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Skin changes may be the first clue to a neoplastic process at a stage when it still is treatable (Such as the development of Acanthosis Nigrican (AN) in an otherwise healthy adult). Ninety percent of the neoplasm responsible for the development of AN originate in the abdomen. The tumor, even in a subclinical state, seems to possess unidentified properties that activate the dermatosis.
Acanthosis nigricans (AN) and scleredema are two skin conditions that have been reported in association with diabetes mellitus. Few cases associating scleredema and AN have been reported. A literature search did not reveal any reports of diabetic patients developing AN on top of a scleredema plaque. Here we report a patient with diabetes mellitus who developed AN within the same indurated scleredema plaque.
Malignant acanthosis nigricans is a dermatosis that appears grossly as a hyperpigmented, velvety, or verrucous hyperplasia of the epidermis, most marked in flexural areas. It is always associated with a malignancy. In 277 cases reviewed, the condition was associated with gastric carcinomas in 55.5%, with other intra-abdominal carcinomas in 17.7%, and with malignancies in other sites in 26.8%. Current theories for the association and pathogenesis of the cutaneous process are discussed.
Diabetes affects 6% of the national population, yet approximately 50% of persons with diabetes remain undiagnosed and receive no treatment. In specific populations, Acanthosis Nigricans (AN) may serve as an early clinical proxy marker of increased risk of type II diabetes. The results of this pilot project to screen selected school age students in New Mexico for AN indicate that a large number of these students may be at increased risk for developing type II diabetes as young adults. The future burden of diabetes on individuals, families, communities, and health care systems may be greater than previously recognized.
Hypothyroidism is not commonly associated with acanthosis nigricans (AN). We examined a 13-year-old girl with AN, hypertrichosis, and Hashimoto's thyroiditis. Overt biochemical hypothyroidism, thyroid enlargement, and positive titers of antimicrosomal and antithyroglobulin antibodies confirmed Hashimoto's thyroiditis. Both AN and hypertrichosis resolved with thyroid hormone replacement. There was no evidence of insulin resistance, polycystic ovarian disease, lipoatrophy, or other endocrine dysfunction, or of malignancy. In two patients from the literature with AN and hypothyroidism, AN was attributed to associated thyroid carcinoma or insulin resistance, rather than coexisting hypothyroidism. Since the skin lesions improved with thyroid hormone therapy in those two patients and in ours, hypothyroidism appears to be directly involved in the pathogenesis of AN.
A number of craniofacial malformation syndromes are characterized by prominent abnormalities of the skin, hair, nails, and mucous membranes. Crouzon disease has been reported in association with severe acanthosis nigricans in 12 patients. We report a new case of this association in a 16-year-old woman with multiple melanocytic nevi. Melanocytic nevi have been already reported in the medical literature in association with several congenital syndromes, although, to our knowledge, not with Crouzon disease.
We present a case of malignant acanthosis nigricans (AN) that initially manifested in the oral cavity. In the present report, the patient had typical clinical and histological findings of oral and esophageal AN, with subtle skin changes, associated with a gallbladder adenocarcinoma. The importance of the clinical oral examination is emphasized because the recognition of oral lesions led to the diagnosis of AN and to the following detection of the internal malignancy. Since the tumours associated with AN are highly malignant, it is of the utmost importance to recognize the skin and mucous membrane changes in adults.
In a series of transgenic mice, the human tissue collagenase gene was expressed in the suprabasal layer of the skin epidermis. Visually, the mice had dry and scaly skin which upon histological analysis revealed acanthosis, hyperkeratosis, and epidermal hyperplasia. At the ultrastructural level, intercellular granular materials were absent in the transgenic skin epidermis but contact was maintained through the intact desmosomes. Despite a diversity of underlying etiologies, similar morphological hyperproliferative changes in the epidermis are observed in the human skin diseases of lamellar ichthyosis, atopic dermatitis, and psoriasis. Subsequent experiments demonstrate that when the transgenic mouse skin was treated once with an initiator (7,12-dimethyl-benz[a]anthracene) and then twice weekly with a promoter (12-O-tetradecanoylphorbol-13-acetate), there was a marked increase in tumor incidence among transgenic mice compared with that among control littermates. These experiments demonstrate that by overexpressing the highly specific proteolytic enzyme collagenase, a cascade of events leading to profound morphological changes which augment the sensitivity of the skin towards carcinogenesis is initiated in the epidermis.
