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PubMed2003

[Proliferative verrucous leukoplakia. Report of five cases].

BACKGROUND: Proliferative verrucous leukoplakia (PVL) is a rare variant of oral leukoplakia (OL) with a high tendency for malignant transformation. PVL starts as a flat hyperkeratosis. During the course of the disease verrucous lesions develop. AIM OF THE STUDY, MATERIAL AND METHODS: Due to the scarcity of reports on PVL five cases of PVL are presented. Clinical and histopathological findings in five female patients with PVL were evaluated retrospectively. RESULTS: The clinical appearance of PVL was characteristic as compared to criteria described in the literature. The average period of observation in these cases was short (1.7 years). There were 3.6 different localizations observed per patient. The buccal mucosa, gingiva, and edentulous alveolar ridge were most often affected. One patient had already developed squamous cell carcinoma prior to referral. The others developed malignancies during follow-up. Recurrences and secondary malignancies could not be avoided using different therapeutic modalities. Two patients died from PVL. The characteristic spectrum of histopathological findings in PVL was observed. Homogeneous flat leukoplakias are characterized by acanthosis, hyperkeratosis, and often parakeratosis. Epithelial dysplasia is not seen. The proliferative verrucous stage of the disease is characterized by papillomatous epithelial growths with signs of slight epithelial dysplasia and subepithelial infiltration with immunocompetent cells. Stages of transformation may result in verrucous carcinoma or squamous cell carcinoma. CONCLUSIONS: PVL is associated with a very high rate of malignant transformations. These, as well as recurrences, cannot be avoided with present-day therapies. In order to define the biological profile of PVL more clearly, multicenter studies are necessary to reveal possible etiologic factors and concepts for therapy.

Aged↗
PubMed2001

[Focal palmoplantar and oral mucosa hyperkeratosis syndrome].

CASE REPORT: Four members of a family in three generations are presented who were affected by a rare syndrome (mucosa hyperkeratosis syndrome). This syndrome is characterized by autosomal-dominant inheritance, white lesions of the gingiva, and palmoplantar hyperkeratosis. The four affected members of the family revealed an abnormal keratinization of the gingiva and palmoplantar epidermis. Biopsies of plantar and gingival lesions histologically showed acanthosis and hyperkeratotic cornification of the epithelium. Electron microscopy demonstrated the features of epidermolytic hyperkeratosis. DISCUSSION: From the differential diagnostic point of view, the mucosa hyperkeratosis syndrome has to be distinguished from the Jadassohn-Lewandowsky syndrome and the Howel-Evans' syndrome, which is associated with esophageal carcinoma.

Adult↗
PubMed2005

Concurrent occurrence of Sweet's syndrome and erythema nodosum: an overlap in the spectrum of reactive dermatoses.

Simultaneous occurrence of Sweet's syndrome and erythema nodosum is very rare. We describe a case of a young male with a recent history of streptococcal infection who presented with concurrent Sweet's syndrome and erythema nodosum. Although the exact pathogenesis of these dermatoses is not yet clear, their similarities and simultaneous occurrence suggest a possible common underlying mechanism and may represent a continuum of reactive dermatoses. Evaluation of the role of cytokines in the etiopathogenesis of these conditions will be useful for further assessment and treatment of these conditions. Like the association of acanthosis nigricans and certain cancers and diabetes, Sweet's syndrome and erythema nodosum may be associated with certain malignancies, autoimmune disorders, or inflammatory bowel disease. Early recognition of these skin lesions can guide a search for underlying disorders. Patients with Sweet's syndrome should undergo an age-appropriate work-up for malignancy.

Adult↗
PubMed2003

Basaloid follicular hamartoma with trichoblastomatous proliferations.

