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PubMed1989

Insulin resistance and acanthosis nigricans, type A: case report.

A 9-year-old Somali girl was referred to the Paediatric Diabetic Clinic, Al-Amiri Hospital for control of her diabetes. On physical examination, she was found to have several somatic abnormalities and acanthosis nigricans. Biochemical and hormonal investigations revealed no major abnormalities apart from that of glucose metabolism. Insulin resistance was detected early on initiating treatment and, even with high doses, it was impossible to achieve normoglycaemia. This case is similar to other cases described in the literature with insulin resistance and acanthosis nigricans type A.

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PubMed1999

A novel skeletal dysplasia with developmental delay and acanthosis nigricans is caused by a Lys650Met mutation in the fibroblast growth factor receptor 3 gene.

We have identified a novel fibroblast growth factor receptor 3 (FGFR3) missense mutation in four unrelated individuals with skeletal dysplasia that approaches the severity observed in thanatophoric dysplasia type I (TD1). However, three of the four individuals developed extensive areas of acanthosis nigricans beginning in early childhood, suffer from severe neurological impairments, and have survived past infancy without prolonged life-support measures. The FGFR3 mutation (A1949T: Lys650Met) occurs at the nucleotide adjacent to the TD type II (TD2) mutation (A1948G: Lys650Glu) and results in a different amino acid substitution at a highly conserved codon in the kinase domain activation loop. Transient transfection studies with FGFR3 mutant constructs show that the Lys650Met mutation causes a dramatic increase in constitutive receptor kinase activity, approximately three times greater than that observed with the Lys650Glu mutation. We refer to the phenotype caused by the Lys650Met mutation as "severe achondroplasia with developmental delay and acanthosis nigricans" (SADDAN) because it differs significantly from the phenotypes of other known FGFR3 mutations.

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PubMed2005

Acanthosis nigricans as an adverse effect of highly active antiretroviral therapy in an adolescent girl with human immunodeficiency virus infection.

We report an 11-year-old girl with acanthosis nigricans that appeared after 4 years of treatment with didanosine, stavudine and amprenavir. Laboratory studies showed hyperglycemia, hyperinsulinemia and hypertriglyceridemia. Withdrawal of amprenavir resulted in disappearance of acanthosis nigricans and improvement of metabolic abnormalities.

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PubMed1997

Acanthosis nigricans associated with hepatolenticular degeneration.

Acanthosis nigricans and hepatolenticular degeneration (Wilson's disease) developed simultaneously in a 16-year-old boy. The diagnosis of Wilson's disease was based on the clinical presentation, including Kayser-Fleischer ring, hypoceruloplasminemia, hypocupremia, and hypercupriuria. His skin lesions were characterized by thick, dark brown, verrucous plaques on the dorsa of both feet, the neck, axillae, and groin. The histological findings were compatible with acanthosis nigricans. Six months after treatment with D-penicillamine, two grams per day, his skin lesions and neurological symptoms were much improved and no complications were observed.

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PubMed1995

Familial acanthosis nigricans with madarosis.

We report familial acanthosis nigricans affecting a 35-year-old woman, her 7-year-old son and 5-year-old daughter. Absence of the eyebrows and eyelashes was noted in this family. The mother had no axillary hair and her pubic hair was sparse. The boy also suffered from congenital heart disease and a congenital cataract in the left eye. The combination of acanthosis nigricans and ectodermal defects in this family may represent a distinct nosological entity.

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PubMed1991

Florid cutaneous papillomatosis, malignant acanthosis nigricans, and pulmonary squamous cell carcinoma.

A 72-year-old man had florid cutaneous papillomatosis (FCP), which is an obligatory paraneoplastic syndrome always associated with an internal malignancy. The cancer, which is usually intraabdominal and most often gastric in origin, evolves parallel to the FCP. This patient is the first case of FCP occurring in association with a lung malignancy. An association of FCP with other signs of internal cancer is common, with malignant acanthosis nigricans usually appearing many times with the sign of Leser-Trélat. FCP, malignant acanthosis nigricans, and the sign of Leser-Trélat are part of a continuum, developing by a common or similar pathogenic pathway due to an underlying malignancy producing a factor possibly similar to human epidermal growth factor.

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PubMed2004

Oral acanthosis nigricans, tripe palms and sign of leser-trélat in a patient with gastric adenocarcinoma.

