAA and BMI, HOMA-IR, waist circumference and total testosterone levels. In the analysis of individuals with abdominal obesity, there were significant differences between PCOS and controls in BCAA (558.13 ± 100.51 vs. 514.22 ± 79.76 nmol/mL) and the concentrations of all the analyzed amino acids were higher in the PCOS patients. Hyperandrogenemia in PCOS patients was associated with significantly higher leucine, isoleucine and total BCAA levels. The increase of BCAA levels among PCOS patients in comparison to healthy controls might be an early sign of metabolic alteration and a predictive factor for other disturbances.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects reproductive-age women and predisposes them to the development of metabolic disturbances. Recent research has shown that several metabolic factors may play a role in PCOS pathogenesis, and it has been suggested that an alteration in the amino acid profile might be a predictive sign of metabolic disorders. Metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO) are concepts that have attracted scientific attention; however, a universal definition has not been established yet for these terms. Already existing definitions of MHO involve the coexistence of obesity with the absence or minimal presence of other metabolic syndrome parameters. A group of 326 women, 209 diagnosed with PCOS and 117 healthy individuals, participated in this study. Multiple parameters were assessed, including anthropometrical, biochemical, and hormonal ones, and gas–liquid chromatography, combined with tandem mass spectrometry, was used to investigate the amino acid profile. Statistical analysis revealed noticeably higher levels of all aromatic amino acids in PCOS women compared to the control group: phenylalanine 47.37 ± 7.0 vs. 45.4 ± 6.09 nmol/mL (p = 0.01), tyrosine 61.69 ± 9.56 vs. 58.08 ± 8.89 nmol/mL (p < 0.01), and tryptophan 53.66 ± 11.42 vs. 49.81 ± 11.18 nmol/mL (p < 0.01); however, there was no significant difference in the “tryptophan ratio” between the PCOS and control group (p = 0.88). A comparison of MHO and MUO PCOS women revealed that LAP, leucine, and isoleucine concentrations were significantly higher among the MUO subgroup: respectively, 101.98 ± 34.74 vs. 55.80 ± 24.33 (p < 0.001); 153.26 ± 22.26 vs. 137.25 ± 25.76 nmol/mL (p = 0.04); and 92.92 ± 16.09 vs. 82.60 ± 18.70 nmol/mL (p = 0.02). No significant differences in BMI, fasting glucose, and HOMA-IR between MHO and MUO were found: respectively, 35.0 ± 4.8 vs. 36.1 ± 4.6 kg/m² (p = 0.59); 88.0 ± 6.0 vs. 87.73 ± 6.28 mg/dL (p = 0.67); and 3.36 ± 1.70 vs. 4.17 ± 1.77 (p = 0.1). The identification of altered amino acid profiles in PCOS holds potential clinical implications. Amino acids may serve as biomarkers for diagnosing and monitoring the metabolic status of individuals with PCOS. The alteration of BCAAs and AAAs may be involved in PCOS pathogenesis, but the underlying mechanism should be further investigated.

Alzheimer disease, the leading cause of dementia, and polycystic ovary syndrome, one of the most prevalent female endocrine disorders, appear to be unrelated conditions. However, studies show that both disease entities have common risk factors, and the amount of certain protein marker of neurodegeneration is increased in PCOS. Reports on the pathomechanism of both diseases point to the possibility of common denominators linking them. Dysregulation of the kynurenine pathway, insulin resistance, and impairment of the hypothalamic-pituitary-gonadal axis, which are correlated with amyloid-beta aggregation are these common areas. This article discusses the relationship between Alzheimer disease and polycystic ovary syndrome, with a particular focus on the role of disorders of tryptophan metabolism in both conditions. Based on a review of the available literature, we concluded that systemic changes occurring in PCOS influence the increased risk of neurodegeneration.

Introduction: Anaplastic thyroid carcinoma (ATC) is one of the most aggressive human malignancies and constitutes approximately 1.6–5% of the malignant neoplasms of the thyroid gland. ATC usually manifests itself with the local symptoms due to a rapidly enlarging thyroid mass, and as other thyroid cancers, has only seldom been reported to cause thyrotoxicosis. Up to now only 9 cases of ATC with concomitant thyrotoxicosis have been described. Case report: We report a rare case of a 66-year-old woman, who had had the preexisting large, euthyroid multinodular goiter for almost 50 years. She was consulted by a doctor because of a 4-week history of thyrotoxicosis, symptoms of the congestive heart failure and a rapid increase in the size of the goiter. Thyroid hormone levels were consistent with a hyperthyroid state. The fine-needle aspiration biopsy confirmed a diagnosis of the anaplastic thyroid carcinoma, the small cells variant. The 99m Tc-pertechnetate scintigraphy visualized non-homogenous tracer distribution with hot nodules. She was given a doxorubicin (20 mg/week) and required the continuous antithyroid treatment. The patient died a one year after the first symptoms of the disease occurred. Discussion: The association between ATC and a thyrotoxic state is very rare. In most cases, thyrotoxicosis concomitant with ATC was thought to be a result of the destruction of the thyroid follicles by the rapid infiltration with malignant cells, resulting in the leakage of preformed hormones to the circulation. In that case the most probable cause of thyrotoxicosis was the multinodular goiter coexisting with ATC. A simultaneous onset of tumor growth, thyrotoxicosis and a relatively long survival time of our patient is worth to notice and discuss. Introduction: Anaplastic thyroid carcinoma (ATC) is one of the most aggressive human malignancies and constitutes approximately 1.6–5% of the malignant neoplasms of the thyroid gland. ATC usually manifests itself with the local symptoms due to a rapidly enlarging thyroid mass, and as other thyroid cancers, has only seldom been reported to cause thyrotoxicosis. Up to now only 9 cases of ATC with concomitant thyrotoxicosis have been described. Case report: We report a rare case of a 66-year-old woman, who had had the preexisting large, euthyroid multinodular goiter for almost 50 years. She was consulted by a doctor because of a 4-week history of thyrotoxicosis, symptoms of the congestive heart failure and a rapid increase in the size of the goiter. Thyroid hormone levels were consistent with a hyperthyroid state. The fine-needle aspiration biopsy confirmed a diagnosis of the anaplastic thyroid carcinoma, the small cells variant. The 99m Tc-pertechnetate scintigraphy visualized non-homogenous tracer distribution with hot nodules. She was given a doxorubicin (20 mg/week) and required the continuous antithyroid treatment. The patient died a one year after the first symptoms of the disease occurred. Discussion: The association between ATC and a thyrotoxic state is very rare. In most cases, thyrotoxicosis concomitant with ATC was thought to be a result of the destruction of the thyroid follicles by the rapid infiltration with malignant cells, resulting in the leakage of preformed hormones to the circulation. In that case the most probable cause of thyrotoxicosis was the multinodular goiter coexisting with ATC. A simultaneous onset of tumor growth, thyrotoxicosis and a relatively long survival time of our patient is worth to notice and discuss.