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PubMed2002

Clinical and biochemical findings of a patient with thanatophoric dysplasia type I: additional finding of dicarboxylic aciduria.

OBJECTIVE: A long-surviving thanatophoric dysplasia type I patient to age of 6 years is presented. RESULTS AND CONCLUSIONS: Molecular studies revealed a heterozygous point mutation, S249C in the fibroblast growth factor receptor 3 gene. Most of the clinical course was similar to previous reports, including hearing loss and acanthosis nigricans. Abnormal urinary excretion of dicarboxylic acids and 3-hydroxydicarboxylic acids was observed. We hypothesize that this was a consequence of the FGFR3 mutation.

Acanthosis Nigricans↗
PubMed2006

Confluent and reticulated papillomatosis : a review of the literature.

Confluent and reticulated papillomatosis (CARP) was first described >60 years ago. It is distinct from acanthosis nigricans. This article presents the results of a review of the literature in MEDLINE through May 2006 using the terms 'confluent and reticulated papillomatosis', 'reticulated and confluent papillomatosis of Gougerot and Carteaud', and 'reticulated papillomatosis'. A recent report has linked the presence of Dietzia spp. (family: Dietziaceae; suborder: Corynebacterineae; order: Actinomycetales) in the skin to CARP. CARP has also been linked to defects in keratinization. Other possible causes of CARP that have been suggested but seem less likely include endocrine abnormalities, Pityrosporum, a reaction to UV light, and a variation of cutaneous amyloidosis. CARP has been reported worldwide and occurs in both sexes, all age groups, and all races. The disorder can initially manifest as hyperkeratotic or verrucous papules that coalesce to form a reticular pattern peripherally and confluent plaques centrally. Although a variety of treatments for CARP exist, oral minocycline 50-100mg twice daily has been the preferred treatment. However, recent reports of the effectiveness of azithromycin 250-500mg three times weekly may make azithromycin the preferred treatment for CARP, since it has a more benign adverse effect profile than minocycline. Other effective antibacterial treatments include fusidic acid 1000mg daily, clarithromycin 500mg daily, erythromycin 1000mg daily, tetracycline 500mg twice daily, and cefdinir 300mg twice daily. If a recent finding that CARP is caused by a bacterial microorganism is replicated, treatment should likely be determined by bacterial sensitivities, antibacterial adverse effect profiles, and cost considerations. Other oral treatments of CARP that are effective but currently disfavored because of the effectiveness of minocycline include isotretinoin, acitretin, and etretinate. There have been mixed reports regarding the effectiveness of topical treatments, which include selenium sulfide, ketoconazole cream, tretinoin, tazarotene, tacalcitol, and calcipotriene (calcipotriol).

Acanthosis Nigricans↗
PubMed1977

Diffuse finely nodular lesions of the esophagus.

Double contrast study of the esophagus revealed a variety of diffuse finely nodular lesions, some of which have not been adequately reported. Acanthosis nigricans, superficial spreading esophageal cancer, leukoplakia, moniliasis, and esophagitis were found to produce this appearance. Typical cases of the first three diseases are demonstrated and the differential diagnosis discussed.

Acanthosis Nigricans↗
PubMed1986

Characterization of binding and phosphorylation defects of erythrocyte insulin receptors in the type A syndrome of insulin resistance.

