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Acanthosis nigricans of the groin, axillae, and neck developed in a patient on long-term steroid therapy for dermatomyositis after eight years. The dermatosis resolved spontaneously ten years after the steroid use had been discontinued. Review of three personal cases and the literature suggests that acanthosis nigricans may have a hormonal basis.
2 cases of acanthosis nigricans associated with an adenocarcinoma (signet ring cell carcinoma) of the stomach and a metastasizing small-cell carcinoma of unknown origin are reported. In both cases the skin lesions preceded the diagnosis of the carcinoma by months and acanthosis nigricans maligna was suspected by onset and localization of the dermatosis. There was no evidence of a papillomavirus etiology of the warty skin lesions. Virus particles could not be demonstrated either in ultrathin sections or in buffer extracts. Virus-specific DNA was not detectable after CsCL-ethidium bromide gradient centrifugation and cellular DNA did not hybridize under stringent or relaxed conditions with 32P-labelled human papillomavirus 6 or human papillomavirus 8 DNA.
Skin biopsy specimens of acanthosis nigricans (AN) lesions were obtained from seven women with the polycystic ovary (PCO) syndrome and insulin resistance (IR). All the patients had normal thyroid function test results and fasting hyperinsulinemia with an exaggerated insulin response to oral glucose. Acanthosis nigricans lesions exhibited prominent deposits of glycosaminoglycan (GAG) consisting mostly of hyaluronic acid in the papillary dermis. Normal amounts of GAGs were found in control biopsy specimens obtained from areas of the skin not involved by AN and from skin of the nape of the neck or axillae in three normal women. These studies demonstrate that GAG deposition is a regular component of AN skin in patients with PCO and IR. The cause of these infiltrates remains to be determined.
Two patients are described with obesity, acanthosis nigricans, acral hypertrophy, basal hyperinsulinism and exaggerated insulin responses to oral glucose. One patient, a diabetic female showed features of virilisation due to polycystic ovarian disease and underwent gonadectomy with some resolution of her androgenisation and acanthosis nigricans. Binding of labelled insulin to erythrocytes was significantly decreased in both patients compared with normal or obese control subjects. In contrast, the receptor concentration in adipose tissue obtained from the patient undergoing gonadectomy was higher than seen in obese control subjects. Thus, somatic growth may be stimulated by insulin in some tissues in these hyperinsulinaemic patients due to relative preservation of receptor numbers.
A 37-year-old man is reported who, as a schoolboy and during puberty, showed the clinical aspects of acanthosis nigricans benigna. In correlation with an obvious obesity the picture has meanwhile developed into pseudoacanthosis nigricans. On the basis of this case the delimitating criteria of the various acanthosis nigricans subgroups and their etiologic factors are discussed.
A case is reported of acanthosis nigricans associated with a gastric carcinoma. The gastric cancer was of the diffuse, infiltrating type. Many tumour cells were identified by means of histochemistry and electron microscopy as neoplastic enterochromaffin-like cells. It is suggested that cancers associated with acanthosis nigricans might constitute a certain group of carcinomas in which parts of the tumour cells arise from the APUD-series of endocrine cells.
Six women (age range 17-38 years), who presented to the dermatology services with biopsy-proven acanthosis nigricans of variable duration were evaluated to rule out endocrine diseases. Menstrual abnormalities (5/6 patients), pallid striae (4/6 patients), hirsutism (4/6 patients) and acne vulgaris (2/6 patients) were found on physical examination. All the patients had body mass indices in the obese (> 27 kg/m2) range, and in association we found ovarian hyperthecosis, PCOD, premature ovarian failure, glucose intolerance and hyperprolactinaemia in the above six patients. The importance of appropriate endocrinal evaluation in patients with biopsy-proven acanthosis nigricans is emphasized.
The authors describe a clinical case of AIDS presented by three opportunistic infections (esophageal candidiasis, tuberculosis and atypical mycobacteriosis) and a dermatological manifestation--acanthosis nigricans--not described in medical literature as accompanying those entities. The exclusion of most common etiologies of acanthosis nigricans and its regression following treatment for those infections suggests that with AIDS it behaves like a paraneoplastic syndrome. Screening for HIV antibodies should be the rule whenever this dermatological manifestation is present.
We report a case of an incidental finding of glycogenic acanthosis of the larynx on autopsy in a 79-year-old man who died of myocardial infarction. The lesion was grossly recognized as a white plaque (leukoplakia) on the subglottic compartment of the left side of the larynx. Histological sections revealed thickened squamous mucosa positive for abundant glycogen on periodic acid-Schiff staining. No epithelial dysplasia was noted. The patient had a history of smoking. This case represents the first report of glycogenic acanthosis involving the larynx. This benign condition should be added to the vast differential diagnosis of leukoplakia in this anatomical location.
Diagnostic features of glycogenic acanthosis of the esophagus on air-contrast radiography, endoscopy, and histopathologic studies in 10 selected cases are presented. Glycogenic acanthosis of the esophagus is a common benign entity, characterized by multifocal plaques of hyperplastic squamous epithelium with abundant intracellular glycogen deposits. At esophagoscopy or on autopsy specimens these lesions appear as slightly raised grey-white plaques which are usually 2-10 mm in diameter and may be confluent. They cause a finely nodular or cobblestone mucosal pattern demonstrable on double-contrast views of the well-distended esophagus. The findings are not associated with mucosal ulcerations, luminal narrowing, or mobility disturbance, although some patients may have coexistent hiatal hernia and gastroesophageal reflux.
