pigmented naevus were irregularly shape macule, papules, and plaques of various colours.Multiple pigmented satellite lesions of size 4-5 cm were present over the body, head, face and extremities. Tufts of coarse hair were present over the satellite lesions, with finer hair covering the abdominal areas of pigmentation. Three nodular lesions were present in the perianal region. Areas of excoriation were noted on the flank areas. No other physical abnormalities were present. Neurological examination was unremarkable.MRI examination revealed extensive intracranial melanocytic infiltrate, confirming a diagnosis of CGMN with NCM. Discussion CGMN is an extremely rare condition with incidence estimated at 1/500000 births. Lesions are caused by genetic mutations which lead to defective proliferation, differentiation and migration of melanoblasts. Risk of transformation of GCMN to malignant melanoma varies between 0 and 3.8%, with 80% of this number symptomatic by the age of seven.CNN originates between the 5th-24th week of gestation and arises from gain of function mutations in either BRAF or NRAS. The protooncogenes c-met and c-kit have also been demonstrated to play a role in the formation of CMN. CMN are predominantly caused by sporadic de novo mutations.Neurocutaneous melanosis is a rare complication of CMN with just over 100 cases reported. Most patients with NCM are asymptomatic t birth with sequelae appearing later in development.Treatment of GCMN is both symptomatic and palliative, with surgical techniques including serial resection, excision and grafting and the use of tissue expanders. Non-excisional techniques include dermabrasion, laser ablation and curettage.
hyperinsulinemia in 81.8%, insulinresistancy according to results of HOMA-indexin 72.7%, increasing triglycerides levelin 40.9%, decreasing level of LPHDin 77.3%, increasing level of LPLD in 45.6%. CRP was moderately elevated in 31.8%. Liver enzymes (ALT) were increased by 2-3 times in 40.9% obese children. Concentration of sVCAM-1 (1395.23±264.73 ng/ml vs 847.44±190.23 ng/ml; p< 0.0001) and VEGF-A (75.89±54.79 pg/ml vs 6.22±5.74 pg/ ml; p< 0.0001) was higher in patients with obesity compare to the adolescents with the normal BMI. Conclusions Obesity in adolescents characterized by significant metabolic disturbances with the development of insulin resistance in 81.8%, atherogenic dyslipidemia in 41%, low-grade inflammation in 31.8%, elevation of liver enzymes in 40.9% and increased level of endothelial dysfunction markers (sVCAM-1 level in obese teenagers exceeds level of teenagers with normal BMI more than 2 times, VEGF-Amore than 12 times).
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