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PubMed1998

Analysis of the insulin receptor gene tyrosine kinase domain in obese patients with hyperandrogenism, insulin resistance and acanthosis nigricans (type C insulin resistance).

OBJECTIVE: To test the hypothesis that the triad of hyperandrogenism, insulin resistance and acanthosis nigricans (HAIR-AN syndrome) in the presence of obesity, also known as type C insulin resistance (type C), is caused by mutations at the tyrosine kinase domain of the insulin receptor gene. DESIGN: A candidate gene approach to study the molecular basis for a syndrome of obesity. SUBJECTS: 15 patients with type C insulin resistance and 25 control individuals. MEASUREMENTS: Analysis of polymerase chain reaction (PCR) products of exons 17 to 21 of the insulin receptor gene, comprising the tyrosine kinase domain, for single strand conformational polymorphisms (SSCP) and sequence analysis of exons with variant SSCP patterns. RESULTS: A synonymous C to T substitution in position 3 of codon 984, which does not alter the amino acid predicted, was found in one patient and in four of 25 control individuals. CONCLUSION: Type C insulin resistance is not commonly caused by mutations in the tyrosine kinase domain of the insulin receptor gene.

Acanthosis Nigricans↗
PubMed2002

Genes, growth factors and acanthosis nigricans.

Acanthosis nigricans (AN) occurs most commonly in association with hyperinsulinaemia and more rarely as a paraneoplastic syndrome. It is also a feature of several genetic disorders. Indirect evidence suggests a role for tyrosine kinase growth factor receptor signalling in the pathogenesis of AN. Defects in the insulin receptor gene causing insulin resistance and AN are well recognized, but recent data in several other syndromes of this association, including lipodystrophic disorders, have identified causative defects in other pathways. The mechanism of AN due to insulin resistance is most probably direct or indirect activation of the insulin-like growth factor 1 receptor by high levels of circulating insulin. However, more direct evidence for abnormal tyrosine kinase receptor signalling in AN has been provided by studies of craniosynostosis and skeletal dysplasia syndromes with AN, which have identified activating mutations in fibroblast growth factor receptors.

Acanthosis Nigricans↗
PubMed2000

Florid cutaneous and mucosal papillomatosis with acanthosis nigricans revealing a primary lung cancer.

This is the report of an 80-year-old patient with diffuse brownish hyperpigmentation and velvety thickening of the skin with onset 1 year before. Warty lesions on his limbs were present as well as papillomatous and verrucous lesions on his lips, mouth and eyelid conjunctivae with hyperkeratosis of the nipples. Biopsies, performed at different sites, showed histological pictures consistent with a diagnosis of acanthosis nigricans (AN) with florid cutaneous and mucosal papillomatosis. This type of AN is frequently associated with internal malignancy. In our patient serum levels of tissue polypeptide antigen, carcinoembryonic antigen, cytokeratin fragment and squamous cell carcinoma antigen were high and chest computed tomography scan indicated a large tumour infiltrating the right lung and extending to the mediastinum. Cytological examination of bronchial drainage revealed the presence of neoplastic cells, non-small cell type carcinoma. The most frequent cancer associated with malignant AN is gastric adenocarcinoma. Lung tumour has rarely been reported with AN. Malignant AN is sometimes associated with other cutaneous and mucosal warty lesions, as in our patient. These various skin and mucosal lesions are the expression of a systemic epithelial disorder and may help clinicians to suspect a malignant form of AN.

Acanthosis Nigricans↗
PubMedDate not supplied

Generalized acanthosis nigricans in early childhood.

Acanthosis nigricans (AN) is a disorder often accompanied by internal malignancy in adult patients, but in children it is usually benign. Generalized forms of AN, especially in childhood, are extremely rare. We report a 5-year-old boy with a 3-year history of AN who had generalized roughness and hyperpigmentation, numerous skin wrinkles, disseminated skin tags, tripe palms, and intensive pruritus. No clinical evidence of internal disorders, notably of an endocrinologic or neoplastic nature, have been detected thus far.

Acanthosis Nigricans↗
PubMedDate not supplied

Juvenile acanthosis nigricans and insulin resistance.

