Pigmentation Of Mucosa Research Articles

Total hip replacement infected with Mycobacterium tuberculosis complicated by Addison disease and psoas muscle abscess: a case report

IntroductionProsthetic joint infection due to Mycobacterium tuberculosis is occasionally encountered in clinical practice. To the best of our knowledge, this is the first report of a prosthetic joint infection due to Mycobacterium tuberculosis complicated by psoas abscesses and secondary Addison disease.Case presentationA 67-year-old immunocompetent Caucasian woman underwent total left hip arthroplasty because of osteoarthritis. After 18 months, she underwent arthroplasty revision for a possible prosthetic infection. Periprosthetic tissue specimens for bacteria were negative, and empirical antibiotic therapy was unsuccessful. She was then admitted to our department because of complications arising 22 months after arthroplasty. A physical examination revealed a sinus tract overlying her left hip and skin and mucosal pigmentation. Her levels of C-reactive protein, basal cortisol, adrenocorticotropic hormone, and sodium were out of normal range. Results of the tuberculin skin test and QuantiFERON-TB Gold test were positive. Computed tomography revealed a periprosthetic abscess and the inclusion of the left psoas muscle. Results of microbiological tests were negative, but polymerase chain reaction of a specimen taken from the hip fistula was positive for Mycobacterium tuberculosis. Our patient's condition was diagnosed as prosthetic joint infection and muscle psoas abscess due to Mycobacterium tuberculosis and secondary Addison disease. She underwent standard treatment with rifampicin, ethambutol, isoniazid, and pyrazinamide associated with hydrocortisone and fludrocortisone. At 15 months from the beginning of therapy, she was in good clinical condition and free of symptoms.ConclusionsProsthetic joint infection with Mycobacterium tuberculosis is uncommon. A differential diagnosis of tuberculosis should be considered when dealing with prosthetic joint infection, especially when repeated smears and histology examination from infected joints are negative. Clinical outcomes of prosthetic joint infection by Mycobacterium tuberculosis are unpredictable, especially given the limited literature in this field and the uncertainty of whether medical treatment alone can eradicate the infection without prosthesis removal. Furthermore, this case report raises interesting issues such as the necessity of a follow-up evaluation after treatment based on clinical conditions, the utility of a more standardized length of treatment for periprosthetic tuberculous infection, and the importance of a high diffusion capacity of anti-mycobacterial agents in order to eradicate the infection.

A Case of Oral Mucosa Pigmentation Diagnosed as an Amalgam Tattoo

A Case of Oral Mucosa Pigmentation Diagnosed as an Amalgam Tattoo

Mucosal Pigmentation Caused by Imatinib: Report of Three Cases

Imatinib mesylate (STI-571, Gleevec(®)), a tyrosine kinase inhibitor, is a first-line medication for treating chronic myeloid leukemia (CML). Clinical studies revealed very good hematological responses without significant side effects. However, imatinib may lead to mucosal pigmentation. Three patients, two males aged 64 and 53 and one female aged 29 presented with a painless, diffuse, grey-blue pigmentation of the mucosa of the hard palate. Both male patients had a history of CML and had been on imatinib for 4 and 10 years, respectively. The female patient had been on imatinib for 4 years for pelvic fibromatosis. Histopathologically, deposition of fine, dark-brown, spherical granules was noted within the connective tissue. There was no inflammation or hemorrhage, and no melanosis or melanocytic hyperplasia in the epithelium. The granules stained positively for both Fontana-Masson and Prussian blue stains. Imatinib-induced pigmentation is similar to that caused by other medications such as minocycline and anti-malarial medications, namely the deposition of a drug metabolite containing melanin and iron.

