Functional bowel symptoms in quiescent inflammatory bowel diseases: role of epithelial barrier disruption and low-grade inflammation.

OBJECTIVE: To determine the role of colonic barrier defects and low-grade inflammation in irritable bowel syndrome (IBS)-like symptoms in quiescent inflammatory bowel disease (IBD). DESIGN: Caecal biopsies were collected from 51 IBS, 49 quiescent IBD (31 Crohn's disease (CD) and 18 ulcerative colitis (UC)) patients and 27 controls. IBS was assessed using the Rome III criteria and the IBS severity score. Epithelial barrier integrity was evaluated by determining the paracellular permeability of biopsies mounted in Ussing chambers and the mRNA expression of tight junction proteins (ZO-1, α-catenin and occludin). Low-grade inflammation was evaluated by counting cells, including intraepithelial lymphocytes (IELs), eosinophils and mast cells, and by determining the mRNA and protein expression of tumour necrosis factor (TNF)-α in biopsies and culture supernatants. RESULTS: IBS-like symptoms were present in 35.4 and 38% of CD and UC patients, respectively. Paracellular permeability was significantly increased in both quiescent IBD with IBS-like symptoms and IBS compared with quiescent IBD without IBS-like symptoms (p<0.01, respectively) or controls (p<0.01, respectively). Significantly lower expression of ZO-1 and α-catenin was detected in IBS and quiescent IBD with IBS-like symptoms. IELs and TNF-α were significantly increased in quiescent IBD with IBS-like symptoms, but not in IBS. CONCLUSIONS: In quiescent IBD, IBS-like symptoms related to persistent subclinical inflammation associated with increased colonic paracellular permeability. A persistent increase in TNF-α in colonic mucosa may contribute to the epithelial barrier defects associated with abdominal pain in quiescent IBD, but not in IBS. Optimisation of anti-inflammatory therapy may be considered in quiescent IBD with IBS-like symptoms.

Combination of allergic factors can worsen diarrheic irritable bowel syndrome: role of barrier defects and mast cells.

OBJECTIVES: Recent evidence suggests a role for increased colonic permeability and mucosal mast cell (MC) mediators on symptoms related to the irritable bowel syndrome (IBS). Whether allergic factors (AFs) are involved in the pathophysiology of IBS is unclear. We addressed the question of the possible influence of an allergic background on IBS symptoms. METHODS: We assessed paracellular permeability, mucosal MCs counts, and spontaneous release of tryptase of colonic biopsy specimens in 34 IBS patients and 15 healthy subjects. The severity of IBS was assessed through self-reported questionnaires. All individuals were tested for the presence of AF, including self-perception of adverse reaction to food, personal and familial history of atopic disease, elevated total or specific immunoglobulin E against food/inhalant antigens, blood eosinophilia, and skin tests. RESULTS: IBS patients had significant enhanced colonic permeability, higher number of MCs, and spontaneous release of tryptase than healthy subjects. The severity of IBS was significantly correlated with colonic permeability (r=0.48, P=0.004), MCs counts (r=0.36, P=0.03), and tryptase (r=0.48, P=0.01). In 13 IBS patients (38.2%) having at least three AFs, symptoms scores, colonic permeability, MCs counts, and tryptase release by colonic biopsies were significantly higher than in those with less than three AFs. IBS patients with at least three AFs were more prone to diarrhea or alternating symptoms. None AF was found to be predictive of IBS severity. CONCLUSIONS: In IBS patients, the presence of an allergic background correlates with a more severe disease and diarrhea predominance, possibly by enhancing mucosal MC activation and paracellular permeability.

Bone metastasis from endometrioid ovarian carcinoma: a case study and literature review.

INTRODUCTION: Bone metastases from epithelial ovarian carcinoma are rare, usually discovered postmortem. The survival of these patients is poor. Furthermore, only two cases of endometrioid ovarian carcinoma with metastasis to the skeletal structures have been described in the literature. CASE REPORT: We present the case of a 58-year-old woman with a lytic metastasis in the left iliac ramus from endometrioid ovarian carcinoma that occurred seven years after the initial diagnosis. DISCUSSION: A review of the literature since 1966 on bone metastasis of ovarian cancer is also presented. In patients suffering from a neoplasm that rarely metastasises to bone, histological proof should be obtained to diagnose uncommon sites of disease relapse.

Mast cells and cellularity of the colonic mucosa correlated with fatigue and depression in irritable bowel syndrome.

BACKGROUND: A subset of patients with irritable bowel syndrome (IBS) have an increased number of mast cells (MCs) in the colonic mucosa. Psychological factors are believed to contribute to the course of IBS. AIMS: To examine associations between fatigue, depression and MCs of the colonic mucosa in IBS. METHODS: Colonic biopsies were taken from 50 Rome II IBS patients, 21 healthy controls and 11 depressed/fatigued patients without IBS. The cellularity of the lamina propria was determined as the number of inflammatory cells per high power field (hpf) through a 400x microscope. The Fatigue Impact Scale (FIS) and the short form Beck Depression Inventory (BDI) evaluated the severity of fatigue and depression. RESULTS: IBS patients had a significant increase in the cellularity of the lamina propria compared with controls or with depressed patients (mean (SD) 94.5 (48-110) vs 68 (58-82) and 78 (87-90) cells per hpf, p = 0.005 and p = 0.05, respectively), in particular of MCs (9.3 (5.6-11.7) vs 4.0 (2.7-6.8) and 4.3 (2.8-7.8) cells per hpf, p = 0.001 and p = 0.005, respectively). Both the FIS and BDI scores were significantly higher in IBS or in depressed patients than in controls (p<0.001). In IBS, the FIS score correlated significantly with the cellularity of the lamina propria (r = 0.51, p<0.0001) and MCs (r = 0.64, p<0.0001). In IBS, the BDI score correlated significantly with MCs (r = 0.29, p = 0.03). CONCLUSIONS: Elevated MCs counts are a key feature of the low-grade inflammatory infiltrate in the caecal mucosa of IBS. Fatigue and depression are associated with mucosal cell counts, in particular MCs, suggesting that psychological factors are associated with the low-grade inflammatory infiltrate in IBS.

Gene expression profiling of human liver transplants identifies an early transcriptional signature associated with initial poor graft function.

Liver ischemia-reperfusion injury occurring in orthotopic liver transplantation (OLT) may be responsible for early graft failure. Molecular mechanisms underlying initial poor graft function (IPGF) have been poorly documented in human. The purpose of this study was to identify the major transcriptional alterations occurring in human livers during OLT. Twenty-one RNA extracts derived from liver transplant biopsies taken after graft reperfusion were compared with 7 RNA derived from normal control livers. Three hundred seventy-one genes were significantly modulated and classified in molecular pathways relevant to liver metabolism, inflammatory response, cell proliferation and liver protection. Grafts were then subdivided into two groups based on their peak levels of serum aspartate amino transferase within 72 h after OLT (group 1, non-IPGF: 14 patients; group 2, IPGF: 7 patients). The two corresponding data sets were compared using a supervised prediction method. A new set of genes able to correctly classify 71% of the patients was defined. These genes were functionally associated with oxidative stress, inflammation and inhibition of cell proliferation. This study provides a comprehensive picture of the transcriptional events associated with human OLT and IPGF. We anticipate that such alterations provide a framework for the elucidation of the molecular mechanisms leading to IPGF.

Peritoneal implantation of cryopreserved encapsulated porcine hepatocytes in rats without immunosuppression: viability and function.

The bioartificial liver (BAL) represents a promising approach to cell transplantation without immunosuppression as a method to support patients with hepatic insufficiency. The aim of this study was to assess viability and function of cryopreserved encapsulated porcine hepatocytes implanted intraperitoneally in rats without immunosuppression. Isolated porcine hepatocytes were cryopreserved at -196 degrees C for 1 month. Four groups were created: group 1 (n=10), freshly encapsulated porcine hepatocytes cultured in albumin-free medium for 10 days; group 2 (n=10), freshly encapsulated porcine hepatocytes implanted in the rat peritoneum without immunosuppression for 1 month and cultured for 10 days after explantation; group 3 (n=10), cryopreserved encapsulated porcine hepatocytes cultured for 10 days; group 4 (n=10), cryopreserved encapsulated porcine hepatocytes implanted in the rat peritoneum without immunosuppression for 1 month and cultured for 10 days after explantation. We assessed urea and albumin production and hepatocyte viability. The hepatocytes of all groups retained the capacity to produce urea and albumin, although the albumin synthesis was significantly decreased among hepatocytes of group 4 (P< .01). Encapsulated cryopreserved porcine hepatocytes explanted from rat peritoneum after 1 month appeared morphologically viable; their ultrastructure was preserved. In conclusion, long-term cryopreservation of porcine hepatocytes resulted in retention of their biological activity and in significant viability when transplanted into the rat peritoneum without immunosuppression.

Inflammatory cell distribution in colon mucosa as a new tool for diagnosis of irritable bowel syndrome: A promising pilot study.

BACKGROUND: Currently, there are no histological criteria to diagnose irritable bowel syndrome (IBS). Our aims were (i) to examine the distribution of inflammatory cells in the colon of healthy and IBS subjects and (ii) to find histological diagnosis criteria for IBS. METHODS: Colonic biopsies were taken from four distinct regions of the colon from 20 controls (HC) and 11 patients with IBS (4 with constipation (IBS-C) and 7 with diarrhea (IBS-D) and embedded in paraffin. Macrophages, mast cells, eosinophils, and T lymphocytes were immunostained and positive cells counted. KEY RESULTS: In both HC and IBS patients, global cellularity decreased from the cecum to the rectum (P < .01) which is attributed to reduced number of macrophages (P < .05) and eosinophils (P < .001) but not T cells. Mast cells were reduced in IBS (P < .05) but not in HC, particularly in IBS-D (P < .05). Results showed higher number of macrophages in the left colon of IBS subjects than HC (P < .05). CONCLUSION & INFERENCES: Here we report a decreasing gradient of immune cells from the cecum to the rectum of the human colon. Although global cellularity cannot be used to distinguish between IBS and HC, closer analysis of macrophages and mast cells may be useful markers to confirm IBS histologically and to differentiate between IBS-C and IBS-D when clinical presentation alternates between constipation and diarrhoea. This pilot study remains to be confirmed with greater number of patients.

[Imaging of inflammatory pseudotumors of the liver]. / Imagerie des pseudo-tumeurs inflammatoires hépatiques.

PURPOSE: To describe the imaging features of inflammatory pseudotumors of the liver. INTRODUCTION: Inflammatory pseudotumors of the liver are rare benign lesions that may simulate malignancy on imaging studies. Diagnosis is most frequently confirmed after surgical resection of the lesion. MATERIALS AND METHODS: Retrospective study from 1998 to 2006 of histologically proven cases of inflammatory pseudotumors of the liver. A combination of the following imaging modalities were utilized: US, contrast enhanced US, helical CT and MRI. RESULTS: A total of seven lesions (mean diameter of 61.4 mm) were detected in 6 patients (mean age of 66 years). Clinical and laboratory results were non-specific. The following imaging studies were available: US in 5 cases, including one with contrast material, CT in 5 cases and MRI in 3 cases. All tumors were hypoechoic on US, with no enhancement after injection of Levovist. The tumors were generally hypodense on noncontrast CT and enhancement, when present, was delayed and moderate. On MRI, the tumors were iso- or slightly hyperintense on T2W images and iso- or slightly hypointense on T1W images with subtle peripheral enhancement on delayed imaging. CONCLUSION: The differential diagnosis of inflammatory pseudotumor of the liver should be known to radiologists and could be suggested in a clinical context of chronic inflammatory process in patients with non-specific liver mass showing imaging features of partial fibrosis with delayed enhancement.

[MR Features of hepatic macronodular mycobacteriosis]. / IRM des atteintes macronodulaires hépatiques à mycobactéries.

Hepatic macronodular mycobacteriosis is rare. Its diagnosis is challenging and is most often proposed on the basis of histological analysis. Final diagnosis, except for germ-proven cases, is made in conjunction with clinical, biological, and radiological arguments. We retrospectively report the MR features of ten hepatic lesions discovered on five patients. MRI is sensitive but has a low specificity in demonstrating pseudotumoral lesions most often exhibiting hypointensity on the T1-weighted sequence, hyperintensity on the T2-weighted sequence, and a slight rim enhancement after gadolinium-enhanced T1-weighted sequences.

MRI features of a pancreatic schwannoma.

A case of a pancreatic schwannoma is presented. The patient, a previously healthy woman, is hospitalized with the diagnosis of purulent pleuritis. Ultrasonography (US) of the abdomen shows a 3-cm mass in the head of the pancreas. Magnetic resonance imaging (MRI) reveals, in T1-weighted sequences, the mass to be hypointense, and an early and persistent enhanced signal is noted following the administration of gadolinium. In T2-weighted fat saturation sequences, the lesion appears markedly hyperintense. A duodenopancreatotomy is performed, and the pathologic specimen demonstrates a schwannoma of the pancreas with Antoni A pattern.

ER stress induces NLRP3 inflammasome activation and hepatocyte death.

The incidence of chronic liver disease is constantly increasing, owing to the obesity epidemic. However, the causes and mechanisms of inflammation-mediated liver damage remain poorly understood. Endoplasmic reticulum (ER) stress is an initiator of cell death and inflammatory mechanisms. Although obesity induces ER stress, the interplay between hepatic ER stress, NLRP3 inflammasome activation and hepatocyte death signaling has not yet been explored during the etiology of chronic liver diseases. Steatosis is a common disorder affecting obese patients; moreover, 25% of these patients develop steatohepatitis with an inherent risk for progression to hepatocarcinoma. Increased plasma LPS levels have been detected in the serum of patients with steatohepatitis. We hypothesized that, as a consequence of increased plasma LPS, ER stress could be induced and lead to NLRP3 inflammasome activation and hepatocyte death associated with steatohepatitis progression. In livers from obese mice, administration of LPS or tunicamycin results in IRE1α and PERK activation, leading to the overexpression of CHOP. This, in turn, activates the NLRP3 inflammasome, subsequently initiating hepatocyte pyroptosis (caspase-1, -11, interleukin-1ß secretion) and apoptosis (caspase-3, BH3-only proteins). In contrast, the LPS challenge is blocked by the ER stress inhibitor TUDCA, resulting in: CHOP downregulation, reduced caspase-1, caspase-11, caspase-3 activities, lowered interleukin-1ß secretion and rescue from cell death. The central role of CHOP in mediating the activation of proinflammatory caspases and cell death was characterized by performing knockdown experiments in primary mouse hepatocytes. Finally, the analysis of human steatohepatitis liver biopsies showed a correlation between the upregulation of inflammasome and ER stress markers, as well as liver injury. We demonstrate here that ER stress leads to hepatic NLRP3 inflammasome pyroptotic death, thus contributing as a novel mechanism of inflammation-mediated liver injury in chronic liver diseases. Inhibition of ER-dependent inflammasome activation and cell death pathways may represent a potential therapeutic approach in chronic liver diseases.

The histological spectrum of visceral leishmaniasis caused by Leishmania infantum MON-1 in acquired immune deficiency syndrome.

Visceral leishmaniasis (VL) due to Leishmania infantum is endemic in Southern France and can be considered as an opportunistic infection in patients with acquired immunodeficiency syndrome (AIDS). Co-infection with Leishmania sp. and human immunodeficiency virus (HIV) is emerging, but pathological findings of leishmaniasis in AIDS have been poorly documented, and scattered case reports have include morphological descriptions. The clinicopathologic analysis of 16 patients with HIV and VL were evaluated. The clinical presentation was characteristic of VL, with fever, hepatosplenomegaly, and pancytopenia in 6 patients, and the diagnosis was confirmed by finding amastigotes of Leishmania sp. in bone marrow smears and biopsy specimens. In 4 patients, the initial diagnosis of VL was made fortuitously in gastrointestinal biopsies performed systematically (3 patients) or in case of diarrhea (1 patient). In one duodenal biopsy, Leishmania sp. and Mycobacteria sp. were associated. Liver biopsy allowed the diagnosis of VL in 3 cases. Autopsy was performed in 9 patients, showing a disseminated leishmaniasis with very unusual localizations (adrenal and heart) in 2 cases. Cutaneous leishmaniasis involvement was noted before (4 patients), at the same time (2 patient), or after (1 patient) the diagnosis of VL. Inflammatory infiltrates noted with Leishmania sp. infection were made by CD68 macrophages with (8 patients) or without (8 patients) associated CD8 positive lymphocytes. Immunoperoxidase study using polyclonal anti-Leishmania sp. antibodies contributed to the diagnosis in all cases. Electron microscopy of 2 digestive biopsy specimens showed the ultrastructural characteristics of Leishmania sp. amastigotes. The zymodeme MON-1 of L infantum was identified by isoenzyme electrophoresis in all patients. The mean of CD4 counts was 37/mm3 at the time of diagnosis, and the mean duration before the death was 8 months. As shown in this study, VL in AIDS can be diagnosed in gastrointestinal or liver biopsies. Diagnosis of VL was made when the CD4 count was very low and was correlated with a poor prognosis.