Acanthosis nigricans in obese adolescents is frequently associated with hyperinsulinemia and insulin resistance. We report three cases of this condition. In the early stage the skin lesions appeared to be erythematous and pruritic, mimicking an inflammatory dermatitis. Dietary control and oral metformin hydrochloride markedly improved the lesions. Topical calcipotriol may also help to control the skin condition.

Acanthosis Nigricans↗
PubMed2001

Altered GLUT1 and GLUT3 gene expression and subcellular redistribution of GLUT4: protein in muscle from patients with acanthosis nigricans and severe insulin resistance.

Multiple isoforms of glucose transporters are found in muscle, the tissue that normally accounts for 85% of insulin-stimulated glucose uptake. Glucose uptake into muscle cells in the fasting state is mediated primarily by GLUT1 and GLUT3 glucose transporters, whereas postprandial (insulin-stimulated) and exercise-related increments in muscle glucose uptake are mediated primarily by GLUT4. To determine if glucose transporters are abnormally expressed in muscle from insulin-resistant subjects, muscle samples were obtained from 10 normal subjects and 6 obese, nondiabetic subjects with severe insulin resistance and acanthosis nigricans. Both GLUT4 total protein and mRNA were normal in the insulin-resistant subjects. Muscle GLUT3 protein and mRNA were lower than controls by 62% and 71%, respectively. GLUT1 mRNA was twice normal, whereas GLUT1 protein content was not significantly increased. GLUT4 protein was markedly redistributed to the muscle plasma membrane in subjects with severe insulin resistance compared with normals (92% v 40% GLUT4 in plasma membrane-enriched fractions, P <.001), whereas the percentage of GLUT1 and GLUT3 protein found in the plasma membrane-enriched fractions was not different from controls. These data document differences in the expression of genes for GLUT1 and GLUT3 in muscle from normal and insulin-resistant subjects. Further, insulin resistance with fasting hyperinsulinemia was associated with a redistribution of GLUT4 to the muscle cell surface with no change in total GLUT4 protein. These data suggest that glucose transporter gene expression and their basal distribution in human muscle are related to insulin resistance and could be determinants of whole body insulin responsiveness.

Acanthosis Nigricans↗
PubMed2006

[Acanthosis nigricans, papillomatosis mucosae and "tripe palms" in a patient with metastasized gastric carcinoma].

HISTORY AND CLINICAL FINDINGS: A 48-year-old obese man presented with thickening, coarseness and hyperpigmentation of the skin, especially of the intertriginous areas, papillomatous to verrucous lesions of the lips and buccal oral mucosa, and hyperkeratosis of the palms ("tripe palms") and soles. He was obese, reported sleep apnea and had a history of hyperuricemia, mixed hyperlipidemia and previous myocardial infarction. He was on a maintenance dose of a proton pump inhibitor for chronic gastro-esophageal reflux. EXAMINATIONS: Immunohistochemical studies of the skin lesion revealed increased epidermal immunoreactivity for the melanocortin-1-receptor. Increased levels of tumor markers CA 19-9 (141100 U/ml), CA 72-4 (755 U/ml) and CEA (189 ng/ml) were found in the serum. Gastroscopic findings were suspicious of adenocarcinoma of the stomach: it was classified histologically as a signet-ring cell, non-mucinous adenocarcinoma. At the time of diagnosis the tumor had already metastasized to perigastric and peripancreatic lymph nodes with peritoneal carcinosis. TREATMENT AND COURSE: Since a curative resection was impossible a gastrojejunostomy was carried out. After this the patient received several courses of chemotherapy according to different schemes. Serum tumor marker levels and cutaneous signs regressed several times. CONCLUSIONS: Marked acanthosis nigricans -- especially when associated with further cutaneous markers of malignancy, e.g. mucocutaneous papillomatosis or so-called tripe palms -- calls for thorough search for malignant tumor, also if metabolic or endocrinological abnormalities co-exist. A pathogenetic role of a-melanocyte-stimulating hormone in the development of the skin changes is suggested.

Acanthosis Nigricans↗
PubMed1976

The syndromes of insulin resistance and acanthosis nigricans. Insulin-receptor disorders in man.