The type A syndrome of insulin resistance and acanthosis nigricans is characterized by severe insulin resistance due to a cellular defect in insulin action. To better understand the molecular nature of this defect, we have investigated insulin binding to circulating monocytes, erythrocytes, and the Triton X-100-solubilized erythrocyte receptor, and insulin-stimulated receptor autophosphorylation using cells and receptor from three type A patients. Insulin binding in both circulating cells and the soluble extract of erythrocytes indicated a heterogeneity of defects. Patients A1 and A2 both presented a major decrease in tracer insulin binding to intact cells and soluble insulin receptor. Determination of stoichiometric binding parameters using a cooperative model indicated that in patient A1 this was due to a reduction in the number of receptors, whereas in patient A2 the affinity constant for binding was decreased. Patient A3 presented near-normal insulin binding to erythrocytes and normal binding in intact monocytes, solubilized erythrocyte receptors, and cultured fibroblasts. Affinity labeling of erythrocyte receptor from this patient revealed a normal alpha-subunit and also a normal relative distribution of the higher-molecular-weight, nonreduced oligomeric forms of the receptor. Receptor autophosphorylation was measured using the solubilized insulin receptor from erythrocytes. The maximal stimulated phosphorylation was reduced by 79%, 76%, and 52% in patients A1, A2, and A3, respectively, relative to the simultaneous control. In all three patients, the autophosphorylation was stimulated only 1.0-3.5 times the basal level compared with controls, in which the stimulation was 5.7-fold +/- 1.2 (mean +/- 1 SD, P less than 0.005). In addition, in patients A1 and A2 a decrease in basal phosphorylation was observed and in patient A2 there was a rightward shift of the dose-response curve for insulin stimulation. These data and the correlation of coupling of receptor phosphorylation with the fractional occupancy of the receptor measured in the same extract suggest that these patients exhibit three types of defects. In patient A1, there is a loss in receptor number manifested by a parallel decrease in insulin binding and receptor phosphorylation. In patient A2, there is an additional decrease in the affinity constant leading to a decrease in both binding and receptor phosphorylation with an almost linear coupling between receptor occupancy and receptor phosphorylation.(ABSTRACT TRUNCATED AT 400 WORDS)

Acanthosis Nigricans↗
PubMed1988

Inhibition of insulin-stimulated glucose transport by factor extracted from serum of insulin-resistant patient.

We report a 31-yr-old nondiabetic male patient with acanthosis nigricans whose hyperinsulinemia and insulin resistance could not be explained by anti-receptor antibodies or by an intrinsic defect of insulin binding to his cells. An acid-alcohol extract of the patient's serum contained a factor that inhibited insulin-stimulated glucose transport in rat adipocytes. Low levels of the factor could be detected in 9 of 13 unselected patients with non-insulin-dependent diabetes. The factor was heat stable and resistant to treatment with acid, base, and various lytic enzymes. It eluted from a Bio-Gel P-2 column with an apparent molecular weight of 300. The factor also inhibited stimulation of glucose transport in adipocytes by the insulin mimickers hydrogen peroxide and sodium vanadate. In vitro incubation of rat soleus muscles in the presence of the factor resulted in inhibition of insulin-stimulated glucose transport. The factor enhanced 125I-labeled insulin binding in both adipocytes and muscle. A preparation of insulin receptors obtained from muscles incubated with serum factor showed increased binding of 125I-insulin to the alpha-subunit of the insulin receptor. Autophosphorylation of the beta-subunit and phosphorylation of exogenous substrate were increased in the receptor preparation obtained from muscles that had been incubated with serum factor. However, the increase in kinase activity was approximately the same as the increase in binding activity. No difference in kinase activity was observed when assayed under conditions in which 125I-insulin binding activity had been equalized.(ABSTRACT TRUNCATED AT 250 WORDS)

3-O-Methylglucose↗
PubMed1991

Use of in vitro clonogenic assays to differentiate acquired from genetic causes of insulin resistance.

Insulin resistance may be due directly to genetically programmed disorders of insulin action or acquired defects in which environmental factors influence insulin action. To address the issue of this distinction, we studied the ability of insulin to stimulate colony formation in primary cultures of erythroid progenitors (assumed to retain environmental influences) and immortalized T lymphocytes (presumed to reflect only genetic influences). Four patients with hyperinsulinemia and disturbed glucose metabolism were studied (2 patients with acanthosis nigricans, 1 of whom had circulating anti-insulin-receptor antibodies, 1 with partial lipodystrophy, and 1 with Cushing's syndrome). The mean colony-forming ability of their erythroid progenitor cells in response to insulin stimulation (less than or equal to 1.6 pM) was significantly blunted compared with control cells (P less than 0.05). The mean responsiveness of their immortalized T-lymphoblast cell lines to similar insulin concentrations was no different than that of control T-lymphocyte lines, consistent with an acquired cause for the observed insulin resistance in each case. A T-lymphocyte line from a patient with leprechaunism, however, showed no stimulation in response to physiological concentrations of insulin. With these same in vitro methodologies, there was normal T-lymphocyte line responsiveness to insulinlike growth factor I (IGF-I) or insulin concentrations greater than 8.6 pM; both of these responses could be completely blocked by preincubation with an antibody to the IGF-I receptor. These findings suggest that, despite resistance to physiological levels of insulin, the high circulating insulin concentrations present in the serum of these patients could mediate unwanted tissue-specific growth through an intact IGF-I receptor-effector mechanism.