An unusual cause of small-intestine mucosal pigmentation

An unusual cause of small-intestine mucosal pigmentation

Oral manifestations of habitual khat chewing: a case-control study

Khat, or qat (Catha edulis), is a shrub indigenous to Yemen and certain parts of eastern Africa. Chewing the leaves, which have sympathomimetic and euphoric effects, is a popular habit in numerous countries including the Yemenite population in Israel. Khat has potentially significant toxic effects; however, its oral effects have been only sporadically examined and some changes suggested. The aim of this study was to assess the association between habitual Khat use and oral/dental pigmentation, gingival health, and reports of oral dryness. Forty-seven Yemenite Israeli individuals >30 years old, who chewed Khat at least twice a week for over 3 years, and 55 control subjects were studied. All individuals underwent standard clinical oral examinations for color changes and gingival health. White changes were significantly more prevalent in the khat chewers, identified primarily at the chewing site (83% vs. 16%). The difference in the prevalence of oral mucosal pigmentation between nonchewing nonsmoking (66.7%) and the khat-chewing (100%) groups was highly significant. The mean gingival index and the depth of periodontal pockets of the khat-chewing subjects were significantly reduced at the chewing side compared with the nonchewing side. Increased gingival recession was recorded on the khat-chewing side. Discoloration of the teeth adjacent to the site of chewing was recorded. Oral dryness occurring 30 minutes after initiating the khat-chewing session was reported by khat users. Khat chewing may result in a number of changes in the oral mucosa and the dentition. The mechanical and chemical irritation may result in the development of mucosal white lesions and dark pigmentation. Khat chewing may reduce aspects related to risk of gingival and periodontal inflammation, but it appears to be associated with attachment loss at the site of chewing.

Association of clinical findings in Yusho patients with serum concentrations of polychlorinated biphenyls, polychlorinated quarterphenyls and 2,3,4,7,8-pentachlorodibenzofuran more than 30 years after the poisoning event

BackgroundThe Yusho poisoning incident, which was caused by rice bran oil contaminated with polychlorinated biphenyls (PCBs), polychlorinated quarterphenyls (PCQs) and polychlorinated dibenzofurans (PCDFs) generated by heat denaturation of PCB, occurred in 1968 in western Japan. Annual physical, dermatological, dental, ophthalmological and laboratory examinations were conducted for Yusho patients after the incident. From 2001, blood levels of individual PCDF congeners were also measured. The blood levels of 2,3,4,7,8-pentachlorodibenzofuran (2,3,4,7,8-PeCDF), PCBs and PCQs in Yusho patients were found to be significantly higher than those of the general population. We investigated the relationships between blood concentrations of 2,3,4,7,8-PeCDF, PCBs and PCQs in Yusho patients and the items measured in the annual medical examination.MethodsMedical and laboratory examination data from 501 Yusho patients enrolled in the study from 2001 to 2004 were analyzed. The relationships between blood 2,3,4,7,8-PeCDF, PCB and PCQ concentrations and medical/laboratory examination data were investigated using principal components and logistic regression analyses.ResultsSerum Concentrations of 2,3,4,7,8-PeCDF, PCBs and PCQs in blood tended to correlate with either acneform eruptions, black comedones, cutaneous and mucosal pigmentation, and hypersecretion of meibomian glands as well as general fatigue, headaches, cough/sputum, abdominal pain, arthralgia, increased blood sugar, increased serum γ-GTP and decreased total bilirubin. The majority of these signs and symptoms are included in the diagnostic criteria for Yusho.ConclusionAfter Yusho patients had suffered chronic exposure to these chlorinated compounds for more than 35 years, the serum concentration of 2,3,4,7,8-PeCDF in blood was significantly related to arthralgia and decreased albumin/globulin (A/G) ratio; the serum concentration of PCBs was significantly related to ophthalmologic symptoms; and the serum concentration of PCQ to increased total cholesterol. These findings suggest that the co-contaminants may affect other functions than those originally associated with Yusho.

Nasal argyria (deposition of silver-selenium) in the photographic film industry: histopathology and microanalysis

