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Biomedical subjects

J Jessurun

Publications and source records attributed to J Jessurun.

At least 55 records · Page 3Linked to original sources

The development of tumors in experimental gastroenterocystoplasty.

Bladder augmentation with segments of the gastrointestinal tract is commonly used to treat patients with small or noncompliant bladders. Reliable data on the incidence of tumors in patients with enterocystoplasty are not available. In the small number of cases reported in the literature the mean latency period is approximately 18 years. We designed a study in Sprague Dawley rats to try to determine the risk of carcinogenesis in different types of augmentation cystoplasty and its possible relationship with infected urine, and to investigate the possibility of detecting the tumors by cytological analysis. We performed 30 gastrocystoplasties, 35 sigmoid cystoplasties, 30 ileocystoplasties and 10 sham operations, and used 10 nonoperated animals as controls. The animals were sacrificed upon completing 1 year of followup and bladder urine samples were collected at the time of sacrifice. Of 115 animals 86 were available for histological evaluation (26 gastrocystoplasty, 22 sigmoid cystoplasty, 18 ileocystoplasty, and all sham and control animals). Mean followup was 11.2 months in the gastrocystoplasty, 11.8 months in the sigmoid cystoplasty, and 12 months in the ileocystoplasty, sham and control groups. Multifocal or superficial transitional metaplasia was found in 65.4% of the gastrocystoplasty, 50% of the sigmoid cystoplasty and 55.5% of the ileocystoplasty animals. Proliferations that we classified as papillary hyperplasia were present in 53.8% of the gastrocystoplasty, 40.9% of the sigmoid cystoplasty and none of the ileocystoplasty rats. The proliferations occurred either at or close to the anastomosis between the bladder and the gastric or colonic patch, or in areas of transitional metaplasia. Cytological urinalysis was negative for neoplastic cells in all cases. No correlation was found between the occurrence of papillary hyperplasia and urinary infection. These data indicate that in rats transitional metaplasia is common in gastrocystoplasty, sigmoid cystoplasty and ileocystoplasty, and that papillary hyperplasia may occur near or at the anastomosis, or in areas of transitional metaplasia in either gastrocytoplasty or sigmoid cystoplasty. In contrast to other studies, we observed no examples of papillary hyperplasia in the ileocystoplasty group in this series. No transitional cell carcinomas or adenocarcinomas were identified in this study. It is not known if these papillary lesions have an increased malignant potential, thus further studies with longer followup are warranted.

Animals↗

Macrophage production of basic fibroblast growth factor in the fibroproliferative disorder of alveolar fibrosis after lung injury.

In organ repair following injury, macrophages accumulate and granulation tissue, comprised of fibroblasts and endothelial cells, develops in the injured area. Basic fibroblast growth factor (bFGF), a potent stimulator of fibroblast and endothelial cell growth, has been linked to the fibroproliferative process. Macrophages are thought to play a central role in the fibroproliferative response, and prior studies indicate that they produce bFGF. Whereas it is plausible that macrophages produce bFGF in a fibroproliferative process, currently no data exists that directly identifies the macrophage as a source of bFGF in a fibroproliferative disorder. We used the model of acute intraalveolar granulation tissue formation following lung injury to determine if the macrophage was a cellular source of bFGF in a naturally occurring fibroproliferative process. To examine this hypothesis, patients with severe acute lung injury underwent bronchoalveolar lavage during the phase of lung repair. Polymerase chain reaction and Northern analysis of macrophage RNA revealed the presence of two species of bFGF messenger RNA (4.4 kb and 1.9 kb). Metabolic labeling studies of recovered macrophages revealed a newly synthesized 18-kd protein with antigenic similarity to bFGF. Immunohistochemical evaluation of lung tissue from patients who died following acute lung injury, showed numerous bFGF immunoreactive macrophages present within airspaces containing fibroblastic and vascular tissue proliferation. This investigation has identified the alveolar macrophage as a cellular source of bFGF in the fibroproliferative disorder of intraalveolar fibrosis following acute lung injury.

Autoradiography↗

Reproduction of the obliterative bronchiolitis lesion after heterotopic transplantation of mouse airways.