Acanthosis Nigricans↗
PubMed1988

Selective insulin action on skin, ovary, and heart in insulin-resistant states.

States of hyperinsulinemia with resistance to insulin action on glucose disposal are frequently associated with proliferative tissue abnormalities of the skin (acanthosis nigricans), ovary, and heart. That insulin may be involved in the pathogenesis of these growth-related abnormalities despite resistance to its metabolic effects mediated through the insulin receptor is suggested by the known ability of high concentrations of insulin to stimulate DNA synthesis and cell proliferation in vitro through the insulin-like growth factor I (IGF-I) receptor. IGF-I receptors are present in skin keratinocytes, some ovarian tissue compartments, and in the heart. Furthermore, ovarian tissue from hyperinsulinemic insulin-resistant women responds to supraphysiologic insulin concentrations in vitro by enhanced steroidogenesis. Cultured, transformed T-lymphocytes from an infant with leprechaunism fail to augment basal-colony formation in response to physiologic insulin concentrations in vitro (compared to a doubling seen in normal subjects), but respond normally to supraphysiologic insulin concentrations, the effect of which is competitively inhibited by a monoclonal antibody to the IGF-I receptor. Thus, insulin action mediated through the IGF-I receptor may initiate growth-promoting tissue effects in the face of limited insulin effect on glucose metabolism. Such spillover actions may add to the morbidity associated with states of clinical insulin resistance.

Acanthosis Nigricans↗
PubMedDate not supplied

Insulin-resistant diabetes with insulin receptor autoantibodies in a male patient without acanghosis nigricans.

A 51-yr-old, nonobese, male patient presented with hyperglycemia and a recent 40-pound weight loss. Severe insulin resistance was documented in studies in which high amounts of insulin were infused using the Biostator GCIIS. Diabetic control was finally achieved with subcutaneous injections of 470 U of insulin per day. Positive laboratory findings included a mild pancytopenia, elevated erythrocyte sedimentation rate, decreased C3 and properdin, and increased IgA. Antinuclear or other autoantibodies were not present. Insulin antibody levels were within the range usually present in insulin-treated diabetic patients. Acanthosis nigricans was not present. Incubation of the patient's serum with IM-9 lymphoblastoid cells revealed that an insulin receptor antibody was present in a serum dilution of 1:80. Insulin-resistant diabetes mediated by insulin receptor antibodies may present in patients with immunologic findings but without overt dermatologic stigmata.

Acanthosis Nigricans↗
PubMed2001

Establishing surveillance for diabetes in American Indian youth.

OBJECTIVE: To determine prevalence estimates in order to monitor diabetes, particularly type 2 diabetes, in American Indian youth. RESEARCH DESIGN AND METHODS: To explore the feasibility of developing a case definition using information from primary care records, all youth aged <20 years with an outpatient visit or hospitalization for diabetes were identified from the Billings Area Indian Health Service database in Montana and Wyoming from 1997 to 1999, and the medical records were reviewed. Classification for probable type 1 diabetes was based on age < or =5 years, weight per age < or =15th percentile at diagnosis, or positive results of islet cell antibody test. Classification for probable type 2 diabetes was based on weight per age > or =85th percentile or presence of acanthosis nigricans at diagnosis, elevated C-peptide or insulin, family history for type 2 diabetes, or use of oral hypoglycemic agents with or without insulin or absence of current treatment 1 year after diagnosis. RESULTS: A total of 52 case subjects with diabetes were identified, 3 of whom had diabetes secondary to other conditions. Of the remaining 49 case subjects, 25 (51%) were categorized as having probable type 2 diabetes, 14 (29%) as having probable type 1 diabetes, and 10 (20%) could not be categorized because of missing or negative information. Prevalence estimates for diabetes of all types, type 1 diabetes, and type 2 diabetes were 2.3, 0.6, and 1.1, respectively, per 1,000 youth aged <20 years. CONCLUSIONS: Our definitions may be useful for surveillance in primary care settings until further studies develop feasible case definitions for monitoring trends in diabetes among youth.

