By Em. Prof. Dr. med. Walter K. H. Krause (auth.)
Skin lesions are usually the 1st signal of endocrine disorder. the facility to spot such lesions is hence of serious significance for endocrinology experts in addition to dermatologists within the early prognosis and therapy of endocrine sickness.
Lavishly illustrated, this scientific advisor describes the medical and histological gains of epidermis lesions saw in endocrine illnesses. Written within the language of dermatologists to be able to let an easy organization among the good points saw and the endocrine etiology, and with its reader-friendly layout, this publication will help dermatologists and endocrinologists alike, either to find the reason for the ailment and in making the right kind diagnosis.
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Extra resources for Cutaneous Manifestations of Endocrine Diseases
Proliferation of dermal fibroblasts Proliferation of fibroblasts, variable large epitheloid and stellate cells as well as myofibroblasts, thickened collagen bundles, distributed haphazardly. 2 Scleromyxoedema Aetiopathogenesis. Scleromyxoedema (lichen myoedematosus, papular mucinosis) is not associated with hypothyroidism. It shares the proliferation of fibroblasts and deposition of mucin in the dermis with myxoedema, but a thyroid disease is absent. The aetiology is unknown. It is usually associated with paraproteinemia that predominantly consists of immunoglobulin G with κ light chain.
2). The pigmentation increases slowly with the course of the disease and is often not recognized by the patient himself or will not be considered as a threatening disease, since it will remain the only clinical manifestation for years (Feingold and Elias 1988). The pigmentation may occur before signs of adrenal insufficiency are visible. Of the patients 12% show a vitiligo. A so-called ‘white Addison disease’ occurs in rare cases of adrenal insufficiency without skin pigmentation. The mechanism appears to depend on peripheral melanosome degradation of unknown origin, since levels of α-melanocyte-stimulating hormone (α-MSH) are enhanced as typical in these cases (Kendereski et al.
No standard treatment of scleromyxoedema is known. Trials reported included retinoid, melphalan, corticotrophin, cyclophosphamide, chlorambucil, plasmapheresis, high-dose intravenous immunoglobulin, glucocorticoids (topical, intra-lesional, and systemic), UV-A, extra-corporal phototherapy, and electron beam therapy. However, 30 3 3 Thyroid Hormones none of the therapeutic trials appeared to be universally effective. Intravenous immunglobulins appear to be the most promising treatment, although controlled studies are not available (Kulczycki et al.