Les lésions de splénose sont des auto-transplants de tissu splénique le plus souvent décrits dans les suites de traumatismes abdominaux. Rares en sont les localisations pelviennes. Nous rapportons le cas d’une patiente de 36ans, suivie pour une infertilité secondaire, dont le bilan échographique a révélé des images nodulaires para-cervicales vascularisées. Les antécédents de splénectomie ont fait évoquer le diagnostic de tissu splénique ectopique. La localisation de la lésion, l’évaluation du risque lié à la ponction ovarienne pour fécondation in vitro (FIV) et l’impossibilité d’évaluation du risque hémorragique à l’accouchement nous ont fait décider de l’exérèse des lésions. La conduite à tenir généralement recommandée est conservatrice en raison d’une possible fonction immunologique résiduelle.

AimWe analysed local cellular and humoral immunity factors in the anal mucosa in an attempt to explain how HIV infection increases the risk of anal cancer in HPV-infected patients.MethodHIV-positive cases and matched HIV-negative controls with more than one recurrence of condylomas were included in a prospective study following treatment of the initial lesions. Patients were followed every 3 to 6 months for the development of anal intraepithelial neoplasia (AIN3) and cancer for up to 60 months. Tissue CD1a+, CD3+, CD4+, CD8+ cells and mRNAs of selected cytokines and chemokines were quantified and compared in patients with or without AIN3 or cancer using morphometric or immunohistochemistry analysis and qRT-PCR.ResultsSixty-six individuals (22 patients and 44 controls) were included. In the case group, CD1a+ and CD3+ cell counts were significantly lower in biopsies from AIN3 and cancer specimens compared with those from AIN 1-2 or normal biopsies (P < 0.0001). A CD1a+ count of < 10/mm was predictive of AIN3 and cancer (Odds ratio = 9.4, 95% CI: 5.4-18.3, P < 0.0001). IL-8 and IL23 levels were significantly higher in cancer than in non-cancer tissues regardless of HIV status (P = 0.02). FoxP3 expression was significantly higher in HIV-infected cases than in controls with AIN3/cancer (P < 0.04).ConclusionDepletion of CD1a+ and CD3+ cells and overexpression of FoxP3 in the anal mucosa appear likely to contribute to the risk of HPV-related anal cancer in HIV-infected patients. Furthermore, overexpression of IL-8 and IL-23 in the anal mucosa might be responsible for the development of this cancer regardless of HIV status.

: Clinical laboratory assays can be affected by interferents like hemoglobin (Hb), lipids and bilirubin. We evaluated the effect of these interferences on pediatric samples for different chemistry assays. Further we established cut-off indices above which these interferences confound sample results.: Three separate serum pools were spiked with increasing concentrations of hemolysate or intralipid or bilirubin and different analytes were analyzed. The Hemolysis-(H), Lipemia-(T) and Icterus-(I) indices were measured on Vitros 5600. Analytes affected by lipemia were treated with LipoClear ® and re-analyzed. All the measured analytes were compromised by gross hemolysis (H-Index > 1000).: Except lipase and magnesium (Mg++), all other analytes were affected by moderate (H-Index > 250) and significant hemolysis (H-Index > 500). Low estradiol levels showed a significant effect at severe icterus (I-Index > 20.0). C3, C4, Ceruloplasmin, Haptoglobin, Immunoglobulins (Ig) and Vitamin D were significantly affected by moderate (T-Index > 100) and severe (T-Index > 500) lipemia. LipoClear ® treatment significantly attenuated the lipemic interference on the above analytes except for C3, C4, and IgG.: Accurate reporting of pediatric samples for the analytes affected by common interferences will lead to better clinical interpretation.

Objectif. – Analyser les résultats carcinologiques et le pronostic obstétrical de patientes jeunes, présentant un adénocarcinome ou une hyperplasie atypique de l'endomètre et traitées de façon conservatrice en vue d'une grossesse.Patientes et méthodes. – Analyse rétrospective de 13 cas (cinq adénocarcinomes et huit hyperplasies atypiques) suivis dans huit CHU français entre 1997 et 2004.Résultats. – Après 4,6 mois de traitement médical, il n'existe plus de cellules atypiques ou carcinomateuses dans 61,5 % des cas. Les progestatifs semblent être le traitement le plus efficace. Cette régression tumorale permet de programmer une grossesse, avec naissance d'enfant vivant dans 25 % des cas. Toutes les possibilités d'Assistance médicale à la procréation peuvent être envisagées chez ces patientes fréquemment infertiles. Les récidives sont nombreuses à l'arrêt du traitement hormonal (37,5 % des cas), justifiant la réalisation d'une hystérectomie de clôture systématique si une grossesse a pu être menée à terme.Discussion et conclusion. – Le traitement conservateur des adénocarcinomes stade I et hyperplasies de l'endomètre chez la femme jeune peut faire régresser la lésion tumorale, permettant à ces patientes d'obtenir, dans certains cas, une grossesse.Objectives. – To analyse the carcinological and obstetrical results of young women with atypical endometrial hyperplasia or endometrial adenocarcinoma, treated in a conservative way to allow pregnancy.Patients and methods. – A retrospective analysis of 13 cases (5 adenocarcinomas and 8 atypical hyperplasias) followed in 8 French centers between 1997 and 2004.Results. – After 4.6 months of conservative treatment, there were no residual lesions in 61.5% of the cases. Progestatives seem to be the most effective treatment. Tumoral regression makes it possible to plan a pregnancy, with childbirth in 25% of the cases. In these frequently infertile patients, all the techniques of assisted reproduction can be used. Recurrences are not rare after hormonal treatment (37.5%), so, total hysterectomy is justified after delivery.Discussion and conclusion. – Conservative treatment for young women with atypical endometrial hyperplasia or endometrial adenocarcinoma stage I can be considered in some cases to enable pregnancy.