Mutations in the fibroblast growth factor receptor 2 (FGFR2) gene have previously been identified in Crouzon syndrome, an autosomal dominant condition involving premature fusion of the cranial sutures. Several different missense and other mutations have been identified in Crouzon syndrome patients, clustering around the third immunoglobulin-like domain. We report here the identification of a mutation in the transmembrane region of FGFR3, common to three unrelated patients with classical Crouzon syndrome and acanthosis nigricans, a dermatological condition associated with thickening and abnormal pigmentation of the skin. The mutation within the FGFR3 transcript was determined by direct sequencing as a specific gcg to gag transversion, resulting in an amino acid substitution ala391glu within the transmembrane region.
OBJECTIVE: To determine the prevalence of acanthosis nigricans (AN) in type 2 diabetes mellitus (T2DM) and its correlation with various anthropometric measurements in Indians. METHODS: One hundred and fifty consecutive subjects with T2DM attending the diabetes clinic at a tertiary referral centre in North India were considered as cases and 150 age and sex matched healthy attendants of non-diabetic subjects as controls. All the cases and controls were screened for the presence of AN and its severity. Anthropometric measurements of all of them were measured in standard method. Regression analysis was done to determine the association of AN with T2DM and various anthropometric measurements. RESULTS: The prevalence of AN in subjects with diabetes and healthy controls was 62.6% and 40% respectively, and this difference was significant (p<0.05). Body mass index (BMI) between cases and controls was comparable by chance. There was a statistically significant correlation of increasing severity of AN with increasing BMI, waist circumference, hip circumference, waist-hip ratio, skinfold thickness, and body fat percentage in diabetic patients. However, in regression analysis after considering all the confounding factors there was a significant correlation of AN, only with diabetes mellitus and BMI. CONCLUSIONS: Indians have high prevalence of AN and it is an independent cutaneous marker of both T2DM and BMI.
We describe a woman with the syndrome characterised by hyperandrogenism, insulin resistance and acanthosis nigricans (the HAIR-AN syndrome), and an associated insulinoma (islet B-cell tumour), whose signs and symptoms cleared after partial pancreatectomy.
We report on a 27-year-old man with acanthosis nigricans (AN) associated with severe obesity, insulin resistance and hypothyroidism. A very low-calorie diet treatment decreased his weight and then ameliorated the insulin-resistant state. These effects were followed by remarkable improvement of the AN prior to the correction of the hypothyroidism. This confirms that AN may be mainly attributed to insulin resistance rather than hypothyroidism per se.
A 19-year-old Japanese man with confluent and reticulated papillomatosis (CRP) is presented. He was an obese and dark-complexioned man, who had impaired glucose tolerance and hyperinsulinemia. The clinical and histological findings were consistent with the diagnosis of CRP. He also had acanthosis nigricans (AN) on his axillae and nape. Neither spores nor hyphae were detected from scales; antifungal treatment had no benefit. Although the reduction of his weight was unsuccessful, oral etretinate therapy resulted in considerable improvement of both CRP and AN. We reviewed previous case reports in terms of the relation between CRP and AN. Although the two conditions are usually differentiated because of their distinctive clinical features, a close relationship was noted between CRP and AN.
A patient is described who developed hyperkeratotic, hyperpigmented plaques, similar to acanthosis nigricans in re-epithelializing erosions of pemphigus foliaceus. The lesions regressed completely after a few months. This phenomenon can be attributed to a Köbner phenomenon after epidermal damage or can be a result of systemic corticosteroid therapy.
The prevalences of obesity and of non-insulin dependent diabetes mellitus (NIDDM) have increased in the United States population over the past two decades, and thus diabetes prevention has become a major concern of public health agencies such as the National Institutes of Health. Identification of individuals at risk for diabetes is an essential first step in designing and implementing intervention programs. Insulin resistance is the hallmark of the pathophysiology of NIDDM. Subjects with hyperinsulinemia, impaired glucose tolerance, or gestational diabetes are well accepted as being at high risk for diabetes. We propose that the easily identifiable skin lesion, acanthosis nigricans, is common in the major minority groups in the United States and that its presence is a surrogate for laboratory-determined hyperinsulinemia.