In six patients with acanthosis nigricans variable degrees of glucose intolerance, hyperinsulinemia and marked resistance to exogenous insulin were found. Studies of insulin receptors on circulating monocytes suggest that the insulin resistance in these patients was due to a marked decrease in insulin binding to its membrane receptors. When these patients were fasted, there was a fall in plasma insulin but no increase in insulin binding, suggesting that the receptor defect was not secondary to the hyperinsulinemia. The clinical features shared by these cases and several similar ones previously reported may be divided into two unique clinical syndromes: Type A, a syndrome in younger females with signs of virilization or accelerated growth, in whom the receptor defect may be primary, and Type B, a syndrome in older females with signs of an immunologic disease, in whom circulating antibodies to the insulin receptor are found.

Acanthosis Nigricans↗
PubMed2001

Relation of acanthosis nigricans to hyperinsulinemia and insulin sensitivity in overweight African American and white children.

OBJECTIVES: Acanthosis nigricans (AN) has been proposed as a reliable marker of hyperinsulinemia, but its utility for predicting hyperinsulinism has not been systematically evaluated in overweight children. We examined the relationship of AN to hyperinsulinemia and body adiposity. STUDY DESIGN: One hundred thirty-nine children underwent physical examination for AN, body composition studies, an oral glucose tolerance test, and a hyperglycemic clamp. RESULTS: Thirty-five children (25%) had AN. AN was more prevalent in African Americans (50.1%) than in white subjects (8.2%, P < .001). Independent of race, children with AN had greater body weight and body fat mass (P < .001); greater basal and glucose-stimulated insulin levels during oral glucose tolerance test (P < .001); greater first-phase, second-phase, and steady-state insulin levels (P < .001); and lower insulin sensitivity (P < .001) during the hyperglycemic clamp. After adjusting for body fat mass and age, none of these differences remained significant. When categorized by fasting insulin, 35% with fasting insulin levels > 20 microU/mL and 50% with fasting insulin levels > 15 microU/mL did not have AN. Eighty-eight percent of children with fasting insulin levels > or = 15 microU/mL had a body mass index SD score > or = 3.0. CONCLUSIONS: AN is not a reliable marker for hyperinsulinemia in overweight children. Children with a race-, sex-, and age-specific body mass index SD scores > or = 3.0 should be screened for hyperinsulinemia, whether or not they have AN.

Acanthosis Nigricans↗
PubMed2006

Genetic factors and clinical significance of acanthosis nigricans in obese Japanese children and adolescents.

AIM: To clarify the clinical significance of acanthosis nigricans (AN) and the association of gene polymorphisms in the ss2- and ss3-adrenergic receptors (B2ADR and B3ADR) in Japanese obese children and adolescents. METHODS: Seventy obese subjects (56 boys, 14 girls) from 5 to 19 y of age were examined as to clinical features. Genetic analyses were performed in 83 obese subjects (61 boys, 22 girls), 2 to 17 y of age. Typing of gene polymorphisms in B2ADR and B3ADR was achieved by polymerase chain reaction (PCR) of genomic DNA and restriction fragment-length polymorphism analysis (PCR-RFLP). RESULTS: The group with AN (n = 30) had higher values for percent overweight, BMI, waist circumference, fasting insulin, HOMA-R, leptin and PAI-1 than the AN-negative group (n = 40), but there were no significant differences in age, sex or percent body fat between the two groups. The prevalences of B2ADR Gly16 and B3ADR Arg64 were significantly higher in AN-positive (n = 26) than in AN-negative (n = 57) subjects. In addition, the AN frequency was significantly higher in the group with both Gly16 and Arg64 than in the group with neither of these alleles (55.6% vs 12.5%, p < 0.05). CONCLUSION: We demonstrate that AN is a useful clinical marker for the severity of obesity associated with a high BMI, and that B2ADR Gly16 and B3ADR Arg64 are associated synergistically with AN in obese children and adolescents.

Acanthosis Nigricans↗
PubMed1985

Mycosis fungoides simulating acanthosis nigricans.

In this paper, an unusual papillomatous variant of the plaque stage of mycosis fungoides with clinical similarities to acanthosis nigricans is described. In contrast to the classic plaque stage of mycosis fungoides, the dermal infiltrates in this patient showed a rather monomorphous proliferation of blast-like cells that had little or no tendency to infiltrate the epidermis.

Acanthosis Nigricans↗
PubMed1989

Crouzon's syndrome associated with acanthosis nigricans: ramifications for the craniofacial surgeon.