BACKGROUND: Basaloid follicular hamartomas (BFH) are rare, benign, adnexal lesions with diverse clinical presentations. Previous studies documented BFHs with fibroepithelioma of Pinkus-like proliferations, or proliferations that resemble trichoepitheliomas. OBJECTIVE: We report on a patient with linear, unilateral BFH and extensive trichoblastomatous proliferations involving the right arm, torso, and leg. An 18-year-old female presented with multiple, hyperkeratotic, linear nodules and plaques limited to her right side from the shoulder to the leg. The lesions had existed since birth and gradually increased over time. RESULTS: The lesions contained hyperpigmented, exophytic nodules with acanthosis, pseudoepitheliomatous hyperplasia, focally associated with hyperkeratosis, and squamous eddies. Some areas contained trichoepithelioma-like proliferations, or large nodules of basaloid cells with numerous cystic spaces, marked hyperpigmentation, and melanophages. The diagnosis was linear, unilateral BFH with an unusual trichoblastomatous component. CONCLUSION: While trichoblastomatous proliferations could occur in a BFH, to our knowledge this finding has not been reported.

Adolescent↗
PubMed2005

Analysis of PTEN gene mutations in Korean patients with Cowden syndrome and polyposis syndrome.

PURPOSE: PTEN (phosphatase and tensin homologue deleted in chromosome 10) is a candidate tumor suppressor gene. Mutations of this gene are responsible for PTEN hamartoma tumor syndromes, including Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and Proteus -like syndromes. Recently, PTEN mutations were identified in several human neoplasms. We analyzed the DNA of various organs and lesions in Korean patients with Cowden syndrome, their family members, and patients with familial adenomatous polyposis for germline or somatic PTEN mutations. METHODS: The 11 patients included in this study were 5 patients with Cowden syndrome, 4 of their family members, and 2 patients with familial adenomatous polyposis. Deletions and mutations in exons 1 to 9 of the PTEN gene were evaluated by polymerase chain reaction-single strand conformation polymorphism and sequencing analysis in esophageal acanthosis, gastric polyps, colonic polyps, skin lesions, and peripheral blood mononuclear cells. To exclude common polymorphisms, 240 controls were tested. RESULTS: All patients with Cowden syndrome showed several to numerous polyps in the gastrointestinal tract. A missense mutation at codon 217 (GTC to GAC, Val to Asp) in exon 7 was identified in one Cowden syndrome patient, and a nonsense mutation at codon 211 (TGC to TGA, Cys to stop) in exon 6 was identified in a second patient. Identical mutations were found in all tissue samples, including colonic polyps, from each patient. No PTEN mutations were found in their family members or in any patient with familial adenomatous polyposis. None of tested controls contained a mutation. CONCLUSIONS: We have identified two new germline PTEN mutations in Korean patients with Cowden syndrome. Mutations in the introns and regulatory regions of the PTEN gene may be present in additional patients with Cowden syndrome and polyposis syndrome.

Adenomatous Polyposis Coli↗
PubMed2006

The changing spectrum of diabetes in Mexican American youth.

Type 2 diabetes (T2DM) is now a pediatric disease. As in adults, it disproportionately affects ethnic and racial minorities, including Hispanics. The preponderance of Hispanics in south Texas are of Mexican American (MA) heritage. Over the past 16 years, we have accumulated a large cohort of children with diabetes. We have noted distinct differences in numerous parameters between MA children with T2DM and those with type 1 diabetes (T1DM). In order to explore these observations, we have reviewed the records of all children diagnosed with diabetes (n = 669) during the 9 years between January, 1990 and December, 1998 and seen by our pediatric diabetes group. In this cohort were 329 MA, 287 non-Hispanic whites (EA) and 53 African Americans. Compared to EA children with T1DM, MA children were more likely to have a parent with diabetes, to be hospitalized at the time of diagnosis and to lack health insurance. The differences between MA children with T1DM and T2DM were significant: specifically, children with T2DM were more likely to be female and pubertal with a body mass index >25 kg/m(2) and have acanthosis nigricans. Slightly more than 2/3 of the MA children with T2DM had at least one parent already diagnosed with T2DM. Less than 1/3 of the children with T2DM required hospitalization at the time of diagnosis and only a 1/4 have private health insurance. Over this 9-year interval, the apparent incidence of diabetes almost tripled in south Texas with the great majority of that increase due to the increasing numbers of children with T2DM.

