Acanthosis nigricans - Wikipedia, the free encyclopedia

14/05/15 12:09

Acanthosis nigricans
From Wikipedia, the free encyclopedia

Acanthosis nigricans is a brown to

black, poorly defined, velvety
hyperpigmentation of the skin. It is

Acanthosis nigricans

usually found in body folds,[1] such as

the posterior and lateral folds of the
neck, the armpits, groin, navel,
forehead, and other areas.

Contents
1 Classification
2 Signs and symptoms
3 Causes
3.1 Endocrine
3.2 Insulin resistance
and acanthosis nigricans
3.3 Obesity-related
3.4 Drug-related
3.5 Familial
3.6 Acral Acanthotic
Anomaly
3.7 Malignant
4 Pathophysiology
5 Diagnosis
5.1 Differential
Diagnosis
6 Prognosis
7 Treatment
8 History
9 References
10 External links

Acanthosis nigricans on axilla

Classification and external resources
ICD-10

L83
(http://apps.who.int/classifications/icd10/browse/2015/en#/L83)

ICD-9

701.2 (http://www.icd9data.com/getICD9Code.ashx?
icd9=701.2)

OMIM

100600 (http://omim.org/entry/100600)

DiseasesDB 58 (http://www.diseasesdatabase.com/ddb58.htm)
MedlinePlus 000852
(http://www.nlm.nih.gov/medlineplus/ency/article/000852.htm)

Classification

eMedicine

derm/1 (http://www.emedicine.com/derm/topic1.htm)

MeSH

D000052 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?
field=uid&term=D000052)

Acanthosis nigricans is conventionally

divided into benign and malignant forms.,[2][3] although may be divided into syndromes according to
cause.:[4]:506
Benign This may include obesity-related, hereditary, and endocrine forms of acanthosis nigricans.[2]
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Malignant. This may include forms that are associated with tumour products and insulin-like activity, or
tumour necrosis factor.[2]
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.[5][6]

Signs and symptoms

Acanthosis nigricans may present with thickened, relatively darker areas of skin on the neck, armpit and in skin
folds.[2]

Causes
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.

Endocrine
Endocrine syndromes associated with acanthosis nigricans can develop in many conditions, particularly:[2]:978
[7]:86

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.[8]:676 This is also known as "Acanthosis nigricans type
III",[4]:5067 and insulin resistance syndromes may be divided into Type A (HAIR-AN) and type B
syndromes.[2]:978

Insulin resistance and acanthosis nigricans

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.[9]

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Obesity-related
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.[2]:968 This is also known as
"Pseudo-Acanthosis Nigricans", or "Type 3 Acanthosis Nigricans".[7]:86

Drug-related
Acanthosis nigricans has been linked to the use of nicotinic acid,[2] glucocorticoid use, COCP, growth hormone
therapy, and stilbesterol.<.[7] This is also known as Type 4 Acanthosis nigricans.[7]:86

Familial
Familial acanthosis may arise as a result of an autosomal dominant trait, presenting at birth or developing
during childhood.[4]:506[8]:676 This is also known as Acanthosis nigricans type 1.[7]:86

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.[10][11][12][13]
While the etiology remains unknown,[13] its presence does not suggest a likelihood of malignancy.[13]

Malignant

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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.[7]:86[14]
This form of acanthosis nigricans is more likely to involve mucous membranes (25-50% of cases)[3][15] This
variant is also known as Acanthosis nigricans type I[8]:676 or 5.[7]:86 Malignant acanthosis nigricans that may
either precede (18%), accompany (60%), or follow (22%) the onset of an internal cancer.[4]:506 Malignancyassociated acanthosis nigricans is usually rapid in onset and may be accompanied by skin tags, multiple
seborrheic keratoses, or tripe palms.[8]:676

Pathophysiology
The pathogenesis of acanthosis nigricans is poorly understood, and likely to relate to an interplay of factors,[16]
including insulin-mediated activation of ILGF receptors on keratinocytes, and increased growth factor
levels.[16]
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.[16]
Fibroblast growth factor. Hereditary variants are associated with FGFR defects.[16]
Increased TGF, which appears to be the mechanism for malignancy-associated acanthosis nigricans. TGF
acts on epidermal tissue via the EGFR.[7]:86
In conjunction with increased end levels of ILGF, it is likely that perspiration and friction may be necessary
predeterminants for lesions.[16]

Diagnosis
Acanthosis nigricans is typically diagnosed clinically.[2] 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.[7]:87
On biopsy, hyperkaratosis, epidermal folding, leukocyte infltration, and melanocyte proliferation may be
seen.[2]:979[7]:87

Differential Diagnosis
Acanthosis nigricans should be distinguished from the Casal collar appearing in pellegra.
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Prognosis
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 malignancyassociated variants may, after a malignancy is removed, fade.[7] :87

Treatment
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.[17]

History
References
1. "acanthosis nigricans
(http://web.archive.org/web/20090616022448/http://www.mercksource.com/pp/us/cns/cns_hl_dorlands_split.jsp?
pg=/ppdocs/us/common/dorlands/dorland/one/000000524.htm)" at Dorland's Medical Dictionary
2. Habif, Thomas P. (2009). Clinical dermatology (5th ed.). Edinburgh: Mosby. ISBN 978-0-7234-3541-9.
3. Ngan, Vanessa. "Acanthosis nigricans" (http://dermnetnz.org/systemic/acanthosis-nigricans.html). Retrieved 23 August
2013.
4. James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.).
Saunders. ISBN 0-7216-2921-0.
5. Garofalo, L.; A.M. Biscozzi; V. Mastrandrea; E. Bonifazi (2003). "Acanthosis nigricans vulgaris. A marker of
hyperinsulinemia." (http://www.dermatologiapediatrica.com/volume13/acanthosis.pdf) (PDF). Eur. J. Pediat. Dermatol.
13: 858. Retrieved 2010-07-29.
6. Schwartz, Robert A. (1994). "Acanthosis nigricans". Journal of the American Academy of dermatology 31 (1): 119.
doi:10.1016/S0190-9622(94)70128-8 (https://dx.doi.org/10.1016%2FS0190-9622%2894%2970128-8). PMID 8021347
(https://www.ncbi.nlm.nih.gov/pubmed/8021347).
7. 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.
8. Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 14160-2999-0.
9. What causes AN ? - http://www.nuecesmedsociety.org [1] (http://www.nuecesmedsociety.org/Template.aspx?id=873)
10. Schwartz RA (February 2007). "Acral acanthosis nigricans (acral acanthotic anomaly)"
(http://linkinghub.elsevier.com/retrieve/pii/S0190-9622(06)02592-8). J. Am. Acad. Dermatol. 56 (2): 34950.
doi:10.1016/j.jaad.2006.09.027 (https://dx.doi.org/10.1016%2Fj.jaad.2006.09.027). PMID 17224380
(https://www.ncbi.nlm.nih.gov/pubmed/17224380).
11. Schwartz RA (September 1981). "Acral acanthotic anomaly (AAA)". J. Am. Acad. Dermatol. 5 (3): 3456.
doi:10.1016/S0190-9622(81)80155-7 (https://dx.doi.org/10.1016%2FS0190-9622%2881%2980155-7). PMID 7263979
(https://www.ncbi.nlm.nih.gov/pubmed/7263979).
12. Schwartz RA (July 1994). "Acanthosis nigricans". J. Am. Acad. Dermatol. 31 (1): 119; quiz 202. doi:10.1016/S01909622(94)70128-8 (https://dx.doi.org/10.1016%2FS0190-9622%2894%2970128-8). PMID 8021347
(https://www.ncbi.nlm.nih.gov/pubmed/8021347).
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13. 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. 13407. ISBN 3-540-29312-4.
14. Rigel DS, Jacobs MI; Jacobs (1980). "Malignant acanthosis nigricans:a review". J Dermatol Surg Oncol 6 (11): 9237.
PMID 6257767 (https://www.ncbi.nlm.nih.gov/pubmed/6257767).
15. Schnopp C, Baumstark J; Baumstark (2007). "Oral acanthosis nigricans". N Engl J Med 357 (9): e10.
doi:10.1056/NEJMicm062917 (https://dx.doi.org/10.1056%2FNEJMicm062917). PMID 17761587
(https://www.ncbi.nlm.nih.gov/pubmed/17761587).
16. 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
(https://www.ncbi.nlm.nih.gov/pubmed/19061584).
17. Brown J, Winkelmann RK (1968). "Acanthosis nigricans: study of 90 cases". Medicine 47 (1): 3351.
doi:10.1097/00005792-196801000-00002 (https://dx.doi.org/10.1097%2F00005792-196801000-00002). PMID 4868603
(https://www.ncbi.nlm.nih.gov/pubmed/4868603).

External links
AOCD

Wikimedia Commons has

media related to Acanthosis
nigricans.

(http://www.aocd.org/skin/dermatologic_diseases/acanthosis_nigrica.html)
http://www.skinsight.com/adult/acanthosisNigricans-references.htm
00001 (http://chorus.rad.mcw.edu/doc/00001.html) at CHORUS
Retrieved from "http://en.wikipedia.org/w/index.php?title=Acanthosis_nigricans&oldid=659781885"
Categories: Endocrine-related cutaneous conditions Medical signs Medical conditions related to obesity
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