Synonym(s)
HistoryThis section has been translated automatically.
Janovsky, 1890; Politzer & Unna, 1890
DefinitionThis section has been translated automatically.
Clinical descriptive term for gray-brown, papillomatous-hyperkeratotic, mostly asymptomatic, polyetiologic, extensive growths of the skin, which typically occur intertriginously, more rarely additionally in acral expression (nose, ears, palmoplantar skin, also orally). Basically, it is a uniform, "reaction cutanée" in which the skin responds to various endogenous "growth" stimuli with nonspecific proliferation.
Acanthosis nigricans can be:
- idiopathic
- reactive in obese individuals
- associated with endocrinological diseases or pregnancy (carefully exclude gestational diabetes)
- medicinal
- as a symptom of genetic defects
- paraneoplastic (then often called "acanthosis nigricans maligna") in association with adenocarcinomas
occur in the context of adenocarcinomas.
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ClassificationThis section has been translated automatically.
A distinction is made between:
- Paraneoplastic form: Acanthosis nigricans paraneoplastic (maligna).
- Non-paraneoplastic forms:
- Acanthosis nigricans "benigna" (acanthosis nigricans in the narrow sense).
- Acanthosis nigricans in endocrinological disorders (e.g. in obesity and insulin resistance) or obesity(pseudoacanthosis nigricans)
- Hereditary acanthosis nigricans(acanthosis nigricans in hereditary syndromes)
- Acral acanthosis nigricans (acral acanthotic anomaly)
- Unilateral (nevoid) acanthosis nigricans
- Drug-induced acanthosis nigricans.
EtiopathogenesisThis section has been translated automatically.
The pathogenesis depends on the different forms of the disease. An activation of growth factors is assumed, e.g. by formation and activation of growth factor receptors(epidermal growth factor receptor, insulin-like growth factor receptor and fibroblast growth factor receptor (FGFR)) with mitogenic and anti-apoptotic effects on keratinocytes. It is likely that in acanthosis nigricans there is rarely activation of a single growth factor (see Growth Factors below) but rather orchestration of multiple factors.
Drug-induced acanthosis nigricans results from interactions of certain drugs with lipid metabolism.
ManifestationThis section has been translated automatically.
Occurring in all age groups. Men and women fall ill about equally often.
LocalizationThis section has been translated automatically.
In principle, any area of the body can be affected. However, intertrigines, in particular armpits, lateral neck and neck areas, inguinal and genitoanal region are preferentially affected. Less frequently affected are eyelids, nasal entrance, elbows, popliteal or umbilical region. Involvement of palmae, plantae, oral mucosa and tongue is mainly observed in paraneoplastic acanthosis nigricans. In obese women with hyperandrogenism (e.g. in PCOS) without diabetes mellitus, the most frequent localization is the vulvar region.
Clinical featuresThis section has been translated automatically.
Mostly symmetrical development of initially yellow-brown to black hyperpigmentation, later area-like, velvety to verrucous enhancement of the skin texture, indistinctly demarcated from the surroundings. Possibly development of warty hyperkeratoses, which according to the current status are not seen as an independent clinical picture, but are partial symptoms of acanthosis nigricans, mostly acanthosis nigricans maligna. The growths may protrude in a cockscomb-like groin. The most severe changes are seen in the centers of the growths and in the intertriginous areas(ptychotropism).
On the mucosa rather rarely pronounced; here formation of planar, leukoplakic and rarely hyperpigmented areas. More rare is the development of cutis verticis gyrata.
The different forms do not differ clinically, but the paraneoplastic variant is often more extensive and clinically more pronounced. Furthermore, in the paraneoplastic variant, in addition to the classic intertriginous accentuated appearance, hyperkeratosis of the palmae and plantae as well as the flexor sides of the fingers and toes with pachydermodactyly may occur. In most cases there are no subjective complaints; in the malignant form itching may well occur.
HistologyThis section has been translated automatically.
Papillomatosis and hyperkeratosis, slight mostly irregular acanthosis, basal hyperpigmentation, partially pseudohorn cysts. No significant inflammatory infiltrate in the dermis. Discrete parakeratosis with papillomatosis and epithelial hyperplasia on the mucosa, typically without proliferation of melanocytes in the epithelium. The "malignant" and "benign" forms of acanthosis nigricans do not differ histologically.
DiagnosisThis section has been translated automatically.
Differential diagnosisThis section has been translated automatically.
- Pemphigus chronicus benignus familiaris; pemphigus vegetans; dyskeratosis follicularis; papillomatosis confluens et reticularis; M. Dowling-Degos; nevus, epidermal painter; Becker nevus; pellagra; haemochromatosis; M. Addison; rarely parapsoriasis en plaques or cutaneous T-cell lymphoma; tinea corporis; atopic eczema.
