Lichen sclerosus-lichen planus overlap in a patient with hepatitis C virus infection.
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Hepatitis C, Chronic↗
Biomedical subjects
J C Haley
Publications and source records attributed to J C Haley.
"Juvenile" xanthogranuloma: an immunophenotypic study with a reappraisal of histogenesis.
The non-Langerhans histiocytoses, a nosologic category to which juvenile xanthogranuoma (JXG) belongs, represent a heterogenous collection of disorders related to the monocyte/macrophage lineage. The dermal dendrocyte was previously proposed as the cell of origin for JXG on the basis of Factor XIIIa reactivity, a suggestion that does not fully explain the occasional xanthogranulomatous proliferations localizing exclusively to extracutaneous sites. This study applies a panel of recently developed immunohistochemical markers to JXGs and relates the phenotype of this process to new concepts of monocyte/dendritic cell ontogeny. Twenty-seven JXG, ten dermatofibromas (DF), and ten age-matched normal skin specimens were stained using standard immunohistochemistry methods, and all JXGs were fascin+ and CD68+, although 26 of 27 were reactive for HLA-DR, 25 of 27 for Factor XIIIa, 25 of 27 for LCA, 21of 27 for CD4, and 8 of 27 for polyclonal s100. Six of those eight polyclonal S100+ cases were also reactive for monoclonal S100. None of those cases was reactive for CD1a, CD3, CD21, CD34, or CD35. Eight of ten dermatofibromas were FXIIIa+; all were negative for HLA-DR, LCA, CD4, and polyclonal s100. In controls, fascin+ dendritic cells were present but did not stain for Factor XIIIa, S100, or CD4. Based on the morphologic and phenotypic overlap of the lesional cells in JXGs and plasmacytoid monocytes, it would appear that the plasmacytoid monocyte might be considered the putative normal counterpart of the major cellular population of JXGs, a proposal that helps explain the extra-cutaneous, visceral, and soft tissue location that have been reported for occasional cases of JXG. We would also conclude that neither Factor XIIIa-nor S100+ results should preclude the diagnosis of JXG, and find that reactivity for CD4 and LCA may be used to distinguish JXG from DF when the latter is heavily lipidized or the former is not.
Adolescent↗
The utility of submitting epidermoid cysts for histologic examination.
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Epidermal Cyst↗
Proliferative verrucous leukoplakia with cutaneous involvement.
Proliferative verrucous leukoplakia (PVL) is a distinct variant of oral leukoplakia characterized by a high rate of malignant transformation. Histologic features are variable and range from epithelial dysplasia to verrucous squamous cell carcinoma. To our knowledge, there have been no previous reports of cutaneous PVL. We present an interesting case of PVL involving the skin.
Aged↗
Experimental infection of human volunteers with Haemophilus ducreyi does not confer protection against subsequent challenge.
Two groups of human volunteers were inoculated with 2 doses of live Haemophilus ducreyi 35000HP. The reinfection group consisted of 7 subjects who previously had participated in experimental infection with 35000HP to the pustular stage of disease. The control group consisted of 7 naive subjects. Papules developed at 92.8% (95% confidence interval [CI], 66.1%-99.8%) of sites inoculated with live bacteria, in the reinfection group, and at 85.7% (95% CI, 57.2%-98. 2%) of sites in the control group. Sixty-nine percent (95% CI, 36. 8%-90.9%) of papules evolved into pustules in the reinfection group, compared with 41% (95% CI, 15.2%-72.3%) in the control group. The recovery rates of H. ducreyi from surface cultures and the histopathology of biopsies obtained from both groups were similar. Thus, experimental infection to the pustular stage of disease does not provide protective immunity against subsequent challenge.
Adult↗
Expression of sialylated or paragloboside-like lipooligosaccharides are not required for pustule formation by Haemophilus ducreyi in human volunteers.
The lipooligosaccharide (LOS) of Haemophilus ducreyi, the etiologic agent of chancroid, chemically and immunologically resembles human glycosphingolipid antigens. To test whether LOS that contains paragloboside-like structures was required for pustule formation, an isogenic mutant (35000HP-RSM2) was constructed in losB, which encodes D-glycero-D-manno-heptosyltransferase. 35000HP-RSM2 produces a truncated LOS whose major glycoform terminates in a single glucose attached to a heptose trisaccharide core and 2-keto-3-deoxyoctulosonic acid. Five human subjects were inoculated with 35000HP and 35000HP-RSM2 in a dose-response trial. For estimated delivered doses (EDDs) of >/=25 CFU, the pustule formation rates were 80% for 35000HP and 58% for 35000HP-RSM2. Preliminary data indicated that a previously described Tn916 losB mutant made a minor glycoform that does not require DD-heptose to form the terminal N-acetyllactosamine. If 35000HP-RSM2 made this glycoform, then 35000HP-RSM2 could theoretically make a sialylated glycoform. To test whether sialylated LOS was required for pustule formation, a second trial comparing an isogenic sialyltransferase mutant (35000HP-RSM203) to 35000HP was performed in five additional subjects. For EDDs of >/=25 CFU, the pustule formation rates were 30% for both 35000HP and 35000HP-RSM203. The histopathology and recovery rates of H. ducreyi from surface cultures and biopsies obtained from mutant and parent sites in both trials were similar. These results indicate that neither the expression of a major glycoform resembling paragloboside nor sialylated LOS is required for pustule formation by H. ducreyi in humans.
Adult↗
Benign vulvar tumors.
Benign tumors of the vulva, although relatively uncommon, are often referred to dermatologists for evaluation and treatment. The clinical features of benign tumors may overlap with malignant neoplasms, and therefore, a biopsy is often necessary to make a definitive diagnosis. This article discusses benign tumors of the vulva that are not associated with infectious agents and presents their classification according to cell of origin.
Adenoma, Sweat Gland↗
Cost of illness studies for schizophrenia: components, benefits, results, and implications.
Although schizophrenia affects only about 1% of the worldwide population, it is costly to patients, their families, community care centers, hospitals, and society. International cost of illness studies show a wide variation, with annual costs ranging from Australia's $139 million US dollars (1975) to the cost in the United States of $65.2 billion US dollars (1991). Since methodology and assumptions vary widely from study to study and country to country, it is a challenge to directly compare the results of these studies. Nevertheless, the published COI studies reveal several consistent trends. Inpatient care may be the largest cost driver for direct costs, suggesting that relapse prevention is key to reducing healthcare costs. Indirect costs resulting from the patient's and caregiver's inability to fully participate in the work force is extensive due to the debilitating nature of the disease and its early onset. Lastly, when prescription drug costs were reported, they represented no more than 3% of direct cost.
Australia↗
The frequency of histologically dysplastic nevi in 199 pediatric patients.
Many uncertainties surround the definition, frequency, and significance of dysplastic nevi in children. Consequently the management of dysplastic nevi in the pediatric population has been largely derived from the studies of adults. Biopsies are usually performed on this young age group because of lesion change or abnormal appearance. One might therefore assume that the frequency of histologically diagnosed dysplastic nevi would be higher in children than in adults. We decided to attempt to verify this assumption by determining the frequency of dysplastic nevi diagnosed histologically in the pediatric population. To do this we reviewed 199 cutaneous pathology reports of nevi removed from patients less than 18 years old and submitted to a community-based dermatopathology laboratory. The diagnosis of dysplastic nevus was made based on histologic criteria recommended by the World Health Organization Melanoma Program. We found that 3 of 199 nevi submitted for histologic analysis met the histologic criteria for dysplastic nevus. There were no melanomas. Our data suggest that there is an extremely low frequency of histologically confirmed dysplastic nevi within the general pediatric population.
Adolescent↗