Acanthosis Nigricans↗
PubMed1982

Insulin resistance associated with androgen excess in women with autoantibodies to the insulin receptor.

Hirsutism, polycystic ovaries, and elevated levels of plasma testosterone are characteristic clinical features in women with extreme insulin resistance and acanthosis nigricans. Extreme insulin resistance resulting from autoantibodies to the insulin receptor (type B extreme insulin resistance) had been considered an exception to this generalization. A woman with type B extreme insulin resistance developed clinical evidence of masculinization in association with a markedly elevated level of plasma testosterone (1000 ng/dL). In nine women with autoantibodies to the insulin receptor, excessive ovarian production of testosterone was a common feature among the premenopausal patients. Postmenopausal patients rarely developed elevated levels of plasma testosterone, presumably as a result of ovarian failure. Overproduction of testosterone may result from a direct effect of hyperinsulinemia on the ovary.

Acanthosis Nigricans↗
PubMed1999

Cutaneous signs of selected systemic diseases.

In this work we will discuss three cutaneous markers of systemic disease. Acanthosis nigricans is the most widely known in this category. Cutaneous angiokeratomas are usually associated with enzyme defect disorders, such as Fabry's disease, and are linked in this work as a reactive pattern in hepatorenal failure. Mast cell disease may occur in a number of forms, often with systemic involvement.

Acanthosis Nigricans↗
PubMed1999

[Insulin resistance: from clinical diagnosis to molecular genetics. Implications in diabetes mellitus].

Insulin resistance is observed in several diseases such as non insulin dependent diabetes mellitus (NIDDM) or polycystic ovarian syndrome (PCOS). To understand genetic determinism of this abnormality we have developed a multidisciplinary approach including selection of phenotypes with insulin resistance confirmed in vivo by minimal model of Bergman and characterization of cellular defects in insulin action on circulating erythrocytes and monocytes. Exploration of variability in candidate genes by direct sequencing in some genetic syndromes of severe insulin resistance and acanthosis nigricans (mainly the Type A syndrome) revealed mutations of the insulin receptor gene associated with major defects in insulin binding or kinase activity. In other rare genetic syndromes or patients affected by NIDDM or PCOS defects appear to be located at post-receptor level, where IRS (insulin receptor substrate) genes are the most attractive candidates. Prevalence of some allelic variants suggested a potential role of IRS genes in insulin resistance, although their involvement in the pathogenesis of NIDDM remains controversial. Genotype-phenotype correlations in first degree relatives of an index case caring the Type A syndrome, suggested that association of allelic variants of IRS-1 and IRS-2 with insulin receptor mutations contribute, by synergistic effects, to phenotypic expression of defects in signal transduction. These mechanisms through genetic epistasis, involving several genes in insulin action, fit better with the polygenic nature of current forms of NIDDM and represent a good model in the study of pathogenesis of insulin resistance.

Acanthosis Nigricans↗
PubMedDate not supplied

Alstrom syndrome with hepatic dysfunction: report of one case.

Alstrom syndrome is a rare autosomal recessive disorder associated with early childhood retinopathy, progressive sensorineural hearing loss, truncal obesity, and acanthosis nigricans. We report a 10-year-old boy with Alstrom syndrome presenting with general malaise and abnormal liver function for 1 year. In addition to the above mentioned features, he also had hyperglycemia and hyperinsulinemia. The mechanism responsible for the persistent elevation of liver enzymes could not be identified. To the best of our knowledge, this is the first-reported case of Alstrom syndrome with hepatic dysfunction in Taiwan.

Acanthosis Nigricans↗
PubMed2000

[Skin disorders as markers of internal disease. Paraneoplastic dermatoses].

Paraneoplastic dermatoses are markers of internal malignancy characterised by being relatively uncommon, associated with certain forms of cancer and occurring in connection with the cancer either before, during, or after the diagnosis has been made. Furthermore, the skin symptoms typically run a parallel course with the cancer. Most paraneoplastic dermatoses disappear when the primary tumour is removed and reappear in the case of recurrence or metastases of the cancer. Adult dermatomyositis is especially associated with breast and lung cancer. Necrolytic migratory erythema is seen in patients with a glucagon-producing tumour in the pancreas. Bazex's syndrome is associated with cancer in the upper respiratory and digestive tracts. Erythema gyratum repens is an annular erythema associated with lung, breast, stomach and oesophageal cancer. Acquired hypertrichosis lanuginosa, which is extremely rare, is a specific marker of internal malignancy, especially lung and colon cancer. Acanthosis nigricans and Leser-Trélat's sign are cutaneous markers of stomach cancer. Sweet's syndrome is in some cases associated with acute myeloid leukaemia, but not as frequently as formerly believed. Acquired ichthyosis, scleromyxoedema, amyloidosis, paraneoplastic pemphigus, woody hands, and Trousseau's syndrome are mentioned.

Acanthosis Nigricans↗
PubMed2002

Metabolic differences between Caucasian and African-American children and the relationship to type 2 diabetes mellitus.

Type 2 diabetes mellitus (DM) has historically been considered an adult disease. However, the incidence of type 2 DM has increased dramatically in pediatric populations in recent years. This increase parallels the recent rise in childhood obesity and has been greatest among minority adolescents. Differences between African-American and white American youths are discussed, including risk factor differences that may help to account for the overwhelming number of African-American children with type 2 DM as compared with white children. African-American youths have higher rates of insulinemia, obesity, family history, and acanthosis nigricans than their white counterparts. In addition, despite similar declines in insulin action during puberty, there is no compensatory increase in insulin secretion in African-American children, contrary to the observation in white children. These differences are likely to have a genetic basis modulated by environmental and lifestyle influences. Treatment of type 2 DM should focus on identifying individuals at risk and instituting lifestyle changes to reduce the risk and stem the development of DM.

Acanthosis Nigricans↗
PubMed2002

Chronic acquired dyskeratotic papulosis of the face.

A Vietnam veteran who had been exposed to Agent Orange presented with a 28-year history of a papulonodular disease mainly affecting the face. Over those years, pin-sized papules had developed into dark nodules. Multiple biopsies of both fresh and mature papulonodules had been performed for routine histopathology and electron microscopy. Results had been positive for spongiosis with exocytosis, acanthosis, dyskeratotic keratinocytes, and marked incontinence of pigment, which together are suggestive of a previously unreported clinical entity that we term chronic acquired dyskeratotic papulosis.

Acanthosis Nigricans↗
PubMed2003

[Two cases of Costello syndrome].

We report two unrelated cases of Costello syndrome, presenting with poor postnatal growth, mild mental retardation, poor feeding, curly hair, coarse characteristic face, loose skin, hypotonia, and cardiac involvement. Nasal papilloma and acanthosis nigricans were the most characteristic features of this syndrome. Both cases had atrial fibrilation from infancy to early childhood. One patient had hypertonia in the lower extremities and pes equinovarus, while the other had hypotonia and pes planovalgus.

Abnormalities, Multiple↗
PubMed1992

[Bone and visceral manifestations of lipoatrophic diabetes. Apropos of a case].

Lipoatrophic diabetes, known by pediatricians as Lawrence-Seip disease or Berardinelli lipodystrophy syndrome, is an infrequent condition of which approximately one hundred cases have been published to date. A case in a 24-year-old female with a fifteen-year follow-up is reported. Manifestations included acanthosis nigricans, generalized lipoatrophy, hirsutism, muscle hypertrophy, and intellectual impairment. Biologic tests revealed insulin-resistant diabetes mellitus with major diet-dependent type V hypertriglyceridemia. The patient had nephrotic syndrome (focal and segmental endocapillary proliferative glomerulonephritis without dense deposits). Phosphorus and calcium determinations were normal, as were the endocrinologic tests. Roentgenograms of the bones disclosed increased density of axial bones and large epiphyseal defects with increased bone density as determined by osteodensitometric studies. The bone manifestations of this syndrome have been documented but are often overshadowed by the severe metabolic alterations.

Abnormalities, Multiple↗