madman
Super Moderator
Abstract
Recent studies identified the presence of a male polycystic ovarian syndrome (PCOS), which mainly affects men whose female relatives are afflicted with PCOS, caused by genes responsible for the susceptibility of this syndrome in women. Similar hormonal, metabolic, and clinical alterations occurring in PCOS women have also been reported in their male relatives, suggesting an association between the male and female forms of the syndrome. Although the remarkable clinical manifestation of the male equivalent PCOS is diagnosed by the early-onset androgenetic alopecia, characterized by hair recession, pronounced hypertrichosis, insulin resistance, biochemical and hormonal abnormalities, the hormonal/metabolic profile is still controversial. Men affected by early-onset androgenetic alopecia (AGA) are at risk of developing hyperinsulinemia, insulin resistance, dyslipidemia, and cardiovascular diseases. However, there is no consensus on the association of male equivalent PCOS with hypertension and obesity. Moreover, reduced levels of sex hormone-binding globulin have been detected in these male patients, accompanied by increased free androgens. Conversely, literature reported lower concentrations of testosterone in male equivalent PCOS when compared with the normal range, indicating a crucial role for the conversion of cortical androgens. Finally, further studies are warranted to investigate a possible link among AGA, metabolic/hormonal alterations, and acne. Our study assessed the hormonal, metabolic, and clinical aspects of male equivalent PCOS syndrome reported in the literature to evaluate similar and divergent elements involved in the female version of the syndrome.
Conclusion
Male equivalent PCOS may be defined as a disorder that occurs in male members of a family with a PCOS history, characterized by the clinical signs of androgenism, complete hair loss, and the same hormonal pattern seen in PCOS, except for testosterone levels that seem to be in the subnormal range. The metabolic pattern should be represented by hyperinsulinemia and insulin resistance with a side role for overweight and obesity in the case of occurrence. However, these patients have a high risk of developing CVDs, metabolic syndrome, and carotid atherosclerotic plaques. According to this, the early diagnosis of the disease would be necessary to permit the patients to adopt a healthy lifestyle preventing the risk of metabolic and cardiovascular events.
Recent studies identified the presence of a male polycystic ovarian syndrome (PCOS), which mainly affects men whose female relatives are afflicted with PCOS, caused by genes responsible for the susceptibility of this syndrome in women. Similar hormonal, metabolic, and clinical alterations occurring in PCOS women have also been reported in their male relatives, suggesting an association between the male and female forms of the syndrome. Although the remarkable clinical manifestation of the male equivalent PCOS is diagnosed by the early-onset androgenetic alopecia, characterized by hair recession, pronounced hypertrichosis, insulin resistance, biochemical and hormonal abnormalities, the hormonal/metabolic profile is still controversial. Men affected by early-onset androgenetic alopecia (AGA) are at risk of developing hyperinsulinemia, insulin resistance, dyslipidemia, and cardiovascular diseases. However, there is no consensus on the association of male equivalent PCOS with hypertension and obesity. Moreover, reduced levels of sex hormone-binding globulin have been detected in these male patients, accompanied by increased free androgens. Conversely, literature reported lower concentrations of testosterone in male equivalent PCOS when compared with the normal range, indicating a crucial role for the conversion of cortical androgens. Finally, further studies are warranted to investigate a possible link among AGA, metabolic/hormonal alterations, and acne. Our study assessed the hormonal, metabolic, and clinical aspects of male equivalent PCOS syndrome reported in the literature to evaluate similar and divergent elements involved in the female version of the syndrome.
Conclusion
Male equivalent PCOS may be defined as a disorder that occurs in male members of a family with a PCOS history, characterized by the clinical signs of androgenism, complete hair loss, and the same hormonal pattern seen in PCOS, except for testosterone levels that seem to be in the subnormal range. The metabolic pattern should be represented by hyperinsulinemia and insulin resistance with a side role for overweight and obesity in the case of occurrence. However, these patients have a high risk of developing CVDs, metabolic syndrome, and carotid atherosclerotic plaques. According to this, the early diagnosis of the disease would be necessary to permit the patients to adopt a healthy lifestyle preventing the risk of metabolic and cardiovascular events.