Argyria is grayish black discoloration of skin or mucous membrane caused by silver deposition; it may be localized or diffuse. Diffuse argyria occurs as a result of elevated silver levels in blood, whereas localized argyria occurs when there is direct deposition from an external source. Exposure to silver was common in the last century; however, in the present times, argyria is an uncommon entity because of the restrictive use of silver-containing medicines and decreased industrial exposure. Occupational exposure is common among silversmiths [1], mineworkers, photographic film laboratory workers, and individuals involved in the electroplating industry. Cases after prolonged use of silver salts for wound dressing, acupuncture needles, silver earrings [2], eyedrops containing silver, and irrigation of urethral or nasal mucous membranes with silver-containing solutions have been reported. Argyria has also been seen among patients undergoing dental procedures, such as silver amalgam tattooing. 2. Case presentation A 66-year-old man had nasal blockage and intermittent drainage from both nares for many years. The drainage was watery and persistent even after being treated with multiple medications. Nasal examination revealed bilateral bluish black pigmentation of mucosa in the superior-anterior portion of the nasal septum. There was no other area of pigmentation either on the skin or elsewhere. The patient’s history is significant for stroke, myocardial infarction, and hypertension. He worked as a supervisor in the chemical sensitizing paper unit of a photographic film–producing company before retiring in 1992 and was exposed to a large number of chemicals, including silver nitrate. In 2004, a computed tomographic scan of the patient’s paranasal sinuses showed minimal mucosal thickening in the left maxillary sinus. A small biopsy specimen of the pigmented nasal mucosa was taken under local anesthesia and sent for routine histopathologic analysis. Subsequently, analysis using scanning electron microscopy (SEM) and energy dispersive x-ray spectroscopy (EDS) was also performed.

Isolated Adrenocorticotropic Hormone Deficiency Presenting With Delirium

Back to table of contents Previous article Next article Letters to the EditorFull AccessIsolated Adrenocorticotropic Hormone Deficiency Presenting With DeliriumKIYOTAKA NEMOTO M.D.YOICHI KAWANISHI M.D., Ph.D.HIROAKI SUZUKI M.D., Ph.D.KATSUYOSHI MIZUKAMI M.D., Ph.D.TAKASHI ASADA M.D., Ph.D.,KIYOTAKA NEMOTO M.D.Search for more papers by this authorYOICHI KAWANISHI M.D., Ph.D.Search for more papers by this authorHIROAKI SUZUKI M.D., Ph.D.Search for more papers by this authorKATSUYOSHI MIZUKAMI M.D., Ph.D.Search for more papers by this authorTAKASHI ASADA M.D., Ph.D.Search for more papers by this author,Published Online:1 Sep 2007https://doi.org/10.1176/appi.ajp.2007.07010193AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To The Editor: Adrenocortical insufficiency causes various physical symptoms, including weakness, fatigue, and loss of appetite due to cortisol deficiency. It is also known to cause psychiatric symptoms such as depression or apathy. However, there are only a few reports of delirium associated with this insufficiency (1) . We present a case of delirium, which was caused by secondary adrenocortical insufficiency because of isolated adrenocorticotropic hormone deficiency. “Mr. A,” a 74-year-old man without a history of neuropsychiatric disease, complained of diarrhea followed by fatigue and a loss of appetite. A general practitioner found hyponatremia, and an intravenous drip infusion of normal saline solution was performed for 1 week. However, the patient’s fatigue and loss of appetite remained. Two weeks later, he went into a delirious state and was admitted to our psychiatric unit.On admission, a physical examination revealed weakness of the patient’s extremities. He did not have a history of receiving glucocorticoids or skin and mucosal pigmentation. Blood examinations showed hyponatremia (121 mEq/l), neutropenia, and eosinophilia (white blood cell: 4600/ml [20.3% neutrophils and 8.3% eosinocytes]). Potassium and plasma glucose were within normal limits. These findings led us to consider the possibility of adrenocortical insufficiency, and we consulted an endocrinologist for further evaluation. Additional tests revealed low levels of cortisol (1 mg/dl) and adrenocorticotropic hormone (5.9 pg/ml). The growth hormone, luteinizing hormone, follicle-stimulating hormone, all of the thyroid hormones, and prolactin levels were within normal limits. A quad pituitary stimulation with the corticotropin releasing hormone, growth hormone releasing hormone, thyrotropin releasing hormone, and gonadotropin releasing hormone caused a normal elevation of growth hormone, thyroid-stimulating hormone, prolactin, luteinizing hormone, and follicle-stimulating hormone levels. However, the adrenocorticotropic hormone level remained low. A magnetic resonance imaging study showed no tumor or atrophy of the pituitary. These results excluded panhypopituitarism and led us to diagnose the patient with secondary adrenocortical insufficiency because of isolated adrenocorticotropic hormone deficiency. A daily dose of hydrocortisone (20 mg by mouth) was administered, which resulted in a dramatic improvement of the patient’s consciousness level and hyponatremia, followed by recovery from the delirium in 3 days.To our knowledge, our case is the second report of delirium associated with adrenocortical insufficiency because of isolated adrenocorticotropic hormone deficiency. Isolated adrenocorticotropic hormone deficiency is a rare cause of secondary adrenocortical insufficiency generally observed in the elderly. Clinical features overlap greatly in isolated adrenocorticotropic hormone deficiency and Addison"s disease. Since symptoms are nonspecific, diagnosis is often delayed, particularly in the identification of isolated adrenocorticotropic hormone deficiency (2) . In our case, noticing neutropenia and eosinophilia, along with hyponatremia, was the key to the right diagnosis (2) . Delirium can be found in adrenocortical insufficiency as well as cortisol excess. Therefore, in patients with delirium, recognizing the potential role of cortisol as a cause is important. If adrenocortical insufficiency lies behind the delirium, cortisol replacement will be the only effective treatment, and dramatic recovery from the delirious state can be expected. Tsukuba, Ibaraki, JapanThe authors report no competing interests.This letter (doi: 10.1176/appi.ajp.2007.07010193) was accepted for publication in April 2007.

