Acanthosis Nigricans - Human & Disease

Acanthosis Nigricans


 Acanthosis Nigricans

History  ¤ A cutaneous marker of insulin resistance states.  ¤ skin changes leading to patches of dark , velvety skin.  ¤ obesity , insulin resistance and polycystic ovary syndrome (PCOs) are risk factors.  ¤ Other etiologies: hereditary, endocrine disorders, obesity, drugs, hormonal changes and malignancy.  Seen in blacks > Hispanics > whites  ¤ Five types:  ° Type I (Familial)  - Exceedingly rare  - Autosomal dominant  - Present at birth or develops during childhood  - Worsens at puberty  - Not associated with an internal cancer  ° Type II (Benign AN)  - Associated with various endocrine disorders  - Examples include acromegaly, gigantism, Stein-Leventhal syndrome, Cushing’s, diabetes mellitus, hypothyroidism, Addison’s disease, hyperandrogenic states, and hypogonadal syndromes  ° Type III (formerly called Pseudo-AN;   however, this probably is the result of an endocrinopathy, namely insulin resistance)  - Most common form.  - Associated with obesity and insulin resistance states  - Not associated with malignancy  ° Type IV (Drug-induced):  - Nicotinic acid, niacinamide, diethylstilbestrol, triazineate, oral contraceptives, testosterone, topical fusidic acid, and glucocorticoids  - Seen in 10% of renal transplant patients
Acanthosis Nigricans








History


¤ A cutaneous marker of insulin resistance states.

¤ skin changes leading to patches of dark , velvety skin.

¤ obesity , insulin resistance and polycystic ovary syndrome (PCOs) are risk factors.

¤ Other etiologies: hereditary, endocrine disorders, obesity, drugs, hormonal changes and malignancy.

Seen in blacks > Hispanics > whites

¤ Five types:

° Type I (Familial)

- Exceedingly rare

- Autosomal dominant

- Present at birth or develops during childhood

- Worsens at puberty

- Not associated with an internal cancer

° Type II (Benign AN)

- Associated with various endocrine disorders

- Examples include acromegaly,
 gigantism, Stein-Leventhal syndrome, Cushing’s, diabetes mellitus, hypothyroidism, Addison’s disease, hyperandrogenic states, and hypogonadal syndromes

° Type III (formerly called Pseudo-AN; 

however, this probably is the result of an endocrinopathy, namely insulin resistance)

- Most common form.

- Associated with obesity and insulin resistance states

- Not associated with malignancy

° Type IV (Drug-induced):

- Nicotinic acid, niacinamide, diethylstilbestrol, triazineate, oral contraceptives, testosterone, topical fusidic acid, and glucocorticoids

- Seen in 10% of renal transplant patients

° Type V (Associated with malignancy):


- Rare

- Most often in adults

- Highly suspected if occurs in non-obese male

-Tends to be more widespread and involve mucosal surfaces

- Precedes 18%, accompanies 60%, or follows 22% the internal malignancy

- Most often associated with adenocarcinoma of gastrointestinal tract (60% stomach)

- Also associated with lung and breast adenocarcinoma

- Other cancers also seen.

History  ¤ A cutaneous marker of insulin resistance states.  ¤ skin changes leading to patches of dark , velvety skin.  ¤ obesity , insulin resistance and polycystic ovary syndrome (PCOs) are risk factors.  ¤ Other etiologies: hereditary, endocrine disorders, obesity, drugs, hormonal changes and malignancy.  Seen in blacks > Hispanics > whites  ¤ Five types:  ° Type I (Familial)  - Exceedingly rare  - Autosomal dominant  - Present at birth or develops during childhood  - Worsens at puberty  - Not associated with an internal cancer  ° Type II (Benign AN)  - Associated with various endocrine disorders  - Examples include acromegaly, gigantism, Stein-Leventhal syndrome, Cushing’s, diabetes mellitus, hypothyroidism, Addison’s disease, hyperandrogenic states, and hypogonadal syndromes  ° Type III (formerly called Pseudo-AN;   however, this probably is the result of an endocrinopathy, namely insulin resistance)  - Most common form.  - Associated with obesity and insulin resistance states  - Not associated with malignancy  ° Type IV (Drug-induced):  - Nicotinic acid, niacinamide, diethylstilbestrol, triazineate, oral contraceptives, testosterone, topical fusidic acid, and glucocorticoids  - Seen in 10% of renal transplant patients










Signs & Symptoms

¤ Often asymptomatic; skin looks “dirty”

¤ Velvety brown thickening of skin on intertriginous surfaces, most tcommonly the axilla, the neck.