Obliterative bronchiolitis, characterized histopathologically by airway inflammation and occlusion of small airways by vascularized fibrous tissue, constitutes an important threat to the long-term survival of lung and heart-lung transplant recipients. The pathogenesis of obliterative bronchiolitis is poorly understood, and successful preventative or treatment strategies are not available. We sought to develop a preclinical model system of obliterative bronchiolitis by transplanting murine airway grafts, consisting of tracheas and main bronchi, into the subcutaneous tissue of allogeneically mismatched recipient animals. By 10 days after transplantation, allografts demonstrated subepithelial and/or peritracheal inflammation, epithelial necrosis, and early fibroproliferation. Grafts harvested 21 days after transplantation demonstrated fibroproliferation in the airway wall or lumen in nine of 10 allografts versus 0 of 10 isografts (P = 0.0001). In addition, abnormal epithelium (ie, nonciliated cuboidal, squamous, or absent) was seen in all allografts, while nine of nine isografts demonstrated normal respiratory epithelium (P = 0.0003). Although differences exist between this model and the chronic rejection process in human lung transplant recipients, these findings reproduce the characteristic features of obliterative bronchiolitis and demonstrate that this lesion can result from allograft rejection. This model will be useful for studying the pathogenesis, prevention, and treatment of obliterative bronchiolitis after lung transplantation.

Animals↗

The prevalence of invasive amebiasis is not increased in patients with AIDS.

OBJECTIVE: To determine whether the frequency or severity of invasive amebiasis is increased in patients with AIDS. DESIGN: A case-control sampling approach, based on an autopsy registry. SETTING: General Hospital of Mexico City, Mexico, a large government-supported, tertiary care medical institution. PATIENTS, PARTICIPANTS: Ninety-four patients with AIDS and 335 historical and contemporary, age- and sex-matched controls who were defined as dying, but not because of AIDS. RESULTS: The odds ratio (OR) for mortality from invasive amebiasis was the same for cases and controls (0.7; 95% confidence interval, 0.07-7.2). By contrast, the OR for other diseases, such as miliary tuberculosis, cytomegalovirus infection, Pneumocystis carinii pneumonia and toxoplasmosis was greatly increased. Only one patient with AIDS had amebiasis of the common amebic ulcerative colitis type, without extraintestinal involvement. CONCLUSION: In conclusion, we show that the frequency and severity of invasive amebiasis is not increased in Mexican patients with AIDS.

Acquired Immunodeficiency Syndrome↗

The spectrum of clinical and pathological manifestations of AIDS in a consecutive series of autopsied patients in Mexico.

OBJECTIVE: Little is known about the clinical profile of AIDS in Latin American populations. This study characterizes the clinical and pathological manifestations of AIDS in a representative series of Mexican AIDS patients at autopsy. DESIGN: The clinical and pathological findings were abstracted retrospectively for a sequential series of autopsied AIDS patients. SETTING: Autopsies were conducted at the four major tertiary level hospitals that serve the majority of AIDS patients in Mexico City. PATIENTS: Subjects included 177 consecutive patients diagnosed with AIDS between March 1984 and January 1989 who subsequently died and were autopsied in the same period in the study hospitals. MAIN OUTCOME MEASURES: Demographic characteristics, including age, gender, residence, socioeconomic status, and risk group; clinical presentation and autopsy findings, including opportunistic infections and malignancies. RESULTS: Sixty per cent of the AIDS patients presented with wasting syndrome. The most common infections were cytomegalovirus (69%), tuberculosis (25%), and Pneumocystis carinii pneumonia (24%). Central nervous system infections were also common and included toxoplasmosis (19%) and cryptococcoses (10%). Kaposi's sarcoma was present in 30% of cases and non-Hodgkin's lymphoma in 9%. CONCLUSION: Clinical manifestation, and types and frequency of opportunistic infections in our Mexican AIDS patients were more similar to those seen in AIDS patients in Africa and Haiti than in the United States and Europe. These findings suggest that the AIDS epidemic in Mexico has an 'intermediate' pattern and may be a prototype for Latin American countries.

Acquired Immunodeficiency Syndrome↗

Low frequency of intestinal metaplasia in gastric biopsies from Mexican patients: a comparison with Japanese and Swedish patients.

