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F P Chatelet

Publications and source records attributed to F P Chatelet.

12 recordsLinked to original sources

Chronic use of non-steroidal anti-inflammatory drugs does not alter colonic mucosa of patients without diarrhoea.

BACKGROUND: Several types of colitis can be NSAID-induced, but whether chronic use of NSAIDs alters colonic mucosa in patients without diarrhoea is not known. PATIENTS AND METHODS: Biopsy specimens of rectal mucosa were taken in six patients with rheumatoid arthritis without diarrhoea receiving NSAIDs (group 1, n=6). Patients with rheumatoid arthritis without diarrhoea not receiving NSAIDs (group 2, n=9), and patients undergoing surveillance colonoscopy (group 3, n=23) served as controls. In all patients from the three study groups, intraepithelial lymphocyte count and apoptotic cell count were assessed, and sub-epithelial collagen band thickness was measured. Leucocyte population of lamina propria was evaluated semi-quantitatively. HLA-DR and CD25 expression of mucosal cells was appreciated by immunohistochemistry. RESULTS: Intraepithelial lymphocyte count was in the normal range in all three group patients, and not statistically different between groups. Apoptotic epithelial cell count was not different between groups. Sub-epithelial collagen band thickness was normal in all the patients. No patient had a marked infiltration of lamina propria by leucocytes, and HLA-DR and CD25 were normally expressed in all patients. CONCLUSION: These results from a small sample of patients suggest that patients without diarrhoea receiving NSAIDs on a long-term basis do not develop microscopic or inflammatory colitis.

Anti-Inflammatory Agents, Non-Steroidal↗

In situ hybridization determination of the heterophagocytic origin of type 2B prostate epithelial lipochrome pigment granules: histochemical and ultrastructural correlates.

UNLABELLED: Morphologically, polymorphic prostatic lipochrome pigment has been classified and subclassified in the last few years. Type 2B lipochrome pigment granules (LPGs) are frequently found in prostatic epithelium in patients who had died of AIDS. Intensive apoptosis is observed in the same epithelium which lends support to the hypothesis of heterophagocytic (apoptotic) origin of type 2B pigment granules. Detection of nuclear chromatin material is necessary for the differentiation of an autophagosomal from a heterophagosomal structure in the cellular cytoplasm. OBJECT OF THE STUDY: Application of in situ hybridization (ISH) for elucidating the origin of subtype 2B LPGs in the prostate epithelial cells of patients who had died of AIDS. METHODS: ISH was used on routine necropsic prostate epithelial samples from three patients who had died of AIDS. A DNA probe raised against total human DNA was employed. RESULTS: Multiple hybridization signals were detected in type 2B LPGs which shows the presence of nuclear material in those structures. The chromatin material localized to the periphery of pigment granules. CONCLUSION: Type 2B LPGs have a heterophagocytic origin and represent phagocytosed apoptotic bodies in the phase of phagolysosomal degradation. They can be used as a morphologic tissue marker of intensive epithelial apoptosis.

Acquired Immunodeficiency Syndrome↗

The -700/-310 fragment of the apolipoprotein A-IV gene combined with the -890/-500 apolipoprotein C-III enhancer is sufficient to direct a pattern of gene expression similar to that for the endogenous apolipoprotein A-IV gene.

Spatial gene expression in the intestine is mediated by specific regulatory sequences. The three genes of the apoA-I/C-III/A-IV cluster are expressed in the intestine following cephalocaudal and crypt-to-villus axes. Previous studies have shown that the -780/-520 enhancer region of the apoC-III gene directs the expression of the apoA-I gene in both small intestinal villi and crypts, implying that other unidentified elements are necessary for a normal intestinal pattern of apoA-I gene expression. In this study, we have characterized transgenic mice expressing the chloramphenicol acetyltransferase gene under the control of different regions of the apoC-III and apoA-IV promoters. We found that the -890/+24 apoC-III promoter directed the expression of the reporter gene in crypts and villi and did not follow a cephalocaudal gradient of expression. In contrast, the -700/+10 apoA-IV promoter linked to the -500/-890 apoC-III enhancer directed the expression of the reporter gene in enterocytes with a pattern of expression similar to that of the endogenous apoA-IV gene. Furthermore, linkage of the -700/-310 apoA-IV distal promoter region to the -890/+24 apoC-III promoter was sufficient to restore the appropriate pattern of intestinal expression of the reporter gene. These findings demonstrate that the -700/-310 distal region of the apoA-IV promoter contains regulatory elements that, in combination with proximal promoter elements and the -500/-890 enhancer, are necessary and sufficient to restrict apoC-III and apoA-IV gene expression to villus enterocytes of the small intestine along the cephalocaudal axis.

Animals↗

An autopsy study of the prostate in acquired immunodeficiency syndrome: evidence for excessive apoptosis and intracytoplasmic epithelial inclusions.

We describe a combination of epithelial cell apoptosis and intracytoplasmic inclusions in prostatic epithelium in 6 patients who died from the acquired immunodeficiency syndrome. Two different types of apoptosis were detected: simple cell shrinkage and exploding glandular cells. No intracellular or extracellular viral particles were detected, either ultrastructurally or immunohistochemically. Intracytoplasmic inclusions are apoptotic bodies in a state of degradation and in close association with lipofuscin. The cell degeneration we observed confirms the theory that increased apoptotic cell depletion is responsible for weight loss in the acquired immunodeficiency syndrome. In the prostate itself, the combination of excessive apoptosis and active phagosomal digestion of apoptotic bodies presents a "human model" of postcastration rat ventral prostate, under the conditions of severe immune deficiency.

Acquired Immunodeficiency Syndrome↗

Thrombotic microangiopathy and cytomegalovirus disease in patients infected with human immunodeficiency virus.

Thrombotic microangiopathy (TMA) can occur during the course of human immunodeficiency virus (HIV) infection. Clinical and pathological data for 29 patients with TMA and HIV infection were recorded. In a retrospective case-control study, we analyzed the link between opportunistic infections or drug therapies and TMA. Twenty-five patients (mean CD4+ cell count +/- SD, 71.9 +/- 18.3/mm3) had renal impairment, and four had neurological dysfunction. In one-half the cases, the disease was progressive with isolated fragmentation anemia appearing several months before the clinical symptoms. The diagnosis of TMA was confirmed by histological examination of kidney biopsy specimens (18 cases). Endothelial cytomegalovirus (CMV) inclusions were associated with TMA in nine of 18 cases, whereas histological examination did not detect CMV in any control specimens (P < .001). The case-control study demonstrated a link between TMA and clinical CMV infection (odds ratio, 3.9; 95% confidence interval, 1.1-14). We conclude that TMA is a late complication of HIV infection and can be associated with systemic CMV infection in this setting.

AIDS-Related Opportunistic Infections↗

Drug induced lymphocytic colitis.

Three cases are presented of lymphocytic colitis with chronic diarrhoea concurrent with longterm use of Cyclo 3 Fort, a phlebotonic drug used in France. The histological and immunopathological features of lymphocytic colitis are described. We show that lymphocytic colitis is drug induced, particularly in one patient where the immunopathological features of mucosal immune cell activation were induced by drug rechallenge. It is concluded that lymphocytic colitis may be drug induced, secondary to a chronic activation of the mucosal immune system by one or several components of the drug.

Aged↗

[Plurifocal alveolar pneumonia in a patient with AIDS: disseminated Mycobacterium avium intracellulare infection with difficult diagnosis].

In patients with the acquired immunodeficiency syndrome (AIDS), manifestations of generalized Mycobacterium avium intracellulare infection are non-specific and pneumopathy is rarely encountered. We report a case of a patient with AIDS who had clinical and radiological manifestations of multifocal alveolar pneumopathy which was found on autopsy to be due to disseminated Mycobacterium avium intracellulare.

Acquired Immunodeficiency Syndrome↗