A 59-yr-old man with carcinoma of the stomach, concurrent acquired hyperkeratosis (tylosis) of the palms and soles, and acanthosis of the esophageal mucosa is reported. He presented the tylosis and esophageal lesions when the carcinoma was evident. Resection of the stomach resulted in diminution of the skin and esophageal lesions. The association of sporadic tylosis and carcinoma of the stomach is extremely rare. This is the first case report documenting the association of gastric cancer, tylosis, and acanthosis of the esophageal mucosa.
A 62-yr-old man was referred for management of GI polyposis. Large bowel polyps were initially diagnosed >25 yr ago, and the patient had undergone multiple colonoscopies and polypectomies. Personal and family history were notable for thyroid goiter and hypothyroidism. Physical examination was notable for lingular papillomatosis. No cutaneous lesions were seen. Upper endoscopy revealed esophageal glycogen acanthosis. There were multiple polyps throughout the stomach and the small and large intestines. Histology of these polyps showed multiple cell types including juvenile polyps, inflammatory polyps with fibromuscular proliferation and lamina propria ganglion cells, and focal adenomatous change. A clinical diagnosis of Cowden syndrome was made. Mutation analysis revealed a variant in exon 8 of the PTEN gene. Direct sequencing revealed a germline heterozygous C.892-895InsA, which is predicted to result in a truncated PTEN protein. Cowden syndrome is an underdiagnosed, underrecognized, autosomal dominant, inherited syndrome. For the gastroenterologist, esophageal acanthosis and multiple hamartomatous polyps should suggest the diagnosis. Sensitive molecular diagnostic tests looking for mutations in the appropriate genes are clinically available. Together with genetic counseling, molecular diagnostic testing will allow more accurate risk assessment and surveillance for cancer for both the patient and family members.
Cowden's disease is a rare autosomal dominant condition characterized by multiple hamartomas of ectodermal, endodermal, and mesodermal origin affecting many organ systems. Gastrointestinal manifestation includes the formation of multiple polyps of various benign histopathological types throughout the alimentary tract. Recent literature suggests that the frequency of gastrointestinal involvement is approximately 70-85%. The diagnosis of Cowden's disease, however, relies mainly on subtle dermatologic findings, which may not be obvious to the gastroenterologist. We describe a patient with Cowden's disease and review the English literature on the topic of gastrointestinal polyposis and Cowden's disease. These studies suggest that gastrointestinal polyposis is commonly found in this disease, and that diffuse esophageal glycogenic acanthosis is a characteristic feature of Cowden's disease. We propose that the finding of extensive glycogenic acanthosis in the presence of other benign gastrointestinal polyposis should be considered pathognomonic for the diagnosis of Cowden's disease.
The authors report a variation of the clinical picture of acanthosis nigricans in two patients with carcinoma of the stomach.
Phenytoin sodium has been used to treat muscle cramps of diverse causes, and is known to increase insulin sensitivity during long-term use. We have previously described a syndrome of insulin resistance, acanthosis nigricans, and acral hypertrophy with continual muscle cramping. The effect of 300 mg/d of phenytoin (Dilantin) on muscle cramping and carbohydrate economy was studied in three affected patients and four control subjects. Oral glucose tolerance tests, euglycemic insulin infusion studies, and monocyte insulin binding tests were conducted before and after phenytoin administration. All three patients had notable improvement in muscle cramps. In response to phenytoin, metabolic improvements were variable, with improvement characteristically better in patients with less severe baseline metabolic abnormalities. Patient 1, with the mildest degree of glucose intolerance, had decreased fasting insulin and blood glucose levels, improved glucose tolerance, and insulin-mediated glucose disposal, associated with an increase in monocyte insulin receptors. Patient 2 had reduced fasting plasma glucose and insulin levels and improved oral glucose tolerance, suggesting a beneficial effect on carbohydrate metabolism. Patient 3, with the most severely impaired carbohydrate economy, showed no metabolic improvement despite marked lessening of muscle pain. These clinical characteristics were unaffected in control subjects. We conclude that phenytoin is of value in the therapy of muscle cramps and glucose intolerance in patients with this syndrome.
Two sibs, whose parents are first cousins, had diabetes mellitus with hyperinsulinism, insensitive insulin receptors, and acanthosis nigricans. Both patients had pigmentary retinopathy, secondary cataracts, labyrinthine deafness, mental retardation, and cerebral atrophy. They were disproportionately short with relatively broad hands and feet and slightly coarse face. The young woman had secondary amenorrhea and polycystic ovaries and the boy gynecomastia and hypergonadotrophic hypogonadism. This appears to be the second family with a new autosomal recessive disorder differing from Alström syndrome by the presence of mental retardation and absence of renal insufficiency. Impaired insulin receptor binding and polycystic ovaries are described as part of this syndrome.
Malignant acanthosis nigricans is rarely associated with carcinoma of the bowel or cervix. However, this dermatosis is described in a case of adenocarcinoma of the ascending colon, and in another with carcinoma of the cervix.
This report analyzes the in vitro characteristics of 125I-insulin binding to the monocytes of nine patients with the syndromes of acanthosis nigricans and insulin resistance. The 3 Type A patients (without demonstrable autoantibodies to the insulin receptor) had decreased binding of insulin due to a decreased concentration of receptors. In these patients the residual receptors demonstrated normal dissociation kinetics, negative cooperativity, and were blocked by anti-receptor antibodies in a manner similar to normal cells. In contrast, monocytes from the 6 Type B patients (with circulating anti-receptor autoantibodies) had decreased binding of insulin due to a decrease in receptor affinity. Insulin binding to monocytes of Type B patients demonstrated accelerated rates of dissociation with no evidence of cooperative interactions among insulin receptors. When coupled with previous data, the present studies further suggest that different mechanisms account for the defects in insulin binding and insulin resistance observed in these patients.