Smokers’ Melanosis in a Nigerian Population: A Preliminary Study

Terms relating to pigmentation of the oral mucosa include physiologic (racial) pigmentation, oral pigmented nevi, oral melanotic maculae, melanoma, and smokers' melanosis. The literature is replete with studies about oral mucosal pigmentation which is thought to result from melanin incontinence. The documented etiological factors are both local and systemic and include hormones, drugs, smoking, and idiopathic causes. This study investigated the prevalence of melanosis among Nigerian smokers and controls who were non-smokers. A total of 1270 sites were examined in 253 subjects consisting of 60 smokers and 193 non-smokers. They were all systemically healthy adults drawn from 12 factories located in different urban and rural settings in the state of Lagos in Nigeria. Five oral mucosal sites were examined per subject. A single examiner performed all examinations and recorded all findings. Pigmentation was scored either as "present" or "absent." Subjects' smoking status, degree, and duration of smoking were ascertained and recorded using an examiner-administered questionnaire. There were five pigmented sites (0.52%) among non-smokers and 18 (6%) among smokers. The buccal mucosa was the most frequently pigmented site found in smokers while the lingual mucosa was the most common site found for non-smokers. The prevalence of pigmented sites increased directly among smokers with the duration of smoking (years); degree of smoking (cigarettes smoked per day); and smoking pack-years (degree of smoking divided by 20 and multiplied by duration of smoking, where 20 is the average number of cigarettes in a pack of cigarettes). SPSS version 11.0 was used for data entry and analysis. Frequency distributions were generated for all categorical variables for descriptive aspects of the analysis. Means were determined for quantitative variables such as age and number of cigarettes smoked. For homogenous variances, the student's t test was used for quantitative variables between smokers and non-smokers, while for non-homogenous variances the Mann-Whitney test was adopted. Chi-square statistic was used for comparisons between smokers and non-smokers. In tables with low expected frequencies, Fisher's exact test was adopted. Statistical tests yielding p-values = or <0.5 were considered significant. Smokers in this study had a significantly higher prevalence of pigmented oral mucosal sites (melanosis) than non-smokers. The number of pigmented sites increased with the degree and duration of smoking. The buccal mucosa was the most frequently pigmented site found among the smokers in this study.

Endoscopic examination of the upper respiratory tract and oesophagus in small ruminants: Technique and normal appearance

The aim of this study was to describe the technique of rhinolaryngotracheobronchoscopy and oesophagoscopy in small ruminants and to report the normal endoscopic appearance of the structures of the upper respiratory tract and oesophagus. Thirty sheep and 30 goats, all clinically normal, underwent rhinolaryngotracheobronchoscopy and oesophagoscopy using a flexible endoscope (length 100 cm; diameter 4 mm). The anatomical features of the structures and the appearance of the mucosa were investigated. The degree of mucosal pigmentation varied between breeds. The appearance of the pharyngeal tonsil and the shape of the trachea in cross-section showed most individual variation. The technique was easily performed and sedation was necessary in only a few cases. No major complications were encountered. It was concluded that the procedure facilitated more accurate diagnosis and prognosis of conditions of the upper respiratory tract and oesophagus.

