Objective: To investigate the values of serum calculated free testosterone (cFT), testosterone secretion index (TSI), and free testosterone index (FTI) in the diagnosis of ED with androgen deficiency by observing their changes in the patient.
Methods: We conducted this study among 185 men complaining of ED and 35 20-40 years old healthy males presenting at the clinic for premarital medical checkup. We asked them about their medical history, to fill in the International Index of Erectile Function (IIEF-5) Questionnaire, and to complete the nocturnal penile tumescence (NPT) test. According to the data obtained, 150 of the complainants were diagnosed as ED patients and 25 of the healthy examinees were included in the control group. We determined the levels of total serum testosterone (TT), luteinizing hormone (LH), sex hormone-binding globulin (SHBG), serum albumin (ALB), cFT, bio-available testosterone (bio-T), TSI, and FTI in the two groups of subjects. Using cFT ≤0.3 nmol/L, TSI ≤2.8, and FTI ≤0.4 as the critical values and TT ≤11.5 nmol/L as the gold standard for androgen deficiency, we calculated cFT-, TSI-, and FTI-related rates of missed diagnosis, misdiagnosis, and diagnostic coincidence.
Results: With TT ≤11.5 nmol/L as the criterion, the cFT-, TSI-, and FTI-related rates of coincidence in the diagnosis of androgen deficiency in the ED patients were 90.8%, 85.8%, and 80.8%, those of missed diagnosis were 4.0%, 33.3%, and 44.0%, and those of misdiagnosis were 10.5%, 19.4%, and 12.6%, with the Kappa of values 0.755, 0.564, and 0.427, respectively (P <0.05). The levels of serum TT, cFT, Bio-T, TSI, and FTI were decreased with increased age of the 20-40 years old ED patients, with statistically significant differences among different age groups except the serum TT level. However, no statistically significant differences were found in the levels of TT, cFT, Bio-T, TSI, and FTI among the patients with different IIEF-5 scores.
Conclusions: The level of cFT has a higher value than those of TT, TSI, and TSI in the diagnosis of ED with androgen deficiency in 20-40 years old men.
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J Toxicol
December 2024
Department of Agriculture Botany (Genetics), Faculty of Agriculture (Girls Branch), Al-Azhar University, Cairo, Egypt.
The environmental xenobiotic aluminum chloride (AlCl) destroys reproduction via free radicals. The present study aimed at evaluating the impact of purple and white eggplant on rat fertility when exposed to AlCl. A total of 36 male albino rats were divided into six groups: a negative control, the second given AlCl (17 mg/kg b.
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Andrology Unit, Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy.
Study Design: Retrospective study.
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Front Neurol
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Brain Rehabilitation Research Center, Malcom Randall Department of Veterans Affairs Medical Center, North Florida/South Georgia Veterans Health System, Gainesville, FL, United States.
SAGE Open Med
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Department of Endocrinology, Diabetology, and Internal Medicine, Tahar Sfar University Hospital, Mahdia, Tunisia.
Introduction: Polycystic ovary syndrome is a common chronic condition characterized by insulin resistance and hyperandrogenism, leading to significant health risks and impaired quality of life. Sodium-glucose transporter type 2 inhibitors have shown promise in improving the metabolic profile of women with polycystic ovary syndrome. However, their impact on hormonal parameters and cycle disorders remains uncertain.
View Article and Find Full Text PDFJ Obes Metab Syndr
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Department of Obstetrics and Gynecology, Seoul National University Hospital Healthcare System Gangnam Center, Seoul, Korea.
The core pathophysiology of polycystic ovary syndrome involves an overproduction of androgens primarily originating from ovarian thecal cells. Two major external triggers promote androgen overproduction in the ovaries: the increased secretion of luteinizing hormone, a consequence of aberrant hypothalamic gonadotropin-releasing hormone secretion dynamics, and compensatory hyperinsulinemia resulting from insulin resistance. Obesity interacts with polycystic ovary syndrome in multiple ways, but a major role of obesity in its pathophysiology is the exacerbation of insulin resistance.
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