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Acanthosis Nigricans

Author: Jason H Miller, MD; Chief Editor: Dirk M Elston, MD

Updated: Nov 28, 2012Background


Although Addison may have seen a case of acanthosis nigricans (AN) before 1885 and
misdiagnosed it as Addison disease, the first documented case of acanthosis nigricans
was in 1889 in Germany as described by Unna and Pollitzer. By 1909, acanthosis
nigricans had been described in approximately 50 patients and was suspected to be
associated with internal malignancy. In 1976, Kahn et al published their landmark study
in which the association between acanthosis nigricans and insulin resistance was first
described. In 2000, the American Diabetes Association established acanthosis nigricans
as a formal risk factor for the development of diabetes in children.[1]

Pathophysiology
Acanthosis nigricans most likely is caused by factors that stimulate epidermal
keratinocyte and dermal fibroblast proliferation.
In the benign form of acanthosis nigricans, the factor is probably insulin or an insulinlike
growth factor (IGF) that incites the epidermal cell propagation. Other proposed mediators
include other tyrosine kinase receptors (epidermal growth factor receptor [EGFR] or
fibroblast growth factor receptor [FGFR]).
At high concentrations, insulin may exert potent proliferative effects via high-affinity
binding to IGF-1 receptors. In addition, free IGF-1 levels may be elevated in obese
patients with hyperinsulinemia, leading to accelerated cell growth and differentiation.[2]
Familial and syndromic forms of acanthosis nigricans have been identified. Many
syndromes share common features, including obesity, hyperinsulinemia, and
craniosynostosis. These have been subdivided into insulin-resistance syndromes and
fibroblast growth factor defects.
Insulin-resistance syndromes include those with mutations in the insulin receptors (ie,
leprechaunism, Rabson-Mendenhall syndrome), peroxisome proliferator-activated
receptor gamma (ie, type 1 diabetes with acanthosis nigricans and hypertension), 1acylglycerol-3-phosphate O-acyl transferase-2 or seipin (Berardinelli-Seip syndrome),
lamin A/C (Dunnigan syndrome), and Alstrom syndrome gene. Fibroblast growth factor
defects include activating mutations in FGFR2 (Beare-Stevenson syndrome), FGFR3
(Crouzon syndrome with acanthosis nigricans, thanatophoric dysplasia, severe
achondroplasia with developmental delay, and acanthosis nigricans [SADDAN]).
Familial cases of acanthosis nigricans with no other syndromic findings have also been
linked to FGFR mutations.[3, 4]

Perspiration or friction may also play a contributory role, as suggested by the predilection
of acanthosis nigricans for body folds.
In malignant acanthosis nigricans, the stimulating factor is hypothesized to be a substance
secreted either by the tumor or in response to the tumor. Transforming growth factor
(TGF)alpha is structurally similar to epidermal growth factor and is a likely candidate.
TGF-alpha and epidermal growth factor have both been found in gastric adenocarcinoma
cells, and EGFR expression has been identified in skin cells within acanthosis nigricans
lesions. Reports of urine and serum TGF-alpha levels normalizing after surgical tumor
removal exist, with subsequent regression of skin lesions.[5]
Exogenous medications also have been implicated as etiologic factors, including insulin
injections (especially at the injection site), likely due to activation of IGF receptors.[6, 7]
Newer agents such as palifermin (recombinant keratinocyte growth factor used to
decrease mucositis with chemotherapy and stem cell transplantation) have reportedly
produced transient but dramatic acanthosis nigricanslike lesions, presumably due to
activation of the FGFR.[8]
Of interest, ectopic acanthosis nigricans has been described in a syndromic patient who
required skin grafting from the groin for syndactyly repair, with delayed acanthosis
nigricans formation at the graft sites.[9]
Table. Acanthosis Nigricans Associations (Open Table in a new window)
Syndromes Associated With Acanthosis
Malignant Diseases Associated With
Nigricans
Acanthosis Nigricans
Acromegaly
Bile duct cancer
Alstrom telangiectasia
Bladder cancer
Barter syndrome
Breast cancer
Beare-Stevenson syndrome
Colon cancer
Benign encephalopathy
Endometrial cancer
Bloom syndrome
Esophageal cancer
Capozucca syndrome
Gallbladder cancer
Chondrodystrophy with dwarfism
Hodgkin disease
Costello syndrome
Kidney cancer
Crouzon syndrome
Liver cancer
Dermatomyositis
Lung cancer
Familial pineal body hypertrophy
Mycosis fungoides
Gigantism
Non-Hodgkin lymphoma
Hashimoto thyroiditis
Ovarian cancer
Hirschowitz syndrome
Pancreatic cancer
Lawrence-Moon-Bardet syndrome
Pheochromocytoma
Lawrence-Seip syndrome
Prostate cancer
Lipoatrophic diabetes mellitus
Rectal cancer