Child↗
PubMed1976

A new familial syndrome characterized by pigmentary retinopathy, hypogonadism, mental retardation, nerve deafness and glucose intolerance.

Three siblings with retinitis pigmentosa, deafness and mental retardation were studied. Physical abnormalities included nystagmus, acanthosis nigricans and multiple keloids. The two male siblings had gynecomastia, small testes and mild subvirilization whereas the only indication of hypogonadism in the female sibling was oligomenorrhea. Testosterone levels in the males, which were in the low to low normal range, were increased by the administration of large doses of chorionic gonadotropin. The two affected males had elevated plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels which were decreased by the administration of testosterone and increased by the administration of clomiphene. One sibling had mild obesity and diabetes mellitus, one had moderate obesity, normal glucose tolerance and hyperinsulinism and the third had abnormal glucose tolerance and hyperinsulinism. This familial syndrome is distinct from either the Laurence-Moon, Bardet-Biedl or Alström disorders and provides further evidence of genetic heterogeneity in this group of autosomal recessive traits.

Adolescent↗
PubMed1991

Polycystic ovary syndrome and the androgen-insulin connection.

The association of hyperandrogenism, insulin resistance, and polycystic ovarian disease is well established. The accompanying hyperinsulinemia results in acanthosis nigricans, an epiphenomenon of this syndrome. The knowledge that states of insulin resistance of diverse causes are associated with ovarian hyperandrogenism makes the argument for insulin-driven ovarian androgen secretion compelling. However, equally compelling evidence suggests that hyperandrogenism may contribute to insulin resistance and hyperinsulinemia. The irreconcilable differences between these two hypotheses have resulted in an array of contradictory studies. In this article a unified concept of polycystic ovary syndrome and its androgen-insulin connection is proposed. The hypothesis incorporates the role of hyperinsulinemia in the androgen excess observed (and vice versa); the key to this connection is the androgen-dependent change in regional body fat distribution and its metabolic consequence. The pathophysiologic features of polycystic ovary syndrome, which has important clinical sequelae, deserve further consideration.

Androgens↗
PubMed1979

Inverted follicular keratosis.

We reviewed 17 cases of inverted follicular keratosis. The median age of the patients at the time of surgery was 69 years. Follow-up in 14 cases showed no recurrences of inverted follicular keratosis, which is a benign skin lesion, often mistaken clinically and pathologically for a malignancy. Inverted follicular keratosis is characterized histologically by the presence of squamous eddies, acantholysis, acanthosis, and hyperkeratosis.

Aged↗
PubMed1989

Histopathological effects of homocysteine thiolactone on epithelial and stromal tissues.

To study the effects of homocysteine on epithelial and stromal tissues, the free base of homocysteine thiolactone was synthesized and administered to mice. Intraperitoneal and intramuscular doses of 0.2 to 2.0 mg/g are acutely toxic, causing as much as 90% mortality because of intense tissue necrosis at the injection site, congestion and fibrin thrombi in pulmonary vessels, focal necrosis of liver and kidney, and deposition of lipid within hepatocytes. In survivors of intramuscular injection the area of tissue necrosis is surrounded by fibrosis, calcification, hypertrophy of nerves and ducts, and formation of acanthotic squamous epithelium with hyperkeratosis and focal dysplasia. Topical homocysteine thiolactone on skin is not systemically toxic, but ulceration, fibrosis, acute and chronic inflammation, angiogenesis, acanthosis, hyperkeratosis, and dysplastic squamous epithelium are observed. The findings show that homocysteine thiolactone promotes keratin formation by squamous epithelium, interferes with cellular processes necessary for viability, stimulates epithelial dysplasia and stromal hyperplasia, and produces intravascular fibrin thrombi.

Administration, Topical↗
PubMed1987

Skin cancer and papillomaviruses in cattle.