Crouzon's syndrome is one of many disorders that have been associated with acanthosis nigricans. Previously reported cases documenting this association have been reviewed, and additional cases that have been treated at the Institute of Reconstructive Plastic Surgery at New York University Medical Center have been added. Recommendations for the surgical management of this unique group of patients are presented.

Acanthosis Nigricans↗
PubMed1992

Mutations in the insulin receptor gene in patients with genetic syndromes of insulin resistance and acanthosis nigricans.

Mutations of the insulin receptor gene have been identified in patients with genetic syndromes of insulin resistance associated with acanthosis nigricans. These mutations impair insulin responses by reducing the number of insulin receptors on the surface of target cells, or by reducing the receptor's ability to bind insulin or to undergo insulin-stimulated autophosphorylation, an important step in insulin action. Studies of mutant receptors expressed in transfection systems have contributed to our understanding of the structure-function relationships of the insulin receptor.

Acanthosis Nigricans↗
PubMed1978

Complete reversibility of paraneoplastic acanthosis nigricans after operation.

A patient with widespread acanthosis nigricans is described. No abdominal tumour was found. Explorative thoracotomy disclosed numerous enlarged lymph glands containing squamous cell carcinoma. The left lung was removed but meticulous search did not disclose any tumour. The glands were removed as radically as possible. After the operation the skin improved and the lesions have disappeared completely. The observation time is over three years.

Acanthosis Nigricans↗
PubMed1988

Acanthosis nigricans, insulin resistance and cutaneous virilism.

Thirteen patients with the syndrome of acanthosis nigricans and insulin resistance are described. They all had a combination of dermatoses related to hyperandrogenism (cutaneous virilism): hirsuties (II), acne vulgaris (6), hidradenitis suppurativa (5) and androgenic alopecia (4). In addition, 9 out of 13 had keratosis pilaris. The patients had raised fasting plasma insulin levels compared with matched normal controls (P less than 0.01) and increased insulin resistance (P less than 0.02). Insulin resistance correlated with total serum testosterone (rs = 0.65; P less than 0.02).

Acanthosis Nigricans↗
PubMed1995

Association of acanthosis nigricans with insulin resistance in patients with polycystic ovary syndrome.

This study was designed to explore the association of insulin resistance and acanthosis nigricans (AN) in patients with polycystic ovary syndrome (PCOS). Fifty women, 18-37 years old, were included in the study, and divided into five groups consisting of: (I) 10 women with PCOS, abnormal body mass index (BMI) and AN; (II) 10 women with PCOS and abnormal BMI, but without AN; (III) 10 women with PCOS, normal BMI, and no AN; (IV) 10 women with abnormal BMI, but without PCOS or AN; and (V) 10 healthy women with normal BMI. Measurement of fasting glucose and insulin levels before and after oral glucose challenge was performed. Fasting serum insulin levels were found to be significantly lower in groups III, IV and V than in groups I and II, with no significant difference between groups I and II, or between groups III, IV and V. Total insulin response following administration of glucose did not differ significantly between the groups. These findings support the view that obese PCOS patients with AN do not have significantly higher insulin resistance than obese patients without AN. Insulin resistance is a necessary, but not the only, factor leading to the development of AN in patients with PCOS. Other factors should also be considered in the pathogenesis of this cutaneous reaction.

Acanthosis Nigricans↗
PubMed1982

Acanthosis nigricans, hirsutism, insulin resistance and insulin receptor defect.

A 24-year-old negress with the triad of acanthosis nigricans, hirsutism associated with polycystic ovaries and insulin resistance is reported. Metabolic studies were done 3 years after a bilateral ovarian wedge resection. Partial remission of the hirsutism and return of menstrual cycles occurred after surgery. Extreme resistance to endogenous and exogenous insulin was observed. Three studies of insulin receptors on circulating red blood cells (RBC) showed abnormal inhibition-competition curves, characterized by increased percentage insulin binding at higher unlabelled insulin levels. Scatchard plots suggested an apparent increase in the number of low affinity receptors. Despite the changes in receptor-insulin interaction, the defect does not seem to explain the insulin resistance since binding of insulin to a target tissue (RBC) appeared to be quantitatively normal at physiological insulin levels, suggesting a simultaneous post receptor defect.

Acanthosis Nigricans↗