¤ Other sites: genitalia, knuckles, lips, submammary area, umbilicus,eyelids, and conjunctiva.

What can be mistaken for acanthosis nigrican ?

- AN can be confused with physiological hyperpigmentation or lichen-simplex chronicus in some patients.

- it is associated with insulin resistance when found in diabetic or obese persons.

Tests

¤ Use history and physical as guide to appropriate workup

Basic Tests:

¤ Check blood glucose and possibly an insulin level.

History  ¤ A cutaneous marker of insulin resistance states.  ¤ skin changes leading to patches of dark , velvety skin.  ¤ obesity , insulin resistance and polycystic ovary syndrome (PCOs) are risk factors.  ¤ Other etiologies: hereditary, endocrine disorders, obesity, drugs, hormonal changes and malignancy.  Seen in blacks > Hispanics > whites  ¤ Five types:  ° Type I (Familial)  - Exceedingly rare  - Autosomal dominant  - Present at birth or develops during childhood  - Worsens at puberty  - Not associated with an internal cancer  ° Type II (Benign AN)  - Associated with various endocrine disorders  - Examples include acromegaly, gigantism, Stein-Leventhal syndrome, Cushing’s, diabetes mellitus, hypothyroidism, Addison’s disease, hyperandrogenic states, and hypogonadal syndromes  ° Type III (formerly called Pseudo-AN;   however, this probably is the result of an endocrinopathy, namely insulin resistance)  - Most common form.  - Associated with obesity and insulin resistance states  - Not associated with malignancy  ° Type IV (Drug-induced):  - Nicotinic acid, niacinamide, diethylstilbestrol, triazineate, oral contraceptives, testosterone, topical fusidic acid, and glucocorticoids  - Seen in 10% of renal transplant patients














Other Tests:

¤ Exclude malignancy in non-obese patients with no obvious cause.

¤ Screen for malignancy as appropriate for patients age, risk factors, and symptoms.

¤ Screen for endocrinopathy if suspected.

What hormone causes ancathosis nigrican ?

- Insulin , insulin resistance leads to type 2 diabetes , polycystic ovary syndrome and might be a factor in developing acanthosis nigrican. 


Management

What is the best treatment for acanthosis nigrican ?

- There is no specific treatment for acanthosis nigrican , your physician can suggest treatment for pain , color and odor of skin as creams , soaps , medication and laser therapy .


¤ Depends on cause:

° Weight loss if obese

° Treat underlying endocrinopathy

° Discontinue offending drug

° Treat underlying malignancy

What creams are best for AN ? 

- Keratolytics ( topical tretinon 0.05% , ammonium lactate 12% cream or combination of them).


¤ Topical urea, lactic acid and oral etretinate used with varied success.

History  ¤ A cutaneous marker of insulin resistance states.  ¤ skin changes leading to patches of dark , velvety skin.  ¤ obesity , insulin resistance and polycystic ovary syndrome (PCOs) are risk factors.  ¤ Other etiologies: hereditary, endocrine disorders, obesity, drugs, hormonal changes and malignancy.  Seen in blacks > Hispanics > whites  ¤ Five types:  ° Type I (Familial)  - Exceedingly rare  - Autosomal dominant  - Present at birth or develops during childhood  - Worsens at puberty  - Not associated with an internal cancer  ° Type II (Benign AN)  - Associated with various endocrine disorders  - Examples include acromegaly, gigantism, Stein-Leventhal syndrome, Cushing’s, diabetes mellitus, hypothyroidism, Addison’s disease, hyperandrogenic states, and hypogonadal syndromes  ° Type III (formerly called Pseudo-AN;   however, this probably is the result of an endocrinopathy, namely insulin resistance)  - Most common form.  - Associated with obesity and insulin resistance states  - Not associated with malignancy  ° Type IV (Drug-induced):  - Nicotinic acid, niacinamide, diethylstilbestrol, triazineate, oral contraceptives, testosterone, topical fusidic acid, and glucocorticoids  - Seen in 10% of renal transplant patients











Specific therapy:

Urea-containing products may give symptomatic relief.

Follow-up

¤ Varies dependent upon the association with an underlying disorder or disease

Complications and Prognosis

¤ Depends on underlying cause

¤ Obesity related AN improves with weight loss

¤ Endocrinopathy associated AN improves with treatment of underlying disease

¤ Removal of malignancy may be followed by regression of AN.
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