The cutaneous manifestations of internal malignancy include nonmalignant skin disorders that occur in association with malignancy (paraneoplastic dermatoses) and skin lesions that represent infiltration of malignant cells into the skin due to metastatic or locoregional spread of disease or the deposition of circulating tumor cells (eg, leukemia cutis). A wide variety of paraneoplastic dermatoses have been described, including proliferative, inflammatory, bullous, and other types of skin disorders [1,2]. When paraneoplastic dermatoses develop before an internal neoplasm is recognized, recognition of these disorders can aid in the diagnosis of the malignancy.
Curth’s postulates, a set of diagnostic criteria, have been used by some authors to determine whether a cutaneous disorder should be classified as a paraneoplastic dermatosis . Curth’s postulates are provided in a table (table 1).
The most common paraneoplastic dermatoses will be discussed here; a discussion of disorders that represent tumoral infiltration of the skin is beyond the scope of this topic. (See "Paget disease of the breast" and "Clinical manifestations, pathologic features, and diagnosis of acute myeloid leukemia" and "AIDS-related Kaposi sarcoma: Staging and treatment" and "Clinical manifestations, pathologic features, and diagnosis of mycosis fungoides".)
DERMATOSES DUE TO METABOLIC PRODUCTS OF MALIGNANCY
Hyperpigmentation in ectopic Cushing's syndrome — Ectopic Cushing's syndrome is the most common hormonally-induced paraneoplastic syndrome associated with internal malignancy. The syndrome is characterized by generalized hyperpigmentation (cutaneous and mucosal), muscle wasting, proximal muscle weakness, hypokalemic metabolic alkalosis, abnormal glucose tolerance, and hypertension . (See "Epidemiology and clinical manifestations of Cushing's syndrome".)
Ectopic Cushing’s syndrome is caused by hypersecretion of proopiomelanocortin (POMC) from tumors outside of the pituitary gland. POMC is a prohormone of melanocyte-stimulating hormone (MSH) and adrenocorticotropic hormone (ACTH). Both MSH and ACTH are capable of stimulating melanin synthesis, which leads to the development of hyperpigmentation . (See "Causes and pathophysiology of Cushing's syndrome".)