Antipaludéens de synthèse

The antimalarials, mainly chloroquine and hydroxychloroquine, derive from the quinoleine core of quinine. Their initial therapeutic indication was the treatment of malaria attacks but, because of anti-inflammatory and immuno-modulatory activities, they have been since used to treat many other pathologies, in particular dermatological ones. For some of these pathologies, lupus or porphyria cutanea tarda for example, the use of these molecules is based on obvious scientific evidence. For other pathologies (cutaneous sarcoidosis, polymyositis, polymorphous light eruption...), the data on the medical literature corroborating the daily clinical practice are extremely poor. Their toxicity is limited. Their most common toxic effects are gastrointestinal (mild nausea or diarrhea) or mucocutaneous (reversible skin or mucosal pigmentation). Their most serious and dreaded side effect, retinopathy, can be largely prevented by using amounts of APS adapted to the weight of the patients. The recommended "safe" daily dose for hydroxychloroquine is 6.5 mg per kilogramme of body weight and for chloroquine 4 mg per kilogramme of body weight. However, at 6- to 12 months intervals, follow-up eye examinations should be performed.

Short Communication

We report a case of oral mucosal pigmentation secondary treatment with mepacrine, with sparing of the denture bearing area. To our knowledge this phenomenon has not been reported since the association between antimalarial therapy and mucosal pigmentation was first described.

Complexo de Carney: relato de um caso e revisão da literatura

Carney complex (CNC) is a familial multiple neoplasia syndrome associated with abnormal skin and mucosal pigmentation, primary pigmented nodular adrenocortical disease (PPNAD), cardiac and cutaneous myxomas, GH and PRL pituitary adenoma, testicular tumors, thyroid adenoma or carcinoma and ovarian cysts. CNC is inherited as an autosomal dominant trait and has some clinical similarities to McCune-Albright syndrome. Recently, genes related to stimulation of the cAMP signaling pathway have been considered candidates for causing CNC. We report a 17-yr-old man with PPNAD, lentigines on the face and severe osteoporosis. In this article we aim at describing the clinical aspects and molecular genetics of CNC and also summarizing diagnostic criteria for CNC and recommendations for follow-up.

Oral mucosal pigmentation secondary to minocycline therapy: report of two cases and a review of the literature

Minocycline is a semisynthetic broad-spectrum antimicrobial agent that was first introduced into clinical practice in 1967. The most common use of minocycline is for the long-term treatment of acne vulgaris. A well-recognized side effect of minocycline treatment is pigmentation, which has been reported in multiple tissues and fluids including thyroid, skin, nail beds, sclera, bone, and teeth. While there have been several reports of oral pigmentation following minocycline therapy, these have been, for the most part, pigmentation of the underlying bone with the overlying oral mucosa only appearing pigmented. We report two cases of actual pigmented oral mucosal lesions on the hard palate secondary to minocycline therapy with the accompanying histopathology, followed by a discussion of minocycline-induced oral pigmentation and a differential diagnosis of these lesions.

Oral mucosal pigmentation secondary to treatment with mepacrine, with sparing of the denture bearing area

We report a case of oral mucosal pigmentation secondary treatment with mepacrine, with sparing of the denture bearing area. To our knowledge this phenomenon has not been reported since the association between antimalarial therapy and mucosal pigmentation was first described.