PURPOSE:The incidence of anal cancer is high in patients with anal condyloma. HIV increases this risk. We analyzed anal mucosa from normal individuals and individuals with condyloma.EXPERIMENTAL DESIGN:Normal anal mucosa from 155 consecutively recruited patients (102 HIV-positive and 53 HIV-negative) with anal condyloma was compared with that obtained from 30 HIV-negative patients after hemorrhoid surgery (controls). Langerhans' cells (LCs), T lymphocytes, and viruses [EBV, cytomegalovirus, herpes simplex virus 1, and human papillomavirus (HPV) types] in anal mucosa and HIV load and CD4 T-lymphocyte counts in the serum were characterized.RESULTS:None of the control individuals had anal squamous intraepithelial lesion or HPV versus 19 HIV-positive and 4 HIV-negative patients with anal condyloma (P = 0.07). The number of LCs/mm in anal tissue was significantly higher in HIV-negative patients with condylomata (median, 30; range, 2-130) than in HIV-positive patients (median, 15; range, 0-100) or in controls (median, 17; range, 4-35). In HIV-negative individuals, the occurrence of condylomata was linked with a higher number of LCs. Significant differences were observed between HIV-positive and HIV-negative patients with anal condylomata:number of LCs/mm anal tissue, oncogenic HPV (26% versus 8%), other current infections (35.6% versus 5%), being male (93% versus 74%). Multivariate regression analysis found HIV as the only risk factor for a decrease in the number of LCs (odds ratio, 6; 95% confidence interval, 2.28-16.1; P < 0.001) and the serum HIV load (odds ratio, 4.9; 95% confidence interval, 1.1-21.4 log/ml; P < 0.03) but not the serum CD4 T-lymphocyte rate as a predictive risk factor for having <17 LCs/mm tissue.CONCLUSION:HPV increases the number of LCs in anal mucosa in HIV-negative individuals. HIV alters anal dendritic cells, likely leading to an increase in anal cancer risk.

Alterations of CD44 proteins, a family of cell adhesion molecule, have been linked with tumorigenesis, carcinogenesis, and prognosis in various neoplasms. Our aims were to evaluate and compare CD44 isoforms expression patterns in normal myometrium, uterine leiomyomas, and leiomyosarcomas and to correlate CD44 expression with clinicopathologic parameters. Fresh (n = 15) and formalin-fixed, paraffin-embedded (n = 76) tissues samples of myometrium, leiomyomas, and leiomyosarcomas were used for immunoblotting and immunohistochemistry, respectively. Semiquantitative evaluation was made after immunostaining. Monoclonal antibodies were used. By immunoblotting in myometrium and leiomyomas samples, we observed a band at 85 kd, corresponding to the apparent molecular weight of CD44s, and bands at 140 kd with the monoclonal antibodies against CD44v3 and CD44v6. In leiomyosarcomas, CD44s and CD44v6 were detected, but not CD44v3. By immunohistochemistry, decreased CD44s expression was found in leiomyomas and leiomyosarcomas (73.9% ± 16.6% and 82.1% ± 20.7%, respectively) compared with myometrium (97.3% ± 6.2%; P <.0001). No CD44v6 staining was detected in myometrium, leiomyomas, and leiomyosarcomas. No CD44v3 expression was detected in leiomyosarcomas, whereas myometrium and leiomyomas expressed CD44v3. For the diagnosis of leiomyosarcoma, the absence of CD44v3 staining had a sensitivity, specificity, and positive and negative predictive values of 100%. In patients with recurrence of leiomyosarcomas, CD44s expression was decreased (P =.03). We conclude that CD44s immunostaining in leiomyosarcomas may have prognostic significance. The loss of CD44v3 expression could be used as a putative diagnostic tool for uterine leiomyosarcomas. HUM PATHOL 32:1190-1196. Copyright © 2001 by W.B. Saunders Company