We examined proliferative lesions on the sun-exposed, unpigmented skin of 13 cattle. Ages of animals at first examination ranged from 4 to 15 years, and 4 were observed for from one to 3 years, during which time progression to malignancy occurred in 2 of them. Early lesions consisted of keratin scales and horns; histology showed underlying acanthosis and hyperkeratosis. Advanced lesions were either squamous cell carcinomas or basaloid tumours with sebaceous and/or squamous differentiation; some were locally invasive but no metastases were found in the 6 animals that were available for necropsy. All 3 types of lesion could occur on the same animal. In early lesions from 11 of 12 animals, there was evidence for the presence of papillomavirus, either virions or viral DNA, the latter detected by gel electrophoresis and/or molecular hybridization. Viral DNA was also detected in 3 basaloid tumours and 2 squamous cell carcinomas from 4 animals. The DNA bound to a probe of bovine papillomavirus type 1 DNA under conditions of low stringency. We suggest that both infection with papillomavirus and exposure to sunlight, possibly in conjunction with other factors such as a period of photosensitization, are involved in the production of this spectrum of proliferative lesions, which bear some resemblance to human skin cancer.

Aging↗
PubMed1988

Studies on the pathology of experimental zinc deficiency in guinea-pigs.

Zinc deficiency was produced in guinea-pigs by feeding a diet containing 1.25 micrograms Zn per g of diet over a period of 60 days. A significant reduction in serum and tissue (kidney, liver and testis) Zn concentration was observed in the Zn-deficient (ZnD) group. Gross lesions were thickening of skin, atrophy of testis and thyroid and enlargement of adrenals. Histologically, there was parakeratosis, hyperkeratosis and acanthosis in skin, tongue and oesophagus, degeneration and strophy of testis, necrosis of the pancreas, atrophy of the thyroid, atrophy of the zona glomerulosa and hyperplasia of the zona reticularis and medulla of the adrenals. In order to study the response to Zn supplementation, the Zn-replete diet was fed over a period of 15 days to guinea-pigs which had been given the ZnD diet for 45 days. These animals exhibited marked, though not complete, improvement in the pathological changes.

Adrenal Glands↗
PubMed1975

Microscopic anatomy of edentulous residual alveolar ridges.

The histologic tissue changes of the residual alveolar ridges were studied in five edentulous patients ranging from 55 to 80 years of age. The material studied was obtained from cadavers. The following observations were made: (1) The epithelium was hornified. Acanthosis was found in all specimens. (2) In four of the specimens, the collagen fibers covering the residual bone crest showed a hyalinized area. (3) Mucoid collagen degeneration was seen in all specimens. (4) The most striking finding, common to all specimens, was the epithelial remnants. Resting and proliferating types were identified. (5) Chronic inflammation was found in all specimens. (6) Both osteoid and necrotic bone types were observed. (7) An outstanding characteristic of the residual alveolar ridge was the reinforcement of the internal structure of the bone by endosteal apposition.

Aged↗
PubMed1988

Lipodystrophic diabetes mellitus. Investigations of lipoprotein metabolism and the effects of omega-3 fatty acid administration in two patients.

We investigated the metabolic effects of omega-6 (safflower oil) and omega-3 (fish oil) fatty acid-enriched diets (65% carbohydrate, 20% fat) in two patients with a syndrome of diabetes mellitus, lipodystrophy, acanthosis nigricans, chylomicronemia, and abdominal pain. 3H-glycerol was used to evaluate triglyceride-rich lipoprotein-triglyceride (TRLP-TG) metabolism, and changes in glucose and insulin dynamics were also studied. On the omega-6 diet, both subjects demonstrated four- to five-times normal rates of TRLP-TG production and glycerol biosynthesis, and striking decrements in the fractional catabolic rate (FCR) for TRLP-TG and TRLP-particles. Both subjects had elevations in nonesterified fatty acid (NEFA) concentrations. In one patient, the omega-3 diet markedly decreased serum triglycerides and newly synthesized triglyceride glycerol production, in association with a fall in NEFA. In both subjects, plasma glycerol reutilization for triglyceride synthesis, normal on the omega-6 diet, was abolished on the omega-3 regimen. Plasma postheparin lipolytic activity was normal on both diets. On the omega-3 diet, xanthomas and hepatomegaly decreased and, in the patient who had no reduction in serum triglycerides, pancreatitis attacks virtually ceased. Mean 24-hour serum glucose levels were higher, and both basal and peak C-peptide responses to a carbohydrate meal were blunted on the omega-3 diet. One patient became ketonuric. We conclude the cause of hypertriglyceridemia in these patients was due to increased lipid synthesis and hypothesize that this is secondary to high plasma concentrations of NEFA. In addition, an omega-3 diet in these subjects inhibited insulin secretion and worsened glucose tolerance.

Adult↗
PubMed1994

Body fat distribution has weight-independent effects on clinical, hormonal, and metabolic features of women with polycystic ovary syndrome.

This study was performed to investigate whether different patterns of body fat distribution may have distinct effects on the clinical, hormonal, and metabolic features of women with clinical hyperandrogenism such as polycystic ovary syndrome (PCOS). Ninety-seven consecutive women with PCOS were included in the study after assessment of gynecological and obesity history and careful clinical examination. Women were divided into three tertile groups based on the waist to hip ratio (WHR). Those with peripheral body fat distribution (P-BFD) had a WHR of less than 0.80, those with intermediate body fat distribution (I-BFD) had a WHR of 0.81 to 0.90, and those with abdominal body fat distribution (A-BFD) had a WHR exceeding 0.90. Baseline blood and urine samples were obtained for several hormone and lipid determinations, and the response of glucose, insulin, and C-peptide to a glucose oral challenge (75 g) was investigated. In the PCOS group, WHR values were higher than those used to define P-BFD and A-BFD in the normal female population. As WHR values increased, a significantly greater prevalence of obesity and acanthosis nigricans and a lower prevalence of acne was present. No significant differences were present in any of the other clinical features between the three groups. Ovarian morphology and volumes were similar in all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1978

Benign enlargement of the labia minora: report of two cases.

2 cases of bilateral hypertrophy of the labia minora are recorded. The patients presented with vulvar discomfort and redundant labia and reduction vulvoplasty was carried out. The resected specimens showed marked hyperplasia of the non-hair-bearing sebaceous glands, acanthosis, keratosis, and hyperpigmentation of the epithelium and a variable degree of neoangiogenesis and fibrosis in the upper dermis. No cause was established clinically or pathologically. The etiology and pathogenesis of this condition are briefly discussed.

Adult↗
PubMed1975

Ultrastructural study of focal epithelial hyperplasia.

Biopsy material from two young Israeli patients with focal epithelial hyperplasia revealed acanthosis, papillomatosis, and the presence of many epithelial cells with a clear cytoplasm in the basale and stratum spinosum. Many of the inclusions seen with the electron microscope had the morphologic appearance of lysosomes, but definite identification must await cytochemical evidence.

Adolescent↗
PubMed1980

Focal palmoplantar and oral mucosa hyperkeratosis syndrome: a report concerning five members of a family.

Focal palmoplantar and oral mucosa hyperkeratosis is a rare inherited disease that is transmitted as an autosomal dominant trait. Five affected members of a Greek family are described. All affected members of this family had hyperkeratosis of the palms, soles and attached gingiva. In addition, less severe hyperkeratosis was observed in areas of the oral mucosa subject to pressure and friction (palate, lateral border of the tongue, and retromolar pad). On histologic examination of biopsy material from the gingiva and the soles, severe hyperkeratosis and acanthosis were noted. Because hyperkeratotic lesions were located in areas of the oral mucosa in addition to the attached gingiva, the name Focal palmoplantar and oral mucosa hyperkeratosis syndrome is proposed.

Adult↗