Acanthosis nigricans (AN), tripe palms (TP) and the sign of Leser-Trélat (LT) may be seen with the presence of malignancy. Acanthosis nigricans may have a mucocutaneous localization involving the oral mucosa with papillomatous and verrucous lesions usually on the lips and buccal mucosa. These paraneoplastic dermatoses are generally linked with intra-abdominal malignancy, most often gastric adenocarcinoma. Improvement of the associated dermatoses after the treatment of the malignancy has been frequently observed. We report the case of a 53-year-old man suffering from advanced gastric adenocarcinoma, in which metastases seemed to sustain all three paraneoplastic dermatoses. To the best of our knowledge this is the first case of a patient showing manifestations of all three paraneoplastic dermatoses. Patients presenting with this set of dermatoses should be suspected to harbor an occult malignancy, or have persistence of a known malignancy.

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PubMed2003

Acanthosis nigricans is a reliable cutaneous marker of insulin resistance in obese Japanese children.

BACKGROUND: Acanthosis nigricans (AN) is a skin condition characterized by darkening and thickening of skin with formation of irregular folds, usually limited to a few specific areas of the body. Recently, AN has been reported to be linked to hyperinsulinemia and obesity. The aim of the present study was to determine whether or not the presence of AN in obese Japanese children is a reliable cutaneous marker. METHODS: The authors analyzed the clinical characteristics of 439 obese Japanese children (260 boys, 179 girls; mean age 10.1 years; mean percentage overweight 51.9%), who had visited Tsuruoka City Shonai Hospital in 1990-2000. Eighty-two of the 439 children were examined using an oral glucose tolerance test (OGTT). Of these children, the authors retrospectively studied 16 subjects: eight with AN and eight without AN (age range: 10.8-13.9 years; percentage overweight range: 54.3-97.0%). They were age and percentage obesity-matched males with normal glucose tolerance during OGTT. Females with normal glucose tolerance during OGTT were excluded from the 16 subjects because the number was too small and children with impaired glucose tolerance or type 2 diabetes during OGTT were also excluded because of glucose toxicity. Eighty-two children including the 16 subjects were analyzed at their first visit for the presence or absence of AN on the posterior of the neck, and for characteristics including age, birthweight, body height, bodyweight, percentage overweight, blood pressure, liver function markers serum lipid concentrations, fasting plasma glucose concentrations and insulin concentrations shown by the results of OGTT. RESULTS: (1) Children with AN showed significantly more glucose intolerance including impaired glucose tolerance and type 2 diabetes compared with those children without AN, and fasting plasma insulin concentrations were most significantly correlated with the presence of AN. (2) Insulin resistance based on fasting plasma insulin concentrations was seen in significantly more children with AN than in children without AN, even in age and percentage obesity-matched subjects with normal glucose tolerance during OGTT. CONCLUSIONS: Acanthosis nigricans could be a reliable cutaneous marker of insulin resistance in obese Japanese children.

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PubMed1995

Acanthosis nigricans: a marker for hyperinsulinemia.

A 12-year-old girl developed acanthosis nigricans due to increased levels of serum insulin. Hyperinsulinemia has been recognized as the underlying cause in most cases of acanthosis nigricans. In this paper we outline a typical clinical case with special regard to the proposed pathogenesis.

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PubMed1982

Insulin resistance in a child with Acanthosis nigricans type A.

The patient, a female 6 years 4 months old, diagnosed as affected by Acanthosis nigricans and diabetes mellitus was referred to our Clinic for further investigation of her glucose metabolism. She had a typical face with hypertelorism, prognathism, macroglossia and large auricles. The skin was hyperpigmented, verrucous, hyperkeratotic especially in the folds and flexural areas with small papillomatous or nodular growth; diffused hypertrichosis and hypertrophic clitoris were also present. Biochemical and hormonal investigations revealed no major abnormalities apart from glucose metabolism. After an unsuccessful trial with conventional insulin therapy, endovenous continuous insulin infusion was started: even with 32 U/kg/h it was not possible to achieve normoglycemia. Insulin receptors were studied on erythrocytes: 125I-insulin binding (specific) was clearly lower than normal. The concentration of insulin receptors was reduced, while the average affinity profile was normal. The study of erythrocyte insulin receptors has demonstrated that insulin resistance in this patient is due to a decrease in the number of receptors, i.e. Acanthosis nigricans type A.