An Atlas of Diseases of the Nail

Readers are attracted to books by their appearance as well as their subject, and this one looks tempting, with stylish layout, clear headings and a good balance of pictures and text. The introductory chapter on nail anatomy and basic science is straightforward, although the two references are at least 7 years old. An alphabetical catalogue of nail signs and their definitions is neat and concise until ‘O’, where it digresses into aetiology and management. A classification by colour is marred by linguistic indecision, with separate sections on ‘red nails’ and ‘erythronychia’. Chapters on infections, signs of cutaneous and systemic disease, and age-related disorders contain repetitions, inaccuracies and the sort of pictures most dermatologists keep in their collections. By the time we reach ‘nail surgery’ and ‘nail cosmetics’ the temptation has worn off. It is unclear who this book is aimed at. Those keen to differentiate onychorrhexis, onychauxis and onychocryptosis (caused by ‘faulty biomechanics in the elderly’) would want more facts. It is impossible to look them up because the index, at least in my copy, stops abruptly and mysteriously at N (for nail). Those seeking treatment advice will find it unreferenced, incomplete and sometimes bizarre: examples include biotin for brittle nails, omission of amorolfine and tioconazole as topical antifungals, and digital amputation for keratoacanthoma. Illustrations of ‘epidermolysis bullosa simplex’ (which rarely affects the nails) clearly show the scarring, milia and nail dystrophy characteristic of dystrophic epidermolysis bullosa. I would like the lay public to learn that those ubiquitous little white dots and lines (‘punctate and transverse leuconychia’) are caused by minor trauma, not calcium deficiency, but despite its coffee-table format this is not a book to leave in your sitting room. Some gruesome pictures are rendered more lurid by unfortunate colour balancing, while others are mercifully overexposed. To their credit, these authors clearly love their subject. They particularly like Beau's lines, which pop up with almost the same text in three different chapters. They enthuse over longitudinal ridges and bands. They enjoy nail pits. And they cannot resist the visual economy of photographing nails next to an associated anomaly. This is sometimes effective—for example, in showing the nail and mucosal pigmentation of Laugier-Hunziger syndrome. More often one or both abnormalities are out of focus, the patients apparently gesturing incomprehensibly. At least this atlas demonstrates a trick unknown to medical photographers, that fingernails are better photographed from the palmar aspect of the hand with fingers flexed and nails approximated, than from the dorsal aspect with fingers straight and nails far apart.

Mutations of the gene encoding the protein kinase A type I-alpha regulatory subunit (PRKAR1A) in patients with the "complex of spotty skin pigmentation, myxomas, endocrine overactivity, and schwannomas" (Carney complex).

Carney complex (CNC) is a familial multiple neoplasia syndrome associated with abnormal skin and mucosal pigmentation. The complex has features overlapping those of McCune-Albright syndrome (MAS) and the other multiple endocrine neoplasias (MENs). CNC is inherited as an autosomal dominant trait, and the responsible genes have been mapped by linkage analysis to loci at 2p16 and 17q22-24. Because of its unusual biochemical features (e.g., paradoxical responses to various endocrine signals) and its clinical similarities to MAS, genes implicated in cyclic nucleotide-dependent signaling, including GNAS1 (which is responsible for MAS), had been considered likely candidates for causing CNC. The gene encoding the protein kinase A (PKA) type I-alpha regulatory subunit (RI alpha), PRKAR1A, had been mapped to 17q22-24; loss-of-heterozygosity (LOH) analysis using polymorphic markers from this region revealed consistent changes in tumors from patients with CNC, including those from one family previously mapped to 17q22-24. Investigation of a polymorphic site within the 5' of the PRKAR1A gene showed segregation with the disease and retention of the allele bearing the disease gene in CNC tumors. Mutations of the PRKAR1A gene were also found to have occurred de novo in sporadic cases of CNC; no mutations were found in kindreds mapping to 2p16. Thus, genetic heterogeneity in CNC was confirmed; in total, 41% of all patients with CNC had mutations in the PRKAR1A gene. All mutations were frameshifts, insertions, and deletions that led to nonsense mRNA and premature termination of the predicted peptide product. Functional studies in CNC tumors suggested that inactivating mutations of the PRKAR1A gene led to nonsense mRNA decay (the mutant peptide product was not present) and were associated with dysregulated PKA activity, increased responsiveness to cAMP, and excess of type-II PKA activity. We conclude that the PRKAR1A gene, coding for the RIalpha subunit of PKA, a critical cellular component of a number of cyclic nucleotide-dependent signaling pathways, is mutated in a subset of patients with CNC. In their tumors, there is LOH of the normal allele, suggesting that normal RI-alpha may have tumor suppression function in the tissues affected by CNC. An excess of type-II PKA activity was present in affected tissues, which may be responsible for the apparent tumorigenicity of PRKAR1A mutations in endocrine tissues.