Lupoid hepatitis
Testicular cancer
Lupus erythematosus
Thyroid cancer
Phenylketonuria
Wilms tumor
Pituitary hypogonadism
Pseudoacromegaly
Prader-Willi syndrome
Pyramidal tract degeneration
Rud syndrome
Scleroderma
Stein-Leventhal syndrome
Type A syndrome (HAIR-AN syndrome)
Werner syndrome
Wilson syndrome

Epidemiology
Frequency

United States
The exact incidence of acanthosis nigricans is unknown. In an unselected population of
1412 children, the changes of acanthosis nigricans were present in 7.1%. Obesity is
closely associated with acanthosis nigricans, and more than half the adults who weigh
greater than 200% of their ideal body weight have lesions consistent with acanthosis
nigricans.
The malignant form of acanthosis nigricans is far less common, and, in one study, only 2
of 12,000 patients with cancer had signs of acanthosis nigricans. The most frequent
associations were with adenocarcinomas of the gastrointestinal tract (70-90%),
particularly gastric cancer (55-61% of malignant acanthosis nigricans cases).
Approximately 61.3% of cases are diagnosed simultaneously with the cancer
manifestation, while 17.6% of malignant acanthosis nigricans cases predate the diagnosis
of malignancy.[5]

International
Epidemiologic studies performed in Iran, United Arab Emirates, and Japan all show
statistically significant increases in insulin resistance among obese patients with
acanthosis nigricans compared with matched obese controls without acanthosis nigricans,
suggesting that acanthosis nigricans is a useful marker for insulin resistance among obese
patients regardless of geographic setting.[10]

Mortality/Morbidity
Patients with the benign form of acanthosis nigricans experience very few, if any,
complications of their skin lesions. However, many of these patients have an underlying
insulin-resistant state that is the cause of their acanthosis nigricans. The severity of the
insulin resistance is highly variable and ranges from an incidental finding after routine
blood studies to overt diabetes mellitus. The severity of skin findings may parallel the
degree of insulin resistance, and a partial resolution may occur with treatment of the
insulin-resistant state.
Insulin resistance is the most common association of acanthosis nigricans in the younger
population. New studies indicate that children with acanthosis nigricans have higher
levels of basal and glucose-stimulated insulin compared with obese children without
acanthosis nigricans, suggesting an association of acanthosis nigricans with
hyperinsulinemia independent of body mass index.[11, 12]
Malignant acanthosis nigricans is associated with significant complications because the
underlying malignancy is often an aggressive tumor. Average survival time of patients
with signs of malignant acanthosis nigricans is 2 years, although cases in which patients
have survived for up to 12 years have been reported. In older patients with new-onset
acanthosis nigricans, most have an associated internal malignancy.

Race
Acanthosis nigricans is much more common in people with darker skin pigmentation.
The prevalence in whites is less than 1%. In Latinos, the prevalence in one study was
5.5%, and, in African Americans, the prevalence is higher, at 13.3%. The incidence is
also increased in the Native American population, with one study showing 34.2% of
Cherokee patients age 5-40 years with acanthosis nigricans, increasing to 73% of those
Cherokee patients with diabetes.[13, 14]
The prevalence in overweight children aged 7-17 years increases to 23% in Latino
patients and 19.4% in African American patients. Children of any race with a body mass
index greater than the 98th percentile have a 62% prevalence of acanthosis nigricans.[15, 16,
17]

In contrast to the benign form, malignant acanthosis nigricans has no racial predilection.

Sex
The incidence of acanthosis nigricans is equal for men and women. Acanthosis nigricans
has no known sex predilection.[1]

Age
Lesions of benign acanthosis nigricans may be present at any age, including at birth,
although it is found more commonly in the adult population. Malignant acanthosis
nigricans occurs more frequently in elderly persons; however, cases have been reported in
children with Wilms tumor, gastric adenocarcinoma, and osteogenic sarcoma.[1]

History
Patients usually present with an asymptomatic area of darkening and thickening of the
skin. Pruritus occasionally may be present. Lesions begin as hyperpigmented macules
and patches and progress to palpable plaques.
In approximately one third of cases of malignant acanthosis nigricans, patients present
with skin changes before any signs of cancer. In another one third of cases, the lesions of
acanthosis nigricans arise simultaneously with the neoplasm. In the remaining one third
of cases, the skin findings manifest sometime after the diagnosis of cancer. Malignant
acanthosis nigricans has been reported to appear abruptly and exuberantly and may be
associated with a higher rate of pruritus.[1]
Onset may be related to medication or supplement usage.

Physical
Acanthosis nigricans is characterized by symmetrical, hyperpigmented, velvety plaques
that may occur in almost any location but most commonly appear on the intertriginous
areas of the axilla, groin, and posterior neck. The posterior neck is the most commonly
affected site in children.
Acrochordons (skin tags) are often found in and around the affected areas. Occasionally,
lesions of acanthosis nigricans may be present on the mucous membranes of the oral
cavity, nasal and laryngeal mucosa, and esophagus. The areola of the nipple also may be
affected. Eye involvement, including papillomatous lesions on the eyelids and
conjunctiva, may occur. Nail changes, such as leukonychia and hyperkeratosis, have been
reported.
The lesions of malignant acanthosis nigricans are clinically indistinguishable from benign
acanthosis nigricans.
Note the images below.

Brown velvety plaques with skin tags in the axilla of a

patient with acanthosis nigricans.

Acanthosis nigricans.

Acanthosis nigricans, obesity related.

Acanthosis nigricans of the axilla with one skin tag.

Causes
The definitive cause for acanthosis nigricans has not yet been ascertained, although
several possibilities have been suggested. Nine types of acanthosis nigricans have been
described.

Obesity-associated acanthosis nigricans


Obesity-associated acanthosis nigricans, once labeled pseudoacanthosis nigricans, is the
most common type of acanthosis nigricans. Lesions may appear at any age but are more
common in adulthood. The dermatosis is weight dependent, and lesions may completely
regress with weight reduction. Insulin resistance is often present in these patients;
however, it is not universal.

Obesity-associated acanthosis nigricans may be a marker for higher insulin needs in


obese women with gestational diabetes.[18] Acanthosis nigricans has been shown to be a
reliable early marker for metabolic syndrome in pediatric patients.[19]

Syndromic acanthosis nigricans


Syndromic acanthosis nigricans is the name given to acanthosis nigricans that is
associated with a syndrome. In addition to the widely recognized association of
acanthosis nigricans with insulin resistance, acanthosis nigricans has been associated with
numerous syndromes (see the Table in Pathophysiology). The type A syndrome and type
B syndrome are special examples.
The type A syndrome also is termed the hyperandrogenemia, insulin resistance, and
acanthosis nigricans syndrome (HAIR-AN syndrome). This syndrome is often familial,
affecting primarily young women (especially black women). It is associated with
polycystic ovaries or signs of virilization (eg, hirsutism, clitoral hypertrophy). High
plasma testosterone levels are common. The lesions of acanthosis nigricans may arise
during infancy and progress rapidly during puberty.
The type B syndrome generally occurs in women who have uncontrolled diabetes
mellitus, ovarian hyperandrogenism, or an autoimmune disease such as systemic lupus
erythematosus, scleroderma, Sjgren syndrome, or Hashimoto thyroiditis. Circulating
antibodies to the insulin receptor may be present. In these patients, the lesions of
acanthosis nigricans are of varying severity.

Acral acanthosis nigricans


Acral acanthosis nigricans (acral acanthotic anomaly) occurs in patients who are in
otherwise good health. Acral acanthosis nigricans is most common in dark-skinned
individuals, especially those of African American or sub-Saharan African descent. The
hyperkeratotic velvety lesions are most prominent over the dorsal aspects of the hands
and feet, with knuckle hyperpigmentation often most prominent.

Unilateral acanthosis nigricans


Unilateral acanthosis nigricans, sometimes referred to as nevoid acanthosis nigricans, is
believed to be inherited as an autosomal dominant trait. Lesions are unilateral in
distribution and may become evident during infancy, childhood, or adulthood. Lesions
tend to enlarge gradually before stabilizing or regressing. Unilateral acanthosis nigricans
lesions may represent a unilateral epidermal nevus.

Generalized acanthosis nigricans


Generalized acanthosis nigricans is rare and has been reported in pediatric patients
without underlying systemic disease or malignancy.[20]

Familial acanthosis nigricans


Familial acanthosis nigricans is a rare genodermatosis that seems to be transmitted in an
autosomal dominant fashion with variable phenotypic penetrance. The lesions typically
begin during early childhood but may manifest at any age. Familial acanthosis nigricans
often progresses until puberty, at which time it stabilizes or regresses.

Drug-induced acanthosis nigricans


Drug-induced acanthosis nigricans, although uncommon, may be induced by several
medications, including nicotinic acid, insulin, pituitary extract, systemic corticosteroids,
and diethylstilbestrol. Nicotinic acid is most widely recognized association, with
acanthosis nigricans, developing on abdomen and flexor surfaces and resolving within 410 weeks of discontinuation.[1] Rarely, triazinate, oral contraceptives, fusidic acid, and
methyltestosterone have also been associated with acanthosis nigricans. Fibroblast
growth factor receptor ligands such as palifermin may cause drug-induced acanthosis
nigricans.[8]
The lesions of acanthosis nigricans may regress following discontinuation of the
offending medication.

Malignant acanthosis nigricans


Malignant acanthosis nigricans, which is associated with internal malignancy, is the most
worrisome of the variants of acanthosis nigricans because the underlying neoplasm is
often an aggressive cancer (see the Table in Pathophysiology).
Acanthosis nigricans has been reported with many kinds of cancer, but, by far, the most
common underlying malignancy is an adenocarcinoma of gastrointestinal origin, usually
a gastric adenocarcinoma. In an early study of 191 patients with malignant acanthosis
nigricans, 92% had an underlying abdominal cancer, of which 69% were gastric. Another
study reported 94 cases of malignant acanthosis nigricans, of which 61% were secondary
to a gastric neoplasm.
Malignant acanthosis nigricans in pediatric patients has been described with gastric
adenocarcinoma, Wilms tumor, and osteogenic sarcoma.[1]
In 25-50% of cases of malignant acanthosis nigricans, the oral cavity is involved. The
tongue and the lips most commonly are affected, with elongation of the filiform papillae
on the dorsal and lateral surfaces of the tongue and multiple papillary lesions appearing
on the commissures of the lips. Oral lesions of acanthosis nigricans seldom are
pigmented.
Tripe palms may show altered dermatoglyphics due to alteration of epidermal rete ridges

Malignant acanthosis nigricans is clinically indistinguishable from the benign forms;


however, one must be more suspicious if the lesions arise rapidly, are more extensive, are
symptomatic, or are in atypical locations.
Regression of acanthosis nigricans has been seen with treatment of the underlying
malignancy, and reappearance may suggest recurrence or metastasis of the primary
tumor.

Mixed-type acanthosis nigricans


Mixed-type acanthosis nigricans refers to those situations in which a patient with one of
the above types of acanthosis nigricans develops new lesions of a different etiology. An
example of this would be an overweight patient with obesity-associated acanthosis
nigricans who subsequently develops malignant acanthosis nigricans.

Differential Diagnoses

Addison Disease
Hemochromatosis
Pellagra

Laboratory Studies
For patients with adult onset of acanthosis nigricans (AN), perform a basic workup for
underlying malignancy.
Screen for diabetes with a glycosylated hemoglobin level or glucose tolerance test.
Screen for insulin resistance; a good screening test for insulin resistance is a plasma
insulin level, which will be high in those with insulin resistance. This is the most
sensitive test to detect a metabolic abnormality of this kind because many younger
patients do not yet have overt diabetes mellitus and an abnormal glycosylated
hemoglobin level, but they do have a high plasma insulin level.

Procedures
Skin biopsy may be useful if clinical diagnosis is not easily made.

Histologic Findings
Histologic examination reveals hyperkeratosis, papillomatosis, with minimal or no
acanthosis or hyperpigmentation. The dermal papillae project upward as fingerlike
projections, with occasional thinning of the adjacent epidermis. Pseudohorn cysts may be
present. Clinical dyschromia is secondary to the hyperkeratosis and not to increased
melanocytes or increased melanin deposition. Dermal inflammatory infiltrate is minimal
or nonexistent.

Mucosal acanthosis nigricans reveals epithelial hyperkeratosis and papillomatosis along


with parakeratosis.[1]
Note the image below.

Acanthosis nigricans biopsy. The epidermis is


papillomatous (undulates) and pigmented ("nigricans"). Acanthosis (thickening of the
spinous layer) is often not really present, so acanthosis nigricans is often a misnomer in
many cases.

Medical Care
No treatment of choice exists for acanthosis nigricans (AN). The goal of therapy is to
correct the underlying disease process. Treatment of the lesions of acanthosis nigricans is
for cosmetic reasons only. Correction of hyperinsulinemia often reduces the burden of
hyperkeratotic lesions. Likewise, weight reduction in obesity-associated acanthosis
nigricans may result in resolution of the dermatosis.
Note the following:

Cessation of inciting agent in drug-induced acanthosis nigricans often results in


resolution. Acipimox may be used in place of nicotinic acid to induce acanthosis
nigricans regression while improving the lipid profile.[21] Dietary fish oil
reportedly is beneficial in patients with lipodystrophic diabetes and generalized
acanthosis nigricans, even if niacin is continued.[22]
Topical medications that have been effective in some cases of acanthosis nigricans
include keratolytics (eg, topical tretinoin 0.05%, ammonium lactate 12% cream,
or a combination of the 2) and triple-combination depigmenting cream (tretinoin
0.05%, hydroquinone 4%, fluocinolone acetonide 0.01%) nightly with daily
sunscreen.[23] Calcipotriol, podophyllin, urea, and salicylic acid also have been
reported, with variable results.[1]
Oral agents that have shown some benefit include etretinate,[24] isotretinoin,[25]
metformin,[26] and dietary fish oils.[27] Octreotide showed sustained improvement in
one patient with insulin resistance 6 months after completing the course.[28]
Hyperandrogenemia, insulin resistance, and acanthosis nigricans syndrome
(HAIR-AN syndrome) patients may be treated with oral contraceptives and
metformin.[1]
Dermabrasion and long-pulsed alexandrite laser therapy may also be used to
reduce the bulk of the lesion, with some long-term remission.[29]

Surgical removal of tumors is the mainstay of treatment for malignant acanthosis


nigricans, if possible, because clearance following primary malignancy excision
has been reported.[30]
Cyproheptadine has been used in cases of malignant acanthosis nigricans because
it may inhibit the release of tumor products.[31]
Psoralen plus UVA (PUVA) has been reported as beneficial for symptomatic relief
in cases of paraneoplastic acanthosis nigricans.[5]

Surgical Care
Dermabrasion and long-pulsed alexandrite laser therapy may also be used to reduce the
bulk of the lesion, with some long-term remission.[32]
Surgical removal of tumors is the mainstay of treatment for malignant acanthosis
nigricans, if possible, because clearance following primary malignancy excision has been
described.[30]

Consultations
Based on underlying etiology, multidisciplinary evaluation may include the following:

Primary care physician (pediatrician, internist, or family practitioner)


Endocrinologist
Oncologist
Geneticist
Dermatologist

Diet
Weight loss and glycemic control are essential for those with obesity-related acanthosis
nigricans or hyperinsulinemic states.

Medication Summary
The goal of pharmacotherapy in acanthosis nigricans is to improve cosmetic appearance.

Topical retinoids
Class Summary
These agents promote shedding of hyperkeratotic skin. They are modifiers of
keratinocyte adhesion, differentiation, and proliferation.
View full drug information

Tretinoin topical (Avita, Retin-A)


Promotes detachment of cornified cells and enhances shedding of corneocytes. Inhibits
microcomedo formation and eliminates lesions that are present. Makes keratinocytes in
sebaceous follicles less adherent and easier to remove.
Available as 0.025%, 0.05%, and 0.1% creams. Available also as 0.01% and 0.025% gels.

Keratolytic Agent
View full drug information

Ammonium lactate
Alpha-hydroxy acid; normal constituent of tissues and blood. Believed to act as
humectant when applied to the skin. This may influence hydration of the stratum
corneum. In addition, when applied to the skin, may act to decrease corneocyte cohesion.
The mechanism(s) by which this is accomplished is not yet known.

Complications
Complications vary depending on the etiology of acanthosis nigricans (AN). Appearance
of acanthosis nigricans during childhood usually is associated with a benign condition,
and no important sequelae are described.
Adult-onset acanthosis nigricans is more worrisome, and an underlying malignancy must
be ruled out. However, most cases of adult-onset acanthosis nigricans are benign and
often are associated with insulin resistance.