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PubMed1984

Insulin-specific binding to erythrocytes in 6 girls with acanthosis nigricans.

6 girls, aged 4-16 years, with acanthosis nigricans and hirsutism were studied. Fasting and postglucose hyperinsulinism was present in the 5 older girls. In the youngest, a transitory diabetes with hyperinsulinism was induced by a cortisone therapy for hepatitis. Insulin resistance, suggested by the failure to significantly decrease blood glucose after insulin injection (0.1 U/kg), was demonstrated in three steps: (1) Patient plasma failed to bind 125I-insulin after a 5-day incubation followed by precipitation by antihuman globulin serum. (2) Specific 125I-insulin binding to rat liver membranes was identical in the presence of patient plasma and control plasma. (3) Specific 125I-insulin binding to the erythrocytes of the 6 patients (3.5-7.0%) was significantly lower (p less than 0.01) than in controls (4.5-19.5%). Moreover, the significant correlation present in controls between total binding and reticulocyte counts (r = 0.824, p less than 0.001) was absent in the patients. These data demonstrate further that, in the juvenile type of acanthosis nigricans, insulin resistance which may precede hyperinsulinism is not related to anti-insulin antibodies nor to antireceptor antibodies, but results from a primary defect of insulin receptors.

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PubMed1990

A syndrome of hyperandrogenism, insulin resistance, and acanthosis nigricans associated with polycystic ovary syndrome: clinical and laboratory features.

We describe an adolescent Japanese girl with acanthosis nigricans and irregular anovulatory menstruation following menarche. Serum LH levels were elevated, whereas serum FSH levels were within normal range. An exaggerated response to LHRH was observed. Further, serum androstenedione levels were markedly elevated. Ultrasonogram revealed bilateral polycystic changes of ovaries. She had a mild degree of insulin resistance. Insulin binding studies using erythrocytes demonstrated a decreased binding capacity of insulin. From the above findings, this patient presents the syndrome consisting of hyperandrogenism, insulin resistance, and acanthosis nigricans and also has clinical and biochemical features compatible with polycystic ovary syndrome.

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PubMed1980

Acanthosis nigricans associated with adenocarcinoma of the thyroid gland.

The association between acanthosis nigricans (malignant type) and internal malignant tumour is well established. In the majority of cases the malignant tumour is localized to the gastrointestinal tract or the thoracic cavity. The malignant tumour is believed to be an adenocarcinoma in most cases. A case of malignant acanthosis nigricans associated with a follicular adenocarcinoma of the thyroid gland in a 31-year-old white male with congenital hypothyroidism and eruptive xanthomas due to hyperlipoproteinemia of type V (Frederickson) is reported.

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PubMed1997

Systemic lupus erythematosus with acanthosis nigricans, hyperpigmentation, and insulin receptor antibody.

Acanthosis nigricans, insulin receptor antibody, and systemic lupus erythematosus are associated in the potentially lethal syndrome of type B insulin resistance. Hyperpigmentation has been reported rarely, while glucose intolerance is common in these patients. We report an adolescent girl with acanthosis nigricans, hyperpigmentation, insulin receptor antibody, and systemic lupus erythematosus without glucose intolerance. Insulin resistance may be mild or transient in some patients with type B insulin resistance. Resolution of skin lesions was noted during therapy of SLE, and was associated with disappearance of insulin receptor antibody.

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PubMed2000

The molecular and genetic basis of fibroblast growth factor receptor 3 disorders: the achondroplasia family of skeletal dysplasias, Muenke craniosynostosis, and Crouzon syndrome with acanthosis nigricans.