- For oral acanthosis nigricans: Goltz-Gorlin syndrome; Cowden syndrome; Wegener's granulomatosis; reticulohistiocytosis; hypertrichosis lanuginosa acquisita.
General therapyThis section has been translated automatically.
Symptomatically in cooperation with the endocrinologist for the treatment of a possible underlying disease. Consistent hygiene of the intertrigines. In the obesity-associated form (Addison's disease, pseudoacanthosis nigricans), the skin changes usually regress when body weight is normalised. In addition, consistent hygiene of the intertriginous areas, washing with syndets.
Notice! The exclusion of malignoma is obligatory for all forms of acanthosis nigricans!
External therapyThis section has been translated automatically.
Internal therapyThis section has been translated automatically.
Operative therapieThis section has been translated automatically.
TablesThis section has been translated automatically.
Malignant form |
Benign forms |
|
Localization |
in addition to the typical localizations, frequent involvement of palmae, plantae, oral mucosa, tongue and eyelids |
in overweight women with hyperandrogenemia often vulva area |
Extension |
mostly extensive involvement, partly generalized |
less extensive affection |
Clinic |
in addition to the classic appearance, hyperkeratosis may occur, especially on palmae and plantae as well as flexor sides of fingers and toes with pachydermatoglyphy ("tripe palms") |
|
mucous membrane involvement |
more frequently |
more rarely |
Subjective complaints |
localized or generalized itching; in mucosal papillomatosis, pain and possibly dysphagia may occur |
usually none |
Associated symptoms |
Malignancy of the internal organs, usually gastric carcinoma. Optionally, other paraneoplastic syndromes such as Leser-Trélat sign, hypertrichosis lanuginosa, pemphigus, palmoplantar keratoses or "tripe palms" may exist. |
Diabetes mellitus, insulin resistance, obesity, hyperhidrosis, fibroma pendulans, hyperandrogenemia |
Course |
acute onset and rapid spread, variable course, often fading after rehabilitation of the underlying malignancy with flare-up in case of metastasis |
often improvement with weight reduction or regulation of the endocrinological disorder |
Note(s)This section has been translated automatically.
Unfortunately, the language rules are inconsistent in Acanthosis nigricans. Some authors define Acathosis nigricans - here called Acanthosis nigricans maligna - as originally described strictly and 100% as a paraneoplastic syndrome. The much more frequent benign variant - here called acanthosis nigricans benigna - is called pseudoacanthosis nigricans. There is no clearly discernible trend in the international literature. There are still no clinically proven morphological distinguishing features between these two groups. In this respect the clinical picture is to be considered as a uniform skin reaction to different endogenous proliferation factors. Helpful for the assumption of a paraneoplastic etiology is the exclusion of obesity and hormonal stimuli as well as the advanced age of the (tumor) patients.
LiteratureThis section has been translated automatically.
- Ceylan C, Alper S, Kilinc I. (2002) Reader's Trelat sign. Int J Dermatol 41: 687-688
- Janovsky V (1890) Acanthosis nigricans. In: Unna PG et al (Ed.) International Atlas of Rare Skin Diseases. Volume 11, Voss, Leipzig
- Lenzner U et al (1998) Acanthosis nigricans maligna. Case description and literature review. Dermatologist 49: 41-47
- Mellor-Pita S, Yebra-Bango M, Alfaro-Martinez J, Suarez E (2002) Acanthosis nigricans: a new manifestation of insulin resistance in patients receiving treatment with protease inhibitors. Clin Infect Dis 34: 716-717
- Pollitzer S (1890) Acanthosis nigricans. In: Unna PG et al (Ed.) International Atlas of Rare Skin Diseases. Volume 11, Voss, Leipzig
- Pollitzer S (1891) Acanthosis nigricans. In: Unna PG et al (eds.) International Atlas of Rare Skin Diseases. Lewis, London, pp. 1-3
- Schroeder B, Ding X, Pfaff-Amesse T (2002) From HAIR-AN to eternity. J Pediatr Adolesc Gynecol 15: 235-240
- Schwartz RA (1994) Acanthosis nigricans. J Am Acad Dermatol 31: 1-22
- Stulberg DL et al (2003) Common hyperpigmentation disorders in adults: Part II. Melanoma, seborrheic keratosis, acanthosis nigricans, melasma, diabetic dermopathy, tinea versicolor, and postinflammatory hyperpigmentation. On Fam Physician 68: 1963-1968
- Torley D, Bellus GA, Munro CS (2002) Genes, growth factors and acanthosis nigricans. British Journal of Dermatology 147: 1096-1101
- Yamazaki H et al (2003) Acanthosis nigricans is a reliable cutaneous marker of insulin resistance in obese Japanese children. Pediatric Int 45: 701-705
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