Prognosis
The prognosis for patients with malignant acanthosis nigricans is often poor. The
associated malignancy frequently is advanced, and the average survival of these patients
is approximately 2 years.

Patient Education
Patients should be instructed that acanthosis nigricans is not a skin disease per se, but
rather a sign of an underlying problem. If a patient does have acanthosis nigricans on the
basis of insulin resistance, which is the most common reason, treatment of the metabolic
abnormality may lead to improvement of the appearance of the skin. Dietary changes and
weight loss may cause the acanthosis nigricans to regress almost completely.
NEW TOPIC

Acanthosis nigricans
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Acanthosis nigricans
Classification and external resources

Acanthosis nigricans on axilla


ICD-10
L83
ICD-9
701.2
OMIM
100600
DiseasesDB
58
MedlinePlus
000852
eMedicine
derm/1
MeSH
D0fff00052
Acanthosis nigricans is a brown to black, poorly defined, velvety hyperpigmentation of
the skin. It is usually found in body folds,[1] such as the posterior and lateral folds of the
neck, the axilla, groin, umbilicus, forehead, and other areas.

Contents

1 Causes
o 1.1 Endocrine
o 1.2 Malignant
o 1.3 Other
2 Types
o 2.1 Classification of Acanthosis nigricans according to Schwartz, 1994 [5][6]
o 2.2 Other Classifications of Acanthosis nigricans
3 Signs, tests, and misdiagnoses
4 Treatment
5 Prognosis
6 References

7 External links

Causes
It typically occurs in individuals younger than age 40, may be genetically inherited, and
is associated with obesity or endocrinopathies, such as hypothyroidism or
hyperthyroidism, acromegaly, polycystic ovary disease, insulin-resistant diabetes, or
Cushing's disease.

Endocrine
The most common cause of acanthosis nigricans is insulin resistance, which leads to
increased circulating insulin levels. Insulin spillover into the skin results in its abnormal
increase in growth (hyperplasia of the skin). The high insulin concentrations probably
activate growth factor receptors (perhaps the IGF1 receptor) that drive the proliferation of
keratinocytes and melanocytes. The condition most commonly associated with insulin
resistance is type 2 diabetes mellitus, but is also a prominent feature of obesity,
polycystic ovary syndrome, Donohue syndrome, and Rabson-Mendenhall syndrome.
Acanthosis nigricans may also be seen with certain medications that lead to elevated
insulin levels (e.g., glucocorticoids, niacin, insulin, oral contraceptives, and protease
inhibitors).[2]

Malignant
In the context of a malignant disease, acanthosis nigricans is a paraneoplastic syndrome
and is then commonly referred to as acanthosis nigricans maligna. Involvement of
mucous membranes is rare and suggests a coexisting malignant condition.[3]
When seen in individuals older than age 40, this disorder is commonly associated with an
internal malignancy, usually adenocarcinoma, and most commonly of the GI tract or
uterus; less commonly of the lung, prostate, breast, or ovary. The stomach is the most

common site.[4] Acanthosis nigricans of the oral mucosa or tongue is highly suggestive of
a neoplasm, especially of the GI tract.

Other
Other causes of acanthosis nigricans are familial, drug-induced and idiopathic.

Types
Classification of Acanthosis nigricans according to Schwartz, 1994 [5]
[6]

Benign acanthosis nigricans


Acanthosis nigricans associated with obesity
Syndromic acanthosis nigricans
Malignant acanthosis nigricans
Acral acanthosis nigricans
Unilateral acanthosis nigricans
Drug-induced acanthosis nigricans
Mixed acanthosis nigricans

Other Classifications of Acanthosis nigricans


Acanthosis nigricans may also be divided into the following types[7]:506:

Acral Acanthotic Anomaly (Acral Acanthosis Nigricans)


Acanthosis nigricans type I
Acanthosis nigricans type II
Acanthosis nigricans type III

Signs, tests, and misdiagnoses


Physicians can usually diagnose acanthosis nigricans by simply looking at a patient's
skin. 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.
Additionally acanthosis nigricans has similar visual characteristics (neck discoloration)
with Casal collar, which is a symptom of pellegra (a nutrient deficiency disease, easily
remedied with supplementation). In early stages of discoloration, it is hard for a non
trained eye to distinguish one from the other.

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. Acanthosis nigricans maligna may resolve if the causative tumor is


successfully removed.[8]

Prognosis
Acanthosis nigricans often fades if the underlying cause can be determined and treated
appropriately.

References