Cases reported "Hyperplasia"

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1/27. persistent hyperplastic primary vitreous with retinal tumor in tuberous sclerosis: report of a case including tumoral immunohistochemistry and cytogenetic analyses.

    OBJECTIVE: The authors describe an ocular lesion combining the characteristics of persistent hyperplastic primary vitreous (PHPV) and a retinal tumor in an infant with tuberous sclerosis complex (TSC). STUDY DESIGN: Case report. methods: immunohistochemistry and cytogenetic studies were performed on TSC cells from an intraocular tumor in a 6-week-old infant. RESULTS: Histopathologic examination showed a thick fibrovascular membrane between the aspect of the lens and the astrocytic component of the mass. glial fibrillary acidic protein (GFAP) showed a variable intracytoplasmic reaction in the astrocytic proliferation, involving approximately 50% of the cells. Tissue culture studies showed a fairly rapid proliferation of fusiform cells, consistent with bipolar astrocytic cells. Cytogenetic studies showed one abnormal clone consisting of three hyperdiploid cells with a loss of chromosome 9 and a gain of chromosomes 6 and 12. CONCLUSION: The atypical localization of the retinal tumor could be explained by the fact that it was trapped during its proliferation by the retinal detachment associated with the PHPV.
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2/27. Dizygotic twin sisters with myelokathexis: mechanism of its neutropenia.

    Dizygotic twin sisters were first found to have neutropenia at 1 year of age when evaluated for recurrent pulmonary infections. Since then they have remained neutropenic (0.05 approximately 0.5 x 10(9)/l). Despite of their neutropenia, myeloid hyperplasia was evident on a marrow smear examination, and a number of cells were hypersegmented with fine interlobular bridging with chromatin strands and cytoplasmic vacuolation. Electron microscopy showed apoptotic cells with condensed nuclei and apoptotic bodies in the cytoplasm. Although life span, hydrogen peroxide production, phagocytosis, spreading, and chemotaxis of peripheral neutrophils were normal, the survival of bone marrow neutrophils in both infants was markedly decreased when compared with that of normal bone marrow neutrophils. During the bone marrow culture apoptotic neutrophils were observed at an earlier stage in both patients than in normal controls, biochemically and morphologically. Morphology of bone marrow neutrophils in both patients resembled that of cultured control bone marrow neutrophils. Peripheral neutropenia and appearance of characteristic neutrophils in the bone marrow in myelokathexis are considered to be an expression of apoptosis of bone marrow neutrophils.
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3/27. food-dependent Cushing's syndrome: possible involvement of leptin in cortisol hypersecretion.

    Stimulation ofcortisol secretion by food intake has been implicated in the pathogenesis of some cases of ACTH-independent Cushing's syndrome, via an aberrant response of the adrenal glands to gastric inhibitory polypeptide (GIP). We report here a novel case of food-dependent Cushing's syndrome in a patient with bilateral macronodular adrenal hyperplasia. In this patient we were able to confirm a paradoxical stimulation of cortisol secretion by GIP in vivo as well as in vitro on dispersed tumor adrenal cells obtained at surgery. In addition to GIP, in vitro stimulation of these cultured tumor adrenal cells with leptin, the secreted product of the adipocyte, induced cortisol secretion. By comparison, no such stimulation was observed in vitro in adrenal cells obtained from another patient with bilateral macronodular adrenal hyperplasia and Cushing's syndrome that did not depend on food intake, in tumor cells obtained from a solitary cortisol-secreting adrenal adenoma, and in normal human adrenocortical cells. These results demonstrate that as in previously described cases of food-dependent Cushing's syndrome, GIP stimulated cortisol secretion from the adrenals of the patient reported here. Therefore, they indicate that such a paradoxical response probably represents the hallmark of this rare condition. In addition, they suggest that leptin, which normally inhibits stimulated cortisol secretion in humans, participated in cortisol hypersecretion in this case. Further studies in other cases of food-dependent Cushing's syndrome, however, will be necessary to better ascertain the pathophysiological significance of this finding.
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4/27. Tumour necrosis factor alpha (TNF-alpha) interferes with Fas-mediated apoptotic cell death on rheumatoid arthritis (RA) synovial cells: a possible mechanism of rheumatoid synovial hyperplasia and a clinical benefit of anti-TNF-alpha therapy for RA.

