AimsThe oesophageal mucosa is a frequent target of opportunistic infections in human immunodeficiency virus (HIV) infection. Langerhans cells (LC) are known as a target and reservoir of HIV in the skin. The aim of this study was to characterize oesophageal LC in HIV‐infected patients.Methods and resultsThirty oesophageal biopsies were obtained from 29 patients (median age 35.5), all in stage IV of the HIV Center of Disease Control Classification. We performed histological assessment of the oesophageal mucosa and immunohistochemical detection of oesophageal LC using an anti‐CD1a antibody, followed by morphometric analysis. Biopsies from 17 noninfected patients were studied using the same procedure. LC in oesophageal mucosa of the HIV positive patients showed a significantly and dramatically decreased number (LC(N) median = 5.85/mm2) and surface/epithelial surface (LC (S) ratio = 0.09) when compared with HIV‐negative controls (LC(N) median = 29.7/mm2, LC(S) ratio = 1.83) with P = 0.003 for LC(N) and P < 0.0001 for LC(S).ConclusionThese data suggest that oesophageal LC are, like their epidermal counterparts, a preferential target for HIV infection. Their alterations may provide a clue to the pathogenesis of the decreased local oesophageal immunity and to the occurrence of opportunistic infections.

We report a case of splenic pneumocystosis in a human immunodeficiency virus-positive individual treated prophylactically with aerosolized pentamidine. Despite this infection with Pneumocystis carinii, the bronchoalveolar lavage revealed no microorganisms. The use of aerosolized pentamidine as prophylaxis for Pneumocystis carinii is not protective against extrapulmonary pneumocystosis because of inadequate systemic distribution of the drug.

Herpetic esophagitis (HE) associated with human immunodeficiency virus (HIV) is a rare condition mainly reported as isolated cases. We thus decided to study this association and analyze the possible predisposing factors, clinical and endoscopic presentations, and clinical response to treatment. Thirty-four HIV-1-infected patients were identified: 27 had histologically or virologically confirmed HE and seven had probable HE, a retrospective diagnosis based on the efficacy of acyclovir given alone. The median CD4 cell count was 15/mm3. Recent predisposing factors (such as nasogastric procedures, steroid therapy, and anticancer therapy) were noted with regard to 16 of the 34 patients (47%). Odynophagia and/or chest pain occurred in 30 patients (88%). At the time of diagnosis of HE, extraesophageal herpes was found in only 13 patients (38%). Superficial ulcers of the distal third of the esophagus were present in 17 (50%). Among 20 of the 27 patients with confirmed HE that could be evaluated, therapy with acyclovir led to complete resolution in 16 and partial response in 3; 1 patient died of HE. Five patients (15%) suffered confirmed or possible relapses. The mean interval between the diagnosis of HE and death was 8.8 months. Herpes simplex virus may be responsible for ulcerated esophagitis that occurs in the advanced stages of AIDS and that can be safely treated with acyclovir before a definitive diagnosis is made.

Objectives: To evaluate the respective diagnostic value of flexible rectosigmoidoscopy and colonoscopy in the cytomegalovirus colitis. Methods: Twenty-four patients with AIDS were studied retrospectivelly. The entry criteria were: flexible rectosigmoidoscopy or colonoscopy, with 2 rectal and 2 caecal biopsies, presenting cytomegalovirus inclusions bodies linked to an inflammation at least on one colonic biopsy. Results: Twenty-four patients had 29 colonoscopies. In 16 cases colonoscopy was performed to the caecum. The endoscopic findings of the 16 full colonoscopies were: 7 right colitis, 5 diffuse colitis, 2 bisegmentary colitis, 1 proctitis and 1 non endoscopic lesion. The histologic findings of the 16 full colonoscopies were: 5 cytomegalovirus inclusions on rectal biopsies and 16 on caecal biopsies. For the 13 incomplete colonoscopies, 11 had inclusions on rectal biopsies. So the flexible rectosigmoidoscopy was not sufficent to find inclusions 13 times out of 29. Conclusion: Our study indicates that in the cytomegalovirus colitis, inclusions predominate in the caecum, isolated right colitis exists and extra-colonic cytomegalovirus disease is not always found. For these reasons full colonoscopy is necessary for diagnosis in patients with normal flexible rectosigmoidoscopy.

OBJECTIVES:To evaluate the respective diagnostic value of flexible rectosigmoidoscopy and colonoscopy in the cytomegalovirus colitis.METHODS:Twenty-four patients with AIDS were studied retrospectively. The entry criteria were: flexible rectosigmoidoscopy or colonoscopy, with 2 rectal and 2 caecal biopsies, presenting cytomegalovirus inclusions bodies linked to an inflammation at least on one colonic biopsy.RESULTS:Twenty-four patients had 29 colonoscopies. In 16 cases colonoscopy was performed to the caecum. The endoscopic findings of the 16 full colonoscopies were: 7 right colitis, 5 diffuse colitis, 2 bisegmentary colitis, 1 proctitis and 1 non endoscopic lesion. The histologic findings of the 16 full colonoscopies were: 5 cytomegalovirus inclusions on rectal biopsies and 16 on caecal biopsies. For the 13 incomplete colonoscopies, 11 had inclusions on rectal biopsies. So the flexible rectosigmoidoscopy was not sufficient to find inclusions 13 times out of 29.CONCLUSION:Our study indicates that in the cytomegalovirus colitis, inclusions predominate in the caecum, isolated right colitis exists and extra-colonic cytomegalovirus disease is not always found. For these reasons full colonoscopy is necessary for diagnosis in patients with normal flexible rectosigmoidoscopy.

In the dexamethasone-treated rat model of cryptosporidiosis, paromomycin was effective at a dosage of 50 mg/kg/day or more for ileal infection and 200 mg/kg/day or more for cecal infection. At 1 and 3 weeks after treatment, a persistent infection was demonstrated in all rats. These results confirm the anticryptosporidial activity of paromomycin and underscore the limitations of this compound because of its potential toxicity at such high dosages and its inability to eradicate the infection.

Disseminated infection by Fusarium is being increasingly reported in immunocompromised patients. We report the first case of Fusarium oxysporum disseminated infection with well-documented fungal myocarditis, Despite antifungal therapy and hematologic recovery, the patient died in cardiogenic shock, myocardial involvement clearly contributing to the fatal outcome.

A dexamethasone-treated rat model of cryptosporidiosis was used to evaluate the curative activity of paromomycin. Although eradication of the parasite could not be demonstrated, statistically significant decreases in oocyst excretion and in the intensity of ileal parasitism were observed in animals receiving 100 mg of paromomycin per kg of body weight per day.