Oral lesions and conditions associated with human immunodeficiency virus infection in 300 south Indian patients.

Human immunodeficiency virus infection/acquired immunodeficiency syndrome (HIV/AIDS) is a major health problem in India. The National AIDS Control Organisation (NACO) of India reports a seropositivity of 25.03 per thousand for the whole country, as of October 1999. In spite of this high prevalence there are very few reports of oral lesions and conditions in Indian HIV/AIDS patients, which are important in early diagnosis and management of these patients. The present report describes the oral lesions in 300 HIV positive symptomatic patients presenting to us at RAGAS-YRG CARE, a non-governmental organisation in Chennai, South India, over a period of 9 months in 1998. Lesions were diagnosed on clinical appearance using international criteria. Of the 300 patients 89% had acquired the infection through heterosexual contact. There were 205 males and 95 females, aged from 7 months to 72 years. Forty-seven percent of the patients were in the age group 21-30 years. CD4 counts were ascertained for 105 patients, 64 (62%) had CD4 counts < or = 200. A total of 217 (72%) of the 300 patients had some oral lesion when examined. Gingivitis (47%) and pseudomembranous candidiasis (33%) were the most common oral lesions. The other oral lesions seen were oral mucosal pigmentation (23%), erythematous candidiasis (14%), periodontitis (9%), angular cheilitis (8%), oral ulcers (3%), oral hairy leukoplakia (3%), hyperplastic candidiasis (1%), oral submucous fibrosis (2%) and one case of leukoplakia. Oral lesions occur commonly in HIV infection. A comprehensive oral examination may not only suggest HIV disease but may also be useful in monitoring the disease progression. This is a cost-effective procedure, which may be useful in screening large populations in developing countries like India.

Genetics of Carney complex and related familial lentiginoses, and other multiple tumor syndromes.

Carney complex is a multiple endocrine neoplasia (MEN) syndrome that affects the adrenal cortex, the pituitary and thyroid glands, and the gonads. The complex is also associated with skin and mucosa pigmentation abnormalities and myxoid and other neoplasms of mesenchymal and neural crest origin. Thus, this syndrome also belongs to another group of genetic disorders, the lentiginoses (or lentigenoses), which include the Peutz-Jeghers, LEOPARD, arterial dissections and lentiginosis, and Laugier-Hunziker syndromes, Cowden disease and Ruvalcaba-Myhre-Smith (Bannayan-Zonana) syndrome and the centrofacial, benign patterned and segmental lentiginoses, all of which can be associated with a variety of developmental defects. The inheritance of Carney complex, just like that of the other MENs and the lentiginoses, is autosomal dominant. Genetic loci or genes have been identified for Carney complex, Peutz-Jeghers and Ruvalcaba-Myhre-Smith syndromes, but not for other lentiginoses. Elucidation of the molecular defects responsible for these disorders is expected to shed light on aspects of early neural crest differentiation, the regulation of pigmentation, the development of autonomous endocrine function, and endocrine and nonendocrine tumorigenesis.

Genetics of Carney Complex and Related Familial Lentiginoses, and other Multiple Tumor Syndromes

Carney complex is a multiple endocrine neoplasia (MEN) syndrome that affects the adrenal cortex, the pituitary and thyroid glands, and the. gonads. The complex is also associated with skin and mucosa pigmentation abnormalities and myxoid and other neoplasms of mesenchymal and neural crest origin. Thus, this syndrome also belongs to another group of genetic disorders, the lentiginoses (or lentigenoses), which include the Peutz-Jeghers, LEOPARD, arterial dissections and lentiginosis, and Laugier-Hunziker syndromes, Cowden disease and Ruvalcaba-Myhre-Smith (Bannayan-Zonana) syndrome and the centrofacial, benign patterned and segmental lentiginoses, all of which can be associated with a variety of developmental defects. The inheritance of Carney complex, just like that of the other MENs and the lentiginoses, is autosomal dominant. Genetic loci or genes have been identified for Carney complex, Peutz-Jeghers and Ruvalcaba-Myhre-Smith syndromes, but not for other lentiginoses. Elucidation of the molecular defect...