BACKGROUND & AIMS The incidence of anal cancer is higher in patients with anal canal condyloma, a sexually transmitted disease, than in the general population. We determined the prevalence of anal dysplasia and cancer in patients with anal canal condyloma with respect to human immunodeficiency virus (HIV) status, immunity status, and human papillomavirus types. METHODS In 174 consecutive patients (114 HIV positive, 60 HIV negative) with anal canal condyloma, lesions were cured, and the patients were then followed up prospectively. Langerhans cells (LCs) in normal anal mucosa were quantified, and viruses (Epstein-Barr virus, cytomegalovirus, human simplex virus 1, and various human papillomavirus [HPV] types) were characterized on inclusion. During follow-up (median 26 months), relapsed condylomas were resected and examined histologically. HIV load and CD4 T-lymphocyte counts in serum were determined at each visit. RESULTS Several factors differed significantly between HIV-positive and HIV-negative patients: LCs/mm anal tissue (15 vs. 30), oncogenic HPV (27% vs. 13%), other current anal infections (44% vs. 0%), and sex ratio (93% vs. 73% male). During follow-up, condylomas relapsed in 75% of the HIV-positive patients, with 19 high-grade dysplasias (HGDs) and 1 invasive carcinoma, but in only 6% of HIV-negative patients, with 1 HGD. Male sex, HIV positivity, and <15 LCs/mm tissue were independent risk factors for condyloma relapse. HIV positivity, HGD before inclusion, and condyloma relapse were independent risk factors for HGD and cancer. Serum HIV load was associated with relapse, whereas CD4 T-lymphocyte counts were not. CONCLUSIONS The prevalence of HGD and carcinoma is higher in HIV-positive than in HIV-negative patients, probably because of HPV activity. HIV-positive patients with high serum HIV load and/or a history of anal dysplasia should be examined by anoscopy, and condylomas should be analyzed histologically.

Background & Aims: Hepatocyte growth factor (HGF) and its receptor c-Met are presumed to play a morphogenic role during embryogenesis. The possible implication of HGF and c-Met during the digestive system development was approached by investigating their ontogeny, distribution, and functionality in human fetal tissues. Methods: Thirty fetuses, 7-24 weeks old, were obtained. HGF and c-Met messenger RNAs and proteins were detected in liver, pancreas, esophagus, stomach, and small and large intestine. Tyrosine phosphorylation assays were realized on homogenates and membrane preparations from fetal tissues. Results: The temporal appearance of HGF and c-Met was established between 7 and 8 weeks of gestation in digestive tissues. Immunoblot analysis showed the presence of the c-Met beta-subunit 145-kilodalton band and of the HGF cc-subunit 70-kilodalton band. c-Met was localized in epithelia, especially in fundic parietal cells, pancreatic and gut endocrine cells, and in muscular layers. HGF immunoreactivity was first detected in epithelia and then in mesenchyme and muscular layers. In young fetal stages, the c-Met immunoprecipitated 145-kilodalton band showed tyrosine phosphorylation after HGF stimulation. Conclusions: This study provides evidence for HGF and c-Met expression early in all human fetal digestive tissues and implicates HGF-c-Met in the digestive system morphogenesis.

In situ polymerase chain reaction is a recent technique which combines the sensitivity of PCR reaction to intracellular localization of genomic sequences with the same specificity as in situ hybridization. This reaction is based on the in situ annealing and polymerisation of oligonucleotides complementary to nucleotides located at each side of the target DNA sequence to amplify. We describe the Hot Start PCR (DNA) and the Hot Start PCR after reverse transcription step (RNA). It allows to amplify some nucleic sequences to a high level, becoming easier to detect. The vizualisation can be realized by direct in situ PCR, the product obtained being directly identifiable by incorporation of labeled nucleotides or primers, or preferentially by indirect in situ PCR. In this case, the amplification is followed by in situ hybridization with labeled probes. This last procedure is more specific. Numerous controls are essential at each step of the technique for validating results.

In situ polymerase chain reaction is a recent technique which combines the sensitivity of PCR reaction to intracellular localizatin of genomic sequences with the same specificity as in situ hybridization. This reaction is based on the in situ annealing and polymerization of oligonucleotides complementary to nucleotides located at each side of the target DNA sequence to amplify. We describe the Hot Start PCR (DNA) and the Hot Start PCR after reverse transcription step (RNA). It allows to amplify some nucleic sequences to a high level, becoming easier to detect. The visualization can be realized by direct in situ PCR, the product obtained being directly identifiable by incorporation of labeled nucleotides or primers, or preferentially by indirect in situ PCR. In this case, the amplification is followed by in situ hybridization with labeled probes. This last procedure is more specific. Numerous controls are essential at each step of the technique for validating results.

T lymphocytes have been assumed to play an essential role in tissue injury in patients with chronