Acanthosis nigricans on axilla
|Classification and external resources|
|Patient UK||Acanthosis nigricans|
Acanthosis nigricans is a brown to black, poorly defined, velvety hyperpigmentation of the skin. It is usually found in body folds, such as the posterior and lateral folds of the neck, the armpits, groin, navel, forehead, and other areas.
- 1 Classification
- 2 Signs and symptoms
- 3 Causes
- 4 Pathophysiology
- 5 Diagnosis
- 6 Prognosis
- 7 Treatment
- 8 History
- 9 References
- 10 External links
- Benign This may include obesity-related, hereditary, and endocrine forms of acanthosis nigricans.
- Malignant. This may include forms that are associated with tumour products and insulin-like activity, or tumour necrosis factor.
An alternate classification system still used to describe acanthosis nigricans was proposed in 1994. This classification system delineates acanthosis nigricans syndromes according to their associated syndromes, including benign and malignant forms, forms associated with obesity and drugs, acral acanthosis nigricans, unilateral acanthosis nigricans, and mixed and syndromic forms.
Signs and symptoms
It typically occurs in individuals younger than age 40, may be genetically inherited, and is associated with obesity or endocrinopathies, such as hypothyroidism, acromegaly, polycystic ovary disease, insulin-resistant diabetes, or Cushing's disease.
Type I - Familial:86
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Type II - Endocrine:506–7
- starts with insulin resistance, such as diabetes mellitus and metabolic syndrome
- excess circulating androgens, particularly Cushing's disease, acromegaly, polycystic ovarian disease
- Addison's disease and hypothyroidism
- Rare diseases, including pinealoma, leprechaunism, lipotrophic diabetes, pineal hyperplasia syndrome, pituitary basophilism, ovarian hyperthecosis, stromal luteoma, ovarian dermoid cysts, Prader-Willi syndrome, and Alstrom syndrome.
Acanthosis nigricans associated with endocrine dysfunction is more insidious in its onset, is less widespread, and the patients are often concurrently obese.:676
Type III - Obesity and Pseudo-Acanthosis Nigricans:86
In young persons, AN is a visible marker which strongly suggests insulin resistance. Higher than normal insulin levels in the blood stream causes the growth of darkened skin over certain areas of the body. There is no skin treatment that will get rid of AN. Acanthosis Nigricans may lighten up and possibly go away by treating the root cause, Insulin Resistance but it can take months or years to do so. Insulin resistance syndromes may be divided into Type A (HAIR-AN) and type B syndromes.:978 The majority of cases of acanthosis nigricans are associated with obesity and otherwise idiopathic. This is likely because of insulin resistance, and more likely to occur in darker-skinned persons.:968 This is can also be referred to as "Pseudo-Acanthosis Nigricans".
Type V - Malignancy:86
Malignant acanthosis nigricans refers to acanthosis nigricans occurring as a paraneoplastic syndrome associated with a cancer. Malignant acanthosis nigricans is most-commonly associated with gastrointestinal adenocarcinomas, as well as genitourinary cancers such as those of the prostate, breast, and ovary. Other cancers, such as those of the lung, stomach, and lymphoma, are occasionally associated with acanthosis nigricans.:86
This form of acanthosis nigricans is more likely to involve mucous membranes (25-50% of cases) Malignant acanthosis nigricans that may either precede (18%), accompany (60%), or follow (22%) the onset of an internal cancer.:506 Malignancy-associated acanthosis nigricans is usually rapid in onset and may be accompanied by skin tags, multiple seborrheic keratoses, or tripe palms.:676
Acral Acanthotic Anomaly
Acral Acanthotic Anomaly refers to a variant of acanthosis nigricans limited to the elbows, knees, knuckles and dorsal surfaces of the feet, in the absence of any other findings, in otherwise healthy individuals. While the etiology remains unknown, its presence does not suggest a likelihood of malignancy.
The pathogenesis of acanthosis nigricans is poorly understood, and likely to relate to an interplay of factors, including insulin-mediated activation of ILGF receptors on keratinocytes, and increased growth factor levels.
Factors involved in the development of acanthosis nigricans include:
- Increased circulating insulin. This activates keratinocyte ILGF receptors, particularly IGF-1. At high concentrations, insulin may also displace IGF-1 from IGFBP. Increased circulating IGF may lead to keratinocyte and dermal fibroblast proliferation.
- Fibroblast growth factor. Hereditary variants are associated with FGFR defects.
- Increased TGF, which appears to be the mechanism for malignancy-associated acanthosis nigricans. TGF acts on epidermal tissue via the EGFR.:86
In conjunction with increased end levels of ILGF, it is likely that perspiration and friction may be necessary predeterminants for lesions.
Acanthosis nigricans is typically diagnosed clinically. A skin biopsy may be needed in unusual cases. If no clear cause of acanthosis nigricans is obvious, it may be necessary to search for one. Blood tests, an endoscopy, or x-rays may be required to eliminate the possibility of diabetes or cancer as the cause.:87
Acanthosis nigricans is likely to improve in circumstances where a known cause is removed. For example, obesity-related acanthosis nigricans will improve with weight loss, and drug-induced acanthosis nigricans is likely to resolve when the drug is ceased. Hereditary variants may or may not fade with age, and malignancy-associated variants may, after a malignancy is removed, fade. :87
People with acanthosis nigricans should be screened for diabetes and, although rare, cancer. Controlling blood glucose levels through exercise and diet often improves symptoms. Topical fade creams (normally used for eliminating age spots) can lighten skin cosmetically in less severe cases. Acanthosis nigricans maligna may resolve if the causative tumor is successfully removed.
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- Ngan, Vanessa. "Acanthosis nigricans". Retrieved 23 August 2013.
- James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0-7216-2921-0.
- Garofalo, L.; A.M. Biscozzi; V. Mastrandrea; E. Bonifazi (2003). "Acanthosis nigricans vulgaris. A marker of hyperinsulinemia." (PDF). Eur. J. Pediat. Dermatol. 13: 85–8. Retrieved 2010-07-29.
- Schwartz, Robert A. (1994). "Acanthosis nigricans". Journal of the American Academy of dermatology 31 (1): 1–19. PMID 8021347. doi:10.1016/S0190-9622(94)70128-8.
- Thomas B. Fitzpatrick et al. (2005). Fitzpatrick's color atlas and synopsis of clinical dermatology (5th ed.). New York: McGraw-Hill Medical Pub. Division. ISBN 0-07-144019-4.
- Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 1-4160-2999-0.
- What causes AN ? - http://www.nuecesmedsociety.org 
- Rigel DS, Jacobs MI; Jacobs (1980). "Malignant acanthosis nigricans:a review". J Dermatol Surg Oncol 6 (11): 923–7. PMID 6257767.
- Schnopp C, Baumstark J; Baumstark (2007). "Oral acanthosis nigricans". N Engl J Med 357 (9): e10. PMID 17761587. doi:10.1056/NEJMicm062917.
- Schwartz RA (February 2007). "Acral acanthosis nigricans (acral acanthotic anomaly)". J. Am. Acad. Dermatol. 56 (2): 349–50. PMID 17224380. doi:10.1016/j.jaad.2006.09.027.
- Schwartz RA (September 1981). "Acral acanthotic anomaly (AAA)". J. Am. Acad. Dermatol. 5 (3): 345–6. PMID 7263979. doi:10.1016/S0190-9622(81)80155-7.
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- Tilgen W (2009). "Benign epidermal tumors". In WHC Burgdorf, G Plewig, HH Wolff, M Landthaler, O Braun-Falco. Braun-Falco's Dermatology (3rd ed.). Heidelberg: Springer. pp. 1340–7. ISBN 3-540-29312-4.
- Higgins, SP; Freemark, M; Prose, NS (Sep 15, 2008). "Acanthosis nigricans: a practical approach to evaluation and management.". Dermatology online journal 14 (9): 2. PMID 19061584.
- Brown J, Winkelmann RK (1968). "Acanthosis nigricans: study of 90 cases". Medicine 47 (1): 33–51. PMID 4868603. doi:10.1097/00005792-196801000-00002.
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