We have studied insulin binding to cultured skin fibroblasts from a patient with the Type A syndrome of insulin resistance and acanthosis nigricans. Insulin binding was decreased aobut 50% at low insulin concentrations. This was due to a decrease in receptor affinity and in increase in the rate of dissociation of insulin from the receptor. In addition, there was a loss of negative cooperativity, as measured by the ability of unlabeled insulin to accelerate dissociation. This defect in the receptor was stable for up to 16 passages of the cells. By contrast, binding of epidermal growth factor did not differ from control. These data suggest that the Type A syndrome of insulin resistance is due to a primary, and possibly genetic, defect in the insulin receptor.
We previously reported that circulating beta-endorphin levels are increased in obese hirsute women and that plasma immunoreactive insulin (IRI) levels are increased in proportion to the degree of hyperandrogenism in women with the polycystic ovary (PCO) syndrome. We, therefore, tested the hypothesis that endogenous opiates are at least partially responsible for the hyperinsulinemia and insulin resistance in this syndrome. In the first study, acute naloxone administration significantly reduced the plasma IRI response and IRI/glucose ratio in three euglycemic obese women with PCO and acanthosis nigricans (AN) and marked insulin resistance, but did not alter the glucose response. Naloxone had no effect on these parameters in the normal weight control subjects. In the second study, nalmefene, a new, orally active opiate antagonist, reduced IRI and the IRI/glucose ratio in four women with PCO-AN and marked hyperinsulinemia in a randomized, double blind, crossover protocol. We conclude that endogenous opiates are at least partially responsible for the hyperinsulinemia and insulin resistance in PCO-AN.
This study examined the prevalence of both basal and glucose-stimulated hyperinsulinemia and acanthosis nigricans (AN) as well as the relationship between insulin and androgen levels in hyperandrogenic women. Sixty-two women who had an elevation of 1 or more plasma androgen levels were studied. The results in these women, grouped for analysis on the basis of obesity and ovulatory status, were compared to those in 36 control women of similar ages and weights. The anovulatory hyperandrogenic women had the clinical and biochemical features of the polycystic ovary syndrome (PCO). Oral glucose tolerance tests were performed with measurement of glucose, insulin, sex hormone-binding globulin (SHBG), and total and non-SHBG-bound sex steroid levels. AN was present in 29% of the hyperandrogenic women, the majority of them obese. Fifty percent of obese PCO women had AN, but they did not otherwise differ from PCO women lacking this dermatological change. Only women with PCO had significant hyperinsulinemia independent of obesity, and obese PCO women with AN had the highest serum insulin levels. Plasma glucose values during the oral glucose tolerance test were significantly increased in obese PCO women independent of the presence of AN, and 20% of these women had frank impairment of glucose tolerance. Ovulatory hyperandrogenic women had normal insulin levels and glucose tolerance. Obese and nonobese women had different relationships between sex steroid and insulin levels; obese women had significant correlations between insulin and non-SHBG testosterone levels (r = 0.30; P less than 0.05), whereas nonobese women had significant correlations between insulin and FSH (r = 0.40; P less than 0.01), dehydroepiandrosterone sulfate (r = 0.33; P less than 0.05), and SHBG (r = 0.37; P less than 0.05) levels, suggesting that the mechanisms underlying the association between sex steroid and insulin levels are complex. These findings suggest that 1) only women with PCO have hyperinsulinemia independent of obesity; hyperinsulinemia is not a feature of hyperandrogenic states in general; 2) AN is a common finding in obese hyperandrogenic women, particularly those with PCO; 3) only obese PCO women are at risk for impairment of glucose tolerance, independent of the presence of AN, suggesting that the negative impact of PCO and obesity on insulin action is additive; and 4) PCO women with AN can be considered as a subgroup of PCO and do not appear to have a distinct endocrine disorder.