    To investigate the mechanism of rheumatoid synovial hyperplasia (RASH), the influence of tumour necrosis factor alpha (TNF-alpha) on Fas-mediated apoptotic cell death (Fas-ACD) was examined on cultured rheumatoid synovial cells (RASCs). RASCs were obtained from the synovial tissues of eight patients with rheumatoid arthritis (RA) and SCs from eight patients with osteoarthritis (OA) were used as a control. To examine the influence of TNF-alpha on Fas-ACD, SCs were cultured with anti-Fas antibody (CH11) for 16 h in the absence or presence of different doses of recombinant TNF-alpha. ACD was determined by electron microscopic analysis and the percentage of apoptotic cells was calculated by trypan blue staining. In addition, the expression of Fas and Bcl-2 on RASCs was examined by flow cytometry. As a result, RASCs were more susceptible to Fas-ACD in vitro than OASCs. TNF-alpha interfered with Fas-ACD on RASCs in a dose-dependent manner. Moreover, removal of TNF-alpha activity by a neutralizing anti-TNF-alpha antibody (cA2) restored Fas-ACD. Flow cytometric analysis showed no significant changes in either Fas or Bcl-2 expression on RASCs after the culture with TNFalpha.These results suggest the following: (1) Fas-ACD might be diminished in vivo by local excessive TNF-alpha and this might contribute in part to RASH. (2) The inhibition of Fas-ACD on RASCs by TNF-alpha might not be associated with changes in the expression of Fas or Bcl-2. (3) In addition, considering a magnetic resonance imaging (MRI) finding of marked reduction in the RASH after cA2 treatment, blockade of TNF-alpha activity could restore Fas-ACD in RA synovium, implicating a clinical benefit of anti-TNF-alpha therapy for RA.
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5/27. Increased expression of vascular endothelial growth factor (VEGF) in Castleman's disease: proposed pathomechanism of vascular proliferation in the affected lymph node.

    Castleman's disease is a lymphoproliferative disorder of unknown etiology characterized by enlarged hyperplastic lymph nodes with marked vascular proliferation. To evaluate the possible involvement of vascular endothelial growth factor (VEGF) in the pathogenesis of Castleman's disease, we studied VEGF expression in sera and lymph nodes from four patients with either the plasma-cell type or mixed type of Castleman's disease. Clinically, one patient had the multicentric type and the others the localized type. The VEGF levels of the sera and the supernatants of the cultured lymph nodes were higher than those of normal controls. VEGF was strongly expressed in plasma cells in the interfollicular region of the lymph nodes, but rarely in normal lymph nodes. The disregulated IL-6 gene expression is considered to be a primary event that could be related to the etiology of this disease. Recently, Kaposi's sarcoma virus/human herpes virus 8 (KSHV/HHV-8) has been reported to be associated with a subset of the multicentric type of Castleman's disease, and a viral homologue of IL-6 (vIL-6) encoded by KSHV/HHV-8 has been shown to induce VEGF expression. Human IL-6 produced in the affected lymph nodes of Castleman's disease may induce paracrine VEGF-production by plasma cells and vascular proliferation in the lymph node. The confirmation of the role of VEGF in the pathogenesis of Castleman's disease may provide a therapeutic strategy.
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6/27. Atypical presentation of herpes simplex (chronic hypertrophic herpes) in a patient with hiv infection.

    A 46-year-old man with hiv infection and AIDS presented with a large perianal ulcerated vegetative lesion that developed over a 1-year period. He had a past history of recurrent genital herpes infection, treated successfully each time with acyclovir. The perianal lesion developed while he was taking prophylactic acyclovir. Clinically, there were features suspicious of a carcinoma and a biopsy was reported as showing dysplasia. Therefore, the lesion was resected in its entirety. Histologically, there were prominent pseudo-epitheliomatous hyperplasia and chronic ulceration associated with herpesvirus infection. There was no evidence of dysplasia or malignancy. It is important to be aware of chronic vegetant herpesvirus infection, as clinical appearances are unusual and some methods of identification, such as smears or biopsy, may not be sufficient for diagnosis. Viral culture or PCR may need to be performed for a definite diagnosis to alleviate prolonged discomfort and avoid unnecessary radical surgery.
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7/27. cytogenetics of multiple endocrine neoplasia syndromes. I. Two different, unique clonal chromosome changes in a medullary thyroid carcinoma and in a C-cell thyroid hyperplasia.