Objective: To determine criteria for the diagnosis of cytomegalovirus (CMV) colitis and to analyse stages of the course and prognosis of CMV colonic involvement in HIV-1-infected patients.Design: Prospective search for CMV colonic involvement with systematic biopsies to search for CMV intranuclear inclusion bodies and for CMV culture. The evolution of CMV colonic involvement was estimated using further coloscopies and autopsy.Setting: Infectious diseases department in a tertiary referral teaching hospital in Paris, France.Participants: Fifty-five consecutive patients with HIV-1 infection, who had not previously received anti-CMV drugs, and who had at least one coloscopy performed.Results: According to initial coloscopy, colitis, either ulcerative or inflammatory, was found in nine (16%) out of the 55 patients, CMV intranuclear inclusions were present in the colon of four (7%) patients, and colonic cultures were positive for CMV in 15 (27%) patients. The results of the initial coloscopy showed a positive correlation between endoscopic colitis (either ulcerative or inflammatory), CMV inclusions and positive CMV culture from colonic biopsies. The absence of endoscopic ulcerative lesions had a 98% (49 out of 50) negative predictive value for recording CMV inclusions in the colon (95% confidence interval, 89-100). CMV inclusions were recorded in three out of five ulcerative colitis. Male homosexuality, HIV-1 infection stages IVB, C1, D or E, according to the Centers for Disease Control and Prevention classification, CD4 lymphocyte count <200 x 10(6)/l and CMV viraemia also correlated positively with CMV colonic involvement. During the observation period (mean, 7.3 months), the estimated incidence of CMV colitis according to coloscopic studies was 13%. Deterioration in condition was the most frequent spontaneous evolution of CMV colonic infection, whereas anti-CMV treatment resulted in an improvement. Ulcerative lesions occurred earlier in patients with colonic CMV inclusions or positive colonic CMV culture than in patients without CMV colonic involvement at the initial coloscopy. CMV colitis occurred late in the course of HIV-1 infection, on average 4 months before death. The presence of CMV inclusions was an indicator of poor prognosis with earlier occurrence of CMV viraemia and retinitis and no survival after 9 months.Conclusions: These results confirm that the colon is a target organ for CMV in HIV-1-infected patients. Coloscopy should be used to diagnose CMV colitis, because of the close correlation between endoscopic and histological data (i.e., intranuclear inclusions). This combination allows us to propose an evolutive staging of CMV colonic involvement and provide stratification criteria to assess the efficacy of anti-CMV drugs.

The infection of liver cells by HIV-1 was investigated in vivo. Liver biopsies from 13 anti-HIV-1 antibody-positive patients were studied and HIV-1 DNA was revealed by polymerase chain reaction (PCR) in eight. In situ hybridization demonstrated the presence of HIV-1 RNA in all eight PCR-positive liver specimens. Mononuclear inflammatory cells in the portal tracts and Kupffer cells were labeled by a HIV-1 35S-RNA probe in all cases and by an anti-p24 monoclonal antibody, in seven cases. In addition, hepatocytes also clearly scored positive for HIV-1 RNA in three cases. These results demonstrate the infection of both parenchymal and non-parenchymal liver cells by HIV-1 in vivo and therefore show that HIV-1 can infect an epithelial CD4-negative cell type.

The case of an immunocompetent woman who died of disseminated cytomegalovirus infection with encephalitis and skin ulcerations is reported. The duration of the disease, from onset to death, was five months. Cytomegalovirus was found in the blood, urine, skin, muscle, liver and periventricular brain tissue, but not in frontal cortex tissue. This case underlines the fact that cytomegalovirus may exceptionally cause life-threatening illness in immunocompetent adults.

The present article describes the clinical and pathological findings in 5 human immunodeficiency virus (HIV)-infected patients with muscle toxoplasmosis. The patients had marked lymphopenia (5/5), with less than five CD4+ cells/mm3 (3/3), when they developed fever (5/5), and multiorgan failure (5/5), including diffuse encephalitis, pneumonia, pancytopenia, and myopathy. Muscle involvement included weakness and wasting (4/5), myalgias (3/5), and high serum creatine kinase levels (3/3). Serology for toxoplasmosis showed high IgG titers in 3 patients (3/4). Anti-Toxoplasma therapy resulted in complete recovery in 2 patients. Muscle toxoplasmosis was detected by biopsy (3/5) or postmortem evaluation (2/5), and was identified using immunocytochemistry and electron microscopy. Toxoplasma cysts were detected in 0.5 to 4% of muscle fibers close to or remote from necrotic fibers and inflammatory infiltrates. Muscle fibers strongly expressed the major histocompatibility complex class I antigen (2/2) as in polymyositis. We suggest that Toxoplasma gondii should be sought by muscle biopsy in patients who have acquired immunodeficiency syndrome with fever, encephalitis, multiorgan dysfunction, and elevated serum creatine kinase levels of obscure origin.

American Journal of HematologyVolume 37, Issue 2 p. 143-143 Letter to the EditorFree Access Hodgkin's disease of the tongue in a homosexual HIV-infected patient Thomas Papo, Thomas Papo Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this authorE. Oksenhendler, E. Oksenhendler Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this authorE. Bouvet, E. Bouvet Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this authorC. Marche, C. Marche Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this authorJ. P. Monteil, J. P. Monteil Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this authorJ. P. Clauvel, J. P. Clauvel Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this author Thomas Papo, Thomas Papo Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this authorE. Oksenhendler, E. Oksenhendler Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this authorE. Bouvet, E. Bouvet Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this authorC. Marche, C. Marche Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this authorJ. P. Monteil, J. P. Monteil Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this authorJ. P. Clauvel, J. P. Clauvel Service ďImmuno-hématologie Hopital Saint Louis 1, Avenue Claude Vellefaux 75010 Paris, FranceSearch for more papers by this author First published: June 1991 https://doi.org/10.1002/ajh.2830370223Citations: 12AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Scheib RG, Siegel RS: Atypical Hodgkin's disease and the acquired immunodeficiency syndrome. Ann Intern Med 102: 554, 1985. 2 Picard O, De Gramont A, Krulik M, Gonzalez G, Debray J, Cady K: Rectal Hodgkin disease and the acquired immunodeficiency syndrome. Ann Intern Med 106: 775, 1987. 3 Ioachim HL, Weinstein MA, Robbins RD, Sohn N, Lugo PN: Primary anorectal lymphoma. A new manifestation of the acquired immune deficiency syndrome. Cancer 60: 1449–1453, 1987. 4 Cooper HS, Patchefsky AS, Marks G: Cloacogenic carcinoma of the anorectum in homosexual men: An observation in four cases. Dis Colon Rectum 228: 557—558, 1979. 5 Ziegler JL, Beckstead JA, Volberding PA, et al: Non-Hodgkin's Lymphoma in 90 homosexual men. N Engl J Med 311: 565–570, 1984. 6 Ho M, Jaffe R, Miller G, Breinig ML, Dummer JS, Makowka L, Atchinson RW, Karrer F, Nalesnik MA, Starzl TE: The frequency of EBV infection and associated lymphoproliferative syndrome after transplantation and its manifestations in children. Transplantation 45: 719–727, 1988. 7 Weiss LM, Movahed LA, Warnke RA, Sklar J: Detection of Epstein–Barr viral genomes in Reed-Sternberg cells of Hodgkin's disease. N Engl J Med 320: 502–506, 1989. 8 Uccini S. Monardo F, Ruco LP, Baroni CD, Faggioni A, Agliano AM, Gradilone A, Manzari V, Vago L, Costanzi G, Carbone AP, Boiocchi M, De Re V: High frequency of Epstein–Barr virus genome in HIV-positive patients with Hodgkin's disease. Lancet 1: 1458, 1989. Citing Literature Volume37, Issue2June 1991Pages 143-143 ReferencesRelatedInformation

Le d’eficit immunitaire du SIDA pr’edispose à de nombreuses infections à germes opportunistes et non opportunistes. Nombre de ces germes d’eterminent des affections gastro-intestinales conduisant à une diarrh’ee et à une malabsorption. Compte tenu du potentiel l’ethal de certains de ces pathogènes, il est souhaitable d’identifier les agents infectieux curables. La d’etection d’un certain nombre de pathogènes n’ecessite, pour des raisons th’eoriques, des biopsies orient’ees par l’endoscopie (Mycobacterium avium, CM). Le diagnostic d’autres bact’eries (salmonelles, Campylobacter, Shigelles, Clostridium difficile) repose sur l’examen des selles sans examen endoscopique. Une troisième cat’egorie (Cryptosporidium, Isospora belli, Giardia, Entamoeba histolytica) peut être identifi’ee soit par l’examen des selles, soit par l’examen du liquide d’aspiration j’ejunal, soit enfin par des biopsies orient’ees endoscopiquement.