A systematic analysis of the cellular and structural components of intestinal metaplasia (IM) was carried out in 691 consecutive endoscopic gastric biopsies from Mexicans patients. Two-thirds of the patients (461 or 66.7%) had chronic gastritis, 27.6% (or 191 patients) had gastric ulcers and 5.6% (39 patients) gastric carcinomas. IM was found in 17.4% of the gastric biopsies. While IM was present in 27.7% of patients with gastric peptic ulcer, patients with gastric malignancy had only 18.7%, and the lowest rate (13.4%) was found in 461 biopsies from patients with chronic gastritis. IM was influenced by the age but not by the sex of the patients. Only one of 120 biopsies with IM (0.8%) had incomplete IM (a lesion claimed to be a precursor of gastric carcinoma). In a previous study it was found that 32.3% of 359 Swedish patients and 59.2% of 625 Japanese patients with chronic gastritis had IM, the proportion of incomplete IM being 23.3% and 25.1%, respectively. The low frequency of IM among Mexicans (a population with a low incidence of gastric carcinoma), contrasts with the moderate frequency of IM among Swedes (who have a moderate gastric cancer incidence) and with the high frequency of IM among Japanese (with a high incidence of gastric carcinoma). These findings recorded in disparate geographical regions strongly support the view that IM is a lesion evoked by environmental factors and associated with gastric carcinogenesis.

Adult↗

Mesenchymal cells isolated after acute lung injury manifest an enhanced proliferative phenotype.

After acute lung injury, mesenchymal cells migrate into the alveolar airspace where they proliferate and deposit connective tissue macromolecules. Early in the disease process, inflammatory cell-derived trophic factors modulate these mesenchymal cell functions. However, in those patients who die, even as the inflammatory response abates, the fibroproliferative response continues, resulting in extensive intraalveolar fibrosis. We therefore hypothesized that lung mesenchymal cells obtained from individuals dying with acute alveolar fibrosis would manifest an enhanced proliferative capacity that was independent of persistent exogenous signals. To examine this hypothesis, the in vitro growth properties of mesenchymal cells prepared from patients dying with acute lung injury (n = 3) were analyzed in defined medium and compared with those of mesenchymal cells similarly prepared from patients dying with histologically normal lungs (n = 3). Isolates were characterized as mesenchymal cells by using morphological and immunohistochemical criteria. In accord with the hypothesis, mesenchymal cells isolated from lung-injured patients doubled within 3 d in the complete absence of exogenous peptide growth factors, reaching a saturation density of approximately 15 x 10(3) cells/cm2. As expected, lung mesenchymal cells from normal individuals failed to significantly increase in number. Consistent with this proliferative phenotype, the immediate early cell division cycle genes c-fos and c-jun were constitutively expressed in each cell strain prepared from injured lungs, but not in those from control lungs. The observed proliferative phenotype was stable through the fifth subcultivation of the cells. Despite these proliferative properties, three separate criteria indicated the mesenchymal cells from injured lungs were not transformed: normal karyotype; finite lifespan in vitro (9-10 subcultivations); and inability to disseminate in mice with severe combined immunodeficiency. These data support the hypothesis that mesenchymal cells manifest an enhanced proliferative state after acute lung injury.

Acute Disease↗

Bronchiolitis obliterans organizing pneumonia as a complication of allogeneic bone marrow transplantation.

We report a patient who underwent two allogeneic bone marrow transplants for chronic myelogenous leukemia, initially in 1984 and again after relapse in 1990, who developed an identical pulmonary syndrome at a similar interval following each transplant. The patient presented with a non-productive cough, bilateral inspiratory crackles, and multiple patchy infiltrates on chest X-ray. Pulmonary function testing revealed a restrictive abnormality but no obstructive defects. The appearance of this pulmonary disorder after each transplant coincided with the development of chronic graft-versus-host disease. In both instances, this pulmonary syndrome completely reversed with corticosteroid therapy. The patient's chest computed tomographic scan and lung biopsy specimens were consistent with the diagnosis of bronchiolitis obliterans with organizing pneumonia (BOOP). While bronchiolitis obliterans has been reported following allogeneic transplant, BOOP has not previously been reported in this setting.

Adult↗

Relapse of acute leukemia presenting as acute cholecystitis following bone marrow transplantation.

Though included in the differential diagnosis of jaundice and abdominal pain, acute acalculous cholecystitis is an uncommon hepatobiliary complication of bone marrow transplantation. Leukemic infiltration of the gallbladder presenting as acute cholecystitis is rare. We describe two cases of acute cholecystitis following marrow transplantation that represented an unexpected relapse with leukemic infiltration of the gallbladder wall.

Acute Disease↗

Evaluation of intrathymic islet transplantation in the prediabetic period.

BACKGROUND: Beta-cell destruction in type I diabetes mellitus results from a chronic autoimmune process. Exposure of thymic T cells to islet antigens during the prehyperglycemic phase of diabetes may alter the likelihood of autoimmune damage to beta cells in the native pancreas. Thus we evaluated whether prophylactic major histocompatibility complex (MHC)-incompatible intrathymic islet allografts could prevent hyperglycemia and native pancreatic beta-cell destruction. METHODS: At 4 to 6 weeks of age, diabetes-prone BioBreeding rats received intrathymic injection of 1500 to 2000 noncultured MHC-incompatible Lewis islets. No immunosuppression was administered. Age-matched littermates underwent intrathymic injection of saline solution. RESULTS: None of 13 BioBreeding rat recipients of prophylactic intrathymic Lewis islet allografts became hyperglycemic versus 13 of 13 control rats (p less than 0.001). The age at onset of diabetes in the control group ranged from 77 to 104 days (mean, 86 days). Normoglycemia in recipients of intrathymic islet allografts persisted for greater than 8 months after transplantation, and thymectomy (graft removal) did not precipitate hyperglycemia. CONCLUSIONS: Prophylactic intrathymic MHC-incompatible islet allografts effectively prevent hyperglycemia and native beta-cell destruction in an animal model of autoimmune diabetes. Rejection and autoimmune destruction of intrathymic MHC-incompatible islet allografts were not seen after transplantation in the prediabetic (prehyperglycemic) period. Intrathymic islet allografts at an early age (before puberty) preserve native beta-cell function and may prevent or retard thymic atrophy.

Animals↗

Carcinoid tumor of the common bile duct: evidence for its origin in metaplastic endocrine cells.

Carcinoid tumors of the extrahepatic bile ducts are extremely rare neoplasms. The authors report the case of a 36-yr-old male patient with a carcinoid tumor that arose in the common hepatic bile duct. The non-neoplastic mucosa showed areas of gastric and intestinal metaplasia that included scattered argyrophil endocrine cells. Since the normal mucosa of the bile ducts lacks the latter type of cells, this case provides evidence for the first time that carcinoid tumors of this anatomic site probably originate from metaplastic endocrine cells.

Adult↗

Crusted scabies in a patient with the acquired immunodeficiency syndrome.

A case of crusted (Norwegian) scabies in a patient with the acquired immunodeficiency syndrome (AIDS) is described and seven previous reports of this association are reviewed. Injury to epidermal Langerhans' cells by the human immunodeficiency virus or cytotoxic cells may explain the appearance of this unusual form of scabies in patients with AIDS.

Acquired Immunodeficiency Syndrome↗

Comparative demographic and autopsy findings in acquired immune deficiency syndrome in two Mexican populations.

In order to identify the characteristics of the acquired immune deficiency syndrome (AIDS) as it occurs in Mexico, a comparative study of the demographic and pathological findings of the first 58 patients who died of AIDS and were autopsied at two Mexican hospitals, Hospital General de Mexico (HG) and Instituto Nacional de la Nutricion (INN), was performed. The patient population consisted of 52 men and 6 women. Their socioeconomic status (SES) was estimated using the occupational prestige and level of education as indicators. As in the U.S.A., most patients (72%) were male homosexuals/bisexuals (HMS/BSX). However, nine patients (31%) at the HG could not be assigned to any of the currently known risk groups. Comparison of the SES of the two series revealed a significantly higher number of poor patients at HG (81 vs. 17%). For the whole group, the most frequent infections were caused by cytomegalovirus (CMV) (65%), Mycobacterium tuberculosis (28%), Pneumocystis carinii (24%), and Toxoplasma gondii (17%). Kaposi's sarcoma (KS) was found in 41% of the cases. The frequency of toxoplasmosis was higher in poor patients (30 vs. 8%, odds ratio of 5.5, 95% confidence limits of 0.83, 39.34, p = 0.04) while the reverse situation was true for KS (18 vs. 61%, odds ratio of 0.14, 95% confidence limits of 0.04, 0.55, p = 0.001). For KS, this difference persisted when only HMS/BSX patients were compared. In conclusion, dissimilarities observed in the frequency of some AIDS-associated diseases in different institutions appear to be mainly influenced by the SES of the patients.

Acquired Immunodeficiency Syndrome↗

Lymphocytic ("microscopic") colitis: a comparative histopathologic study with particular reference to collagenous colitis.

Lymphocytic colitis, previously termed "microscopic colitis", is a clinicopathologic syndrome of watery diarrhea, grossly normal colonoscopy, and mucosal inflammatory changes. Since lymphocytic colitis is a new, incompletely characterized entity, a histopathologic study was performed to compare lymphocytic colitis (n = 16), collagenous colitis (n = 17), idiopathic inflammatory bowel disease (n = 16), acute colitis (n = 16), and histologically normal colon (n = 12). The study was a blinded semiquantitative analysis of histologic features in the surface epithelium, lamina propria, and crypts. The most distinctive feature of lymphocytic colitis was increased intraepithelial lymphocytes, particularly in the surface epithelium (P = .0001 v idiopathic inflammatory bowel disease, acute colitis, and normal colon). Other prominent features of lymphocytic colitis included surface epithelial damage (P less than .005 v idiopathic inflammatory bowel disease and normal colon), increased lamina propria chronic inflammation (P less than .01 v normal), and minimal crypt distortion or active cryptitis. There were striking similarities between lymphocytic colitis and collagenous colitis, but subepithelial collagen thickening was seen only in collagenous colitis. Idiopathic inflammatory bowel disease showed prominent crypt distortion and greater active inflammation, in addition to minimal intraepithelial lymphocytes. Acute colitis occasionally demonstrated prominent surface epithelial damage, but was otherwise dissimilar from lymphocytic colitis. We reached the following conclusions: (1) the entity "microscopic colitis" shows characteristic histopathology including prominent lymphocytic infiltration of epithelium, and thus, a more appropriate designation is lymphocytic colitis; (2) although lymphocytic colitis closely resembles collagenous colitis, each entity is distinct on biopsy; and (3) lymphocytic colitis is readily distinguishable from idiopathic inflammatory bowel disease, acute forms of colitis, and normal colorectum.

Colitis↗

Intracytoplasmic plasma proteins in distended esophageal squamous cells (balloon cells).

Esophageal mucosal biopsy specimens frequently show numerous distended squamous cells with pale cytoplasm, which we term "balloon cells." These cells often occur in clusters, have a patchy distribution, and predominate in the prickle-cell layer in biopsies from patients with gastroesophageal reflux. We studied the immunohistochemical characteristics of balloon cells and their associated clinical findings. We demonstrated by immunoperoxidase technique that balloon cells contain intracytoplasmic albumin and immunoglobulin light chains and show reduced staining for keratin, suggesting cellular injury with resultant uptake of plasma proteins and fluid. Balloon cells were absent or sparse in esophageal mucosal biopsy specimens from 12 normal control persons, but were observed in 7 of 10 patients (70%) with gastroesophageal reflux confirmed by pH-probe test (P = 0.001 versus normal controls), in 16 of 25 patients (64%) with clinically suspected reflux (P less than 0.001), and in 4 of 5 patients with infectious or chemotherapy-associated esophagitis. However, no consistent association was found between balloon cells and the presence of the usual histopathologic criteria for epithelial injury, such as increased height of vascular tufts or width of basal zone. We conclude that balloon cells are most commonly observed in biopsy specimens from patients with various causes of esophageal injury. We propose that balloon cells may be a marker for epithelial injury, possibly even when other histopathologic criteria for injury are absent.

Adolescent↗

Chronic colitis with thickening of the subepithelial collagen layer (collagenous colitis): histopathologic findings in 15 patients.

The histopathologic features of collagenous colitis were studied in 14 women and one man. All but one patient presented with chronic watery diarrhea: 10 had a history of thyroid disease or unspecified arthritis. All 15 patients showed characteristic thickening of the subepithelial collagen layer (SCL) in colorectal biopsy specimens, but in the distal colorectum the thickening was sometimes absent or borderline. Patchy or diffuse injury to the surface epithelium was seen in all cases and was independent of SCL thickening. The injured surface epithelium was infiltrated by lymphocytes and variably by eosinophils and neutrophils, causing it to resemble the surface epithelial injury seen in the small intestine in celiac disease. Crypts were commonly infiltrated by lymphocytes but without associated epithelial injury. The lamina propria in all patients was expanded by lymphocytes, plasma cells, and eosinophils. Neutrophilic cryptitis was seen in seven patients but was usually sparse. Watery diarrhea abated in eight patients treated with corticosteroids or sulfasalazine and was often paralleled by restoration of surface epithelium, reduction in surface epithelial lymphocytes, diminished SCL thickening, and reduced lamina propria eosinophils. Therapy did not consistently alter other inflammatory changes. The possible role of autoimmunity in collagenous colitis should be investigated because of the following circumstantial evidence: the overwhelming female predominance; the frequent presence of possible immunologically mediated disorders such as thyroid and joint disease; the resemblance of surface epithelial changes to those in celiac disease; and the response to corticosteroids.

Adult↗