    In short-term cultures of tumor tissue from a medullary thyroid carcinoma (MTC), we found a large clone of cells with a balanced translocation t(9;12)(p24;q22). A large clone with a balanced translocation t(10;16)(p11;q24) was also found in cultures from a C-cell thyroid hyperplasia. No clearcut evidence for chromosome instability was observed in the lymphocytes of the two patients. The mother of the first patient died of MTC; two relatives of the second patient had MTC and one of them had pheochromocytoma. These findings classify the two subjects as MEN 2A patients with different phenotypic expression but with the same type of chromosomal abnormality.
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8/27. Cushing's syndrome in a patient with bilateral macronodular adrenal hyperplasia responding to cisapride: an in vivo and in vitro study.

    Cortisol secretion in adrenal Cushing's syndrome can be regulated by aberrant hormone receptors, such as gastric inhibitory polypeptide, V1 vasopressin, catecholamines, LH/human chorionic gonadotropin, and serotonin receptors. We report the case of a patient with Cushing's syndrome due to bilateral adrenal macronodular hyperplasia. Extensive in vivo testing for the presence of aberrant receptors revealed a 5-fold increase of plasma cortisol after the administration of cisapride, an agonist of the serotonin 4 (5-HT(4)) receptor. Primary cell cultures were established from adrenocortical specimens obtained at surgery, and in vitro studies also showed that cisapride determined an increase [133.7 /- 5.5% (mean /- SE) of baseline, considered 100%) of cortisol secretion from cultured cells. The presence of 5-HT(4) receptor transcript, and in particular of isoforms c, g, and n, was confirmed by RT-PCR, and the determination of the mRNA levels by real-time RT-PCR revealed a higher expression than in normal adrenal glands. To our knowledge, this is one of the first reports of Cushing's syndrome in which cortisol secretion is regulated mainly by the 5-HT(4) receptor, among known aberrant receptors. In addition, it is noteworthy that hypocortisolism ensued after the removal of the most enlarged adrenal gland, but the in vivo response to cisapride persisted.
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9/27. mycobacterium marinum with different responses to second-generation tetracyclines.

    BACKGROUND: Persistent cutaneous infections with mycobacterium marinum can follow exposure of injured skin to contaminated water or fish, and can be treated with second-generation tetracyclines in addition to other antimicrobials. Due to the rarity of this infection, there are few data comparing the different treatment alternatives. methods: We report a patient with culture-proven M. marinum who was treated with two different second-generation tetracyclines. RESULTS: Our patient failed a 4-week trial of doxycycline, but responded rapidly to minocycline. CONCLUSION: This case suggests that, despite a similar mechanism, pharmacokinetics, and even sensitivity, these two agents may differ in their effectiveness against strains of M. marinum.
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10/27. Bacillary angiomatosis associated with pseudoepitheliomatous hyperplasia.

    Bacillary angiomatosis is an opportunistic bacterial infection caused by either bartonella henselae or B. quintana. The classic histologic presentation of bacillary angiomatosis involves three components: a lobular proliferation of capillaries with enlarged endothelial cells, neutrophilic debris, and clumps of finely granular material identified as bacteria with staining techniques. Pseudoepitheliomatous hyperplasia is a histologic reaction pattern characterized by epithelial proliferation in response to a variety of stimuli, including mycobacterial, fungal, and bacterial infections. We describe a case of bacillary angiomatosis associated with pseudoepitheliomatous hyperplasia in an immunocompromised patient with acquired immunodeficiency syndrome. Histologic examination of a finger lesion demonstrated a capillary proliferation with neutrophilic debris and characteristic amorphous granular deposits. Warthin-Starry and Giemsa staining revealed clumps of coccobacilli. Cervical lymph node tissue also revealed organisms identified as Bartonella with PCR techniques. Stains and cultures for acid fast bacilli, fungus, and bacteria were negative. To our knowledge, there has been only one other report of bacillary angiomatosis presenting with pseudoepitheliomatous hyperplasia. We conclude that the differential diagnosis of entities associated with pseudoepitheliomatous hyperplasia should be expanded to include bacillary angiomatosis.
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