In addition to their lack of affinity for the androgen receptor, norgestimate and norelgestromin have virtually no affinity for SHBG, and therefore do not displace testosterone from this carrier protein (although levonorgestrel does still bind with high affinity to SHBG and hence could increase free testosterone levels via occupation of SHBG). In accordance, clinical trials of norgestimate have observed minimal androgenic side effects in women treated with the medication. As an example, clinical studies have found that norgestimate does not appreciably inhibit the increase in SHBG levels produced by ethinylestradiol. This is of interest because estrogens increase and androgens decrease liver production of SHBG and by extension circulating levels of SHBG.The relative binding affinity of norgestimate and its metabolite norelgestromin for the rat prostatic androgen receptor (AR) are 0.3% and 1.3% of those of dihydrotestosterone (DHT), respectively, whereas the respective values for levonorgestrel and gestodene are 22% and 15%. Based on these findings, the ratios of AR to PR binding are 219 for norgestimate and 48 for norelgestromin, whereas the ratios for progesterone, levonorgestrel, and gestodene are 93, 11, and 28, respectively. As such, norgestimate and norelgestromin would appear to have much lower androgenic potency than other 19-nortestosterone progestins. However, levonorgestrel is an important metabolite of both norgestimate and norelgestromin, and it may serve to increase their androgenic potency to some degree.When norgestimate is combined with ethinylestradiol, which is potently antiandrogenic, there are only antiandrogenic effects overall and the combination is suitable for treatment of hyperandrogenism.
Its symptoms include superficial peeling of small areas of the skin that involve the dorsal and palmar surfaces of the hands and feet, superficial scaling of forearms and legs, and acanthosis. Peeling skin syndrome 6
Peeling skin syndrome 6 is caused by a genetic defect in the filaggrin (filaggrin family member 2) gene. The function for this gene is vital for normal cellular-cell adhesion within the cornified cell layers. It is also critical for the integrity and mechanical strength of the stratum corneum of the epidermis. Its symptom include dryness of the skin, peeling of the skin. erythema at lesion sites, bullae, and hyper-pigmentation. Symptoms and signs
Abnormal blistering of the skin
Abnormality of hair texture
Dry skin
Aminoaciduria
Hyperhidrosis
Ichthyosis

Treatment
There is no remedy for peeling skin syndrome. Treatment focuses on avoiding skin damage and treating symptoms as they occur. Ointments are also used to minimize skin peeling and when the blister grows, sterile needles may be activated. The condition can be exacerbated by hot temperatures, humidity, and friction. Individuals should be informed to avoid exacerbating triggers such as trauma, humidity, heat, perspiration, and water. Frequency
Only several dozen cases have been reported in the literature, making it rare, but because its symptoms are mild and similar to other disorders it could very well be under-diagnosed. See also
Idiopathic calcified nodules of the scrotum
Keratolysis exfoliativa
List of cutaneous conditions
Corneodesmosin
TGM5
Carbohydrate sulfotransferase
Cystatin A
Serpin
Filaggrin

References


== External links ==