Achondroplasia, the most common form of short-limbed dwarfism in humans, occurs between 1 in 15,000 and 40,000 live births. More than 90% of cases are sporadic and there is, on average, an increased paternal age at the time of conception of affected individuals. More then 97% of persons with achondroplasia have a Gly380Arg mutation in the transmembrane domain of the fibroblast growth factor receptor (FGFR) 3 gene. Mutations in the FGFR3 gene also result in hypochondroplasia, the lethal thanatophoric dysplasias, the recently described SADDAN (severe achondroplasia with developmental delay and acanthosis nigricans) dysplasia, and two craniosynostosis disorders: Muenke coronal craniosynostosis and Crouzon syndrome with acanthosis nigricans. Recent evidence suggests that the phenotypic differences may be due to specific alleles with varying degrees of ligand-independent activation, allowing the receptor to be constitutively active. Since the Gly380Arg achondroplasia mutation was recognized, similar observations regarding the conserved nature of FGFR mutations and resulting phenotype have been made regarding other skeletal phenotypes, including hypochondroplasia, thanatophoric dysplasia, and Muenke coronal craniosynostosis. These specific genotype-phenotype correlations in the FGFR disorders seem to be unprecedented in the study of human disease. The explanation for this high degree of mutability at specific bases remains an intriguing question.

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PubMed1985

Insulin resistance, acanthosis nigricans, and polycystic ovaries associated with a circulating inhibitor of postbinding insulin action.

A 21-yr-old moderately obese woman with hirsutism, acanthosis nigricans, and oligomenorrhoea was diagnosed as having polycystic ovary syndrome. Despite hyperinsulinemia, binding of insulin to her red cells was within the range for normal, young adult subjects. Her serum did not bind or degrade [125I]insulin or alter its binding to fat cells, and was negative for insulin receptor antibodies. However, her serum caused a dose-dependent inhibition of insulin-stimulated lipogenesis (conversion of [3-3H]glucose to [3H]lipid) in rat fat cells significantly greater than that produced with control serum (relative potency, 3.5:1) and (at a 1:20 dilution) markedly impaired the response of both lipogenesis and 2-deoxy-D-glucose uptake to maximum concentrations of insulin. After the patient was treated with clomiphene for 4 months, her menses resumed, hair growth slowed, fasting blood glucose and plasma insulin concentrations decreased, and serum inhibitory activity decreased to the control range. Serum inhibitory activity was stable to freezing and thawing and to heating at 56 C for 30 min, and could be extracted into acid-ethanol. By dialysis, its mol wt was below 1000, whereas by ultracentrifugation, it was above 3500; both high and low mol wt forms were detected after Sephadex G-50 gel chromatography of serum, suggesting that the inhibitor was of low mol wt but loosely bound to a higher mol wt component in serum. These findings indicate that insulin resistance in this patient with acanthosis nigricans and polycystic ovaries could be attributed to a circulating low mol wt inhibitor of postbinding insulin action.

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PubMed1986

Functional characteristics of decreased insulin receptors on fibroblasts obtained from a subject with severe insulin resistance and acanthosis nigricans.

In a patient with severe insulin resistance and acanthosis nigricans, a decrease in the number of insulin receptors has been found on freshly isolated monocytes and cultured fibroblasts compatible with a primary or genetic decrease in cell-surface insulin receptors. To determine the functional characteristics of the remaining receptors on these cells, insulin-stimulated glucose uptake, insulin internalization, and insulin-induced receptor loss were evaluated in monolayer fibroblasts obtained from this subject. Maximal insulin stimulation of 2-deoxyglucose was markedly blunted, compatible with abnormal insulin responsiveness due to a functional impairment of the remaining receptors. In the presence of chloroquine, the acanthotic subject's fibroblasts internalized more insulin per available receptor compared with the normal cell line, suggesting an accelerated rate of insulin internalization. When the rate of insulin internalization was more directly determined by assessing the rate of appearance of acid-resistant, cell-associated radioactivity at 37 degrees C, a similar increase in insulin internalization rate was evident. When downregulation was assessed, insulin's ability to induce receptor loss in the acanthotic subject's cell line was augmented. Thus, a primary or genetic decrease in insulin receptors on cultured fibroblasts from a patient with acanthosis nigricans and insulin resistance is associated with functional impairment of the remaining receptors leading to significant alterations in ligand processing and subsequent insulin action.

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PubMed1993

Acanthosis nigricans and bile duct malignancy.

A case of acanthosis nigricans associated with a metastatic adenocarcinoma is presented. To our knowledge this is the first one reported in the literature. The primary tumour is unknown, but it is presumably a cholangiocarcinoma. The skin changes preceded the detection of malignancy by 2 years, during which the skin lesions progressed though the patient was still in good health. If malignant acanthosis nigricans is suspected and the underlying malignancy cannot be found at the initial screening, repeated screenings are necessary because of the time factor.

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