By Thierry Passeron, Jean-Paul Ortonne
The dermis is coloured by means of a mix of pigments, which shape a part of a posh and hugely regulated procedure. Pigmentary defects more often than not current with dyschromia and will be attributable to genetic defects, systemic illness, inflammatory approaches, metabolic defects, infections, tumors, or poisonous or iatrogenic explanations. This atlas is an intensive textual content written through key opinion leaders inside of dermatology, it has a finished structure that publications the reader in the course of the epidemiology, pathophysiology, prognosis, therapy, and differential prognosis of either universal and infrequent pigmentary problems. It illustrates the prognosis and popularity of pigmentary problems with a variety of images.
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Extra info for Atlas of Pigmentary Disorders
This would induce a synergistic response of normal and malignant melanocytes resulting in enhanced proliferation, melanogenesis, and motility. DIFFERENTIAL DIAGNOSIS • Addison’s disease. • Hemochromatosis. • Argyria. KEY REFERENCES • Bork K, Korting GW, Rumpelt HJ. Diffuse melanosis in malignant melanoma. Hautarzt. 1977;28:463-8. • Paulo Filho Tde A, da Trindade Neto PB, Reis JC, Bartelt L, da Costa SA. Diffuse cutaneous melanosis in malignant melanoma. Dermatol Online J. 2007;13:9. CLINICAL DERMATOLOGICAL PRESENTATION Asymptomatic progressive slate-blue hyperpigmentation Localization: entire skin.
Progressive sclerodermatous thickening of the skin, with overlying hyperpigmentation and hypertrichosis. OMIM: #621391 Twenty-year-old man with H syndrome. Note the short stature. Sclerodermatous hyperpigmentation associated with hypertrichosis. decade of life and extend gradually. Localization: middle and lower parts of the body. GENETICS Autosomal recessive inherited disease. EPIDEMIOLOGY Extremely rare disease with less than 100 patients reported, mostly of Arab origin. PATHOPHYSIOLOGY Mutations in the SLC29A3 gene encoding for the human equilibrative nucleoside transporter (hENT3) which mediates passive sodium-independent transport of nucleoside is responsible for this genodermatosis.
TREATMENT None reported. No spontaneous regression of the hyperpigmentation. 29 ADDISON’S DISEASE Hyperpigmentation of the tongue. Hyperpigmentation of the extremities of the ﬁngers associated with acquired melanonychia. Hyperpigmentation of the palmar creases. EPIDEMIOLOGY Addison’s disease is an uncommon disorder affecting approximately 1 in 10,000 individuals. There is no age, race or sexual predilection. PATHOPHYSIOLOGY Addison disease is caused by a deficiency of adrenocortical hormones including glucocorticoids such as cortisone, and mineralocorticoids such as aldosterone.