Jejunal versus ileal segmental allografts in the dog: comparison of immunologic and functional results.

Segmental small-bowel grafts have been advocated as a means of reducing the incidence of rejection and graft-versus-host disease in small-bowel transplant recipients. This study compared the results achieved with heterotopic segmental allografts of the jejunum and the ileum that used 120 cm Thiry-Vella loops in a dog model. Immunosuppressive therapy consisted of 25 mg cyclosporine/kg/day. Results were monitored by histologic examinations, function tests (maltose and xylose absorption), and brush-border enzyme assays. Thirty-three dogs were randomized for use as a donor (n = 11) or recipient of a jejunal allograft (n = 11) or an ileal allograft (n = 11). Eight allografts were technical failures and were excluded from analysis. Fourteen allografts were successful (eight ileal, six jejunal). No case of graft-versus-host disease was observed. Six allografts (42.5%, three jejunal [50%] and three ileal [37.5%]) were rejected during the first 3 months (not statistically significant). Eight allografts (five ileal, three jejunal) were tolerated for up to 3 months and were removed. Two ileal and two jejunal allografts appeared grossly normal at surgical removal, but two ileal and one jejunal allografts exhibited signs of chronic rejection, and one ileal allograft showed advanced rejection. The jejunal and ileal allografts had similar clinical courses, as were revealed by immunologic reactions and functional parameters. We conclude that there is no major difference between jejunal allografts and ileal allografts in the dog.

Oral inflammatory pseudotumour: immunohistochemical investigation of a case involving the submandibular gland and review of the literature.

Inflammatory pseudotumours (IPs) are rare lesions. Most commonly reported in the lung, they are almost ubiquitous, but few oral cases have been described. Their rapid growth, local invasiveness and recurrence, and their ultrasound, computed tomography (CT) and magnetic resonance imaging (MRI) aspects are confusing and mimic benign or malignant neoplasms. Their recognition and distinction from malignant tumors is of importance but their histopathological diagnosis may represent a challenge. In the case reported involving the submandibular gland, the spindle cells had the immunohistochemical profile of myofibroblasts, broader cells with a larger nucleus were CD68 and/or Mac387 positive and the dense plasmacytic infiltrate was polyclonal. Histopathology of IPs covers a spectrum of appearances according to the cellularity and the degree of fibrosis. The recognition of a variable mixture of three main cell types: histiocytes or macrophages, myofibroblasts or fibroblasts and abundant plasma cells, with low mitotic activity and absence of cytological abnormalities in an ill circumscribed and rather fibrous lesion is recommended for the diagnosis of oral IP.

Regression of experimental liver tumor after distant intra-hepatic injection of cytosine deaminase-expressing tumor cells and 5-fluorocytosine treatment.

Cytosine deaminase (CD) gene of E. coli converts the non-toxic compound 5-fluorocytosine (5-FC) into 5-fluorouracil. We have introduced a vector expressing the CD gene in a rat colon carcinoma cell line. Expression of the CD gene confers 5-FC sensitivity to these cells in vitro and in vivo. In a bifocal model consisting in a simultaneous engrafment of a CD+ tumor on one lobe of the liver and a wild-type parental tumor on the opposite lobe, treatment with 5-FC results in regression of both type of tumors, indicating the existence of a distant bystander effect.

Chondrex (YKL-40), a potential new serum fibrosis marker in patients with alcoholic liver disease.

OBJECTIVES: Chondrex (YKL-40) is a mammalian member of a protein family that includes bacterial chitinases. The pattern of its expression in certain tissues such as human liver or cartilage suggests a function in remodelling or degradation of extracellular matrix. The purpose of this study was to assess whether circulating YKL-40 might be a serum fibrosis marker in alcoholics. METHODS: Plasma YKL-40 was determined in 146 consecutive heavy drinkers (106 men, 40 women; mean age, 49.2 +/- 9.0 years). Liver biochemical parameters and serum fibrosis markers such as hyaluronate were also measured. Fibrosis and inflammation in liver biopsy were evaluated using a semi-quantitative scoring system. RESULTS: Plasma YKL-40 increased in parallel with the severity of fibrosis (P<0.00001). YKL-40 also increased in the presence of hepatic inflammation (P<0.01). Receiver operating characteristic curves of Chondrex revealed that a threshold of 330 microg/l gave a specificity of 88.5%; however, the sensitivity was only 50.8%. Only 11.5% of patients without severe fibrosis displayed a Chondrex plasma level above this threshold. A positive correlation was found between Chondrex and hyaluronate (r=0.40, P<0.0001), and a negative correlation was shown between Chondrex and the prothrombin index (r=-0.37, P<0.0001). CONCLUSIONS: The severity of liver fibrosis is associated with elevated circulating Chondrex levels. The overlap in YKL-40 values prevents use of Chondrex in a screening programme. High levels of Chondrex (above 330 microg/l) are predictive of severe liver fibrosis. Increased plasma YKL-40 may reflect the remodelling of liver fibrosis in alcoholics.

Autopsy findings in the acquired immunodeficiency syndrome (AIDS). A report of 395 cases from the south of France.

Necropsy findings in 395 adult patients with the acquired immunodeficiency syndrome (AIDS) who died in Nice, France, between March 1983 and May 1996 were compared retrospectively with antemortem diagnoses, risk factors and number of positive T CD4 lymphocytes at the time of death. Special emphasis on bacterial infections was made in this study. Lesions observed from 1983 through 1989 and from 1990 through 1996 were compared. We assessed the role of organ lesions in the immediate cause of death. The organ system distribution of major opportunistic infections and neoplasms was similar throughout the years of the study. The most common diagnostic disease entities in all organ sites were cytomegalovirus infection, toxoplasmosis and candidiasis. Toxoplasmosis was more common in the intravenous drug abuser group. Bacterial infections were frequent and contributed to the mortality and morbidity of all risk factor groups. Kaposi' sarcoma continued to occur more frequently in the homosexual population. Cytomegalovirus infection remained one of the most common causes of death from 1983 to 1996. Mortality from fungal and bacterial infections, and mycobacteriosis increased in frequency during the course of this study whereas deaths from pneumocystosis declined. The death rate from malignant lymphoma and carcinoma increased after 1989. The clinical cause of death concurred with the pathological cause in 55% of the cases. Lung was the most frequent organ involved followed by the central nervous system the gastrointestinal tract and the heart.

Histiocytoid cardiomyopathy: a cause of sudden death in infancy.

We report the case of an infant aged of 14 months deceased of sudden death. The diagnosis of histiocytoid cardiomyopathy was made on a necropsic basis. The pathologic examination showed a cardiac hypertrophy characterized by yellowish areas with irregular outlines, disseminated in the myocardium, and made of histiocyte-like cells with foamy or granular cytoplasm. These cells reacted positively with desmin and myoglobin labels, and had rare and disorganised myofibrils in electron microscopy, proving their muscular origin. The illness affects infants and usually causes severe cardiac troubles leading to death without treatment. This case is the fourteenth associated with sudden death.

Pathological features of intestinal microsporidiosis in HIV positive patients. A report of 13 new cases.

Enterocytozoon bieneusi is a microsporidian parasite found only in the enterocytes of the small bowel of HIV positive patients, producing chronic diarrhea and malabsorption. Since January 1990, we have seen the 13 first Mediterranean cases, diagnosed on duodenal pinch biopsy samples. Diarrhea was the major symptom in all instances, and E. bieneusi was the sole identified pathogen in 6 cases. The diagnosis was made on HES or Giemsa-stained paraffin sections and on Giemsa-stained smears (9 cases). In 3 cases, the parasite was also found on ileal biopsies, but was never encountered in the colonic mucosa. In all patients, transmission electron microscopy of the duodenal mucosa was used, and it confirmed the diagnosis of intestinal microsporidiosis. No instance with negative optic examination had evidence of an infection by E. bieneusi with electron microscopy. Due to the small size of the spores, routine fecal parasitological diagnosis is still a difficult procedure, but it is possible that greater experience may avoid many of today's invasive investigations. Cytologic and histologic routine examination of paraffin sections of the distal duodenal or ileal mucosae is a reliable method to diagnose intestinal microsporidiosis in HIV-positive patients with diarrhea.

Intestinal and extraintestinal Isospora belli infection in an AIDS patient. A second case report.

A 30-year-old black female, from Burkina Faso, had AIDS in 1990. She died in March 1993 following a cachexia secondary to a chronic intestinal isosporiasis. The autopsy revealed a massive parasitic infection by I. belli of the small intestine mesenteric and mediastinal lymph nodes and liver and spleen. The parasite stage observed in extra intestinal sites corresponded to unizoite tissue cysts. This is the first report of I. belli infection in liver and spleen.