Correlation between insulin resistance and treatment-resistant acne

Physiologically during puberty and adolescence, when juvenile acne usually appears, the response to a glucose load is increased if compared to the one observed in adult and at pre-pubertal age, while insulin sensitivity is reduced. Insulin is a hormone that acts at different levels along the axis which controls the sex hormones. It increases the release of LH and FSH by pituitary gland, stimulates the synthesis of androgens in the gonads and stimulates the synthesis of androgenic precursors in adrenal glands. Finally, it acts in the liver by inhibiting the synthesis of Sex Hormone Binding Globulin (SHBG). Insulin is also able to act directly on the production of sebum and amplify the effects of Iinsulin Growth Factor-1 in the skin, inhibiting the synthesis of its binding protein (IGF Binding Protein-1). In female subjects with acne and Polycystic Ovary Syndrome (PCOS) insulin resistance is a well known pathogenetic factor, while the relationship between acne and insulin resistance has been poorly investigated in males so far. The purpose of this study is to investigate the correlation between insulin resistance and acne in young males who do not respond to common therapies. Clinical and biochemical parameters of glucose, lipid metabolism, androgens and IGF-1 were evaluated. Insulin resistance was estimated by Homeostasis Model assessment (HOMA-IR) and Oral Glucose Tolerance Test was also performed. We found that subjects with acne had higher Sistolic and Diastolic Blood Pressure, Waist/Hip Ratio, Waist Circumference, 120' OGTT serum insulin and serum IGF-1 and lower HDL-cholesterol than subjects of comparable age and gender without acne. The results thus obtained confirmed what other authors have recently reported about a metabolic imbalance in young males with acne. Furthermore, these results support the hypothesis that insulin resistance might play an important role in the pathogenesis of treatment-resistant acne in males.

Female melanoma: the role of ovarian stimulation and antioestrogens cancer therapy A retrospective study with immunohistochemical oestrogen receptors alpha and beta analysis.

Cutaneous melanoma (CM) represents the third most common cancer in Italian women under 49 years old. In the last decades, many molecular studies confirmed that sex hormones have a part in melanogenesis and melanoma genesis. However, many controversies are present regarding the role of exogenous oestrogens intake and endogenous hormonal status in female melanoma. Our study's primary objective is to investigate the features of melanoma in women of fertile age and women in postmenopausal age. The secondary aim is to evaluate the expression of ERα and ERβ by immunohistochemical analysis in women who underwent ovarian stimulation for medically assisted procreation and in women in cancer therapy for breast cancer (BC) comparing to two control groups. The tertiary objective is to correlate ERα and ERβ with the Breslow thickness and other relevant histopathological, clinical and dermoscopic characteristics Results A total of 998 women were included in the study. Women in fertile age are significantly more prone to have CM on the trunk. Conversely, postmenopausal females are more likely to develop CM on acral locations. Breslow thickness and ulceration were statistically significant among postmenopausal women (P-value <0,001). In the group for women with a history of breast cancer (BC), we observed a significantly higher CM percentage with “non-brisk” TILs. Upon immunohistochemical analysis, most cases with inhibitor aromatase therapy displayed a strong cytoplasmatic ERα positivity. Upon the Pearson correlation analysis, no association was shown between nuclear ERβ and Breslow thickness. The meaning of cytoplasmatic ERα in melanoma is still debated. It could suggest a potentially significant role of oestrogen non-genomic pathway in these patients, or it can be a mechanism of ERs modulation in response to aromatase inhibitor therapy. Our work tried to enlighten some of the existing shadows on the role of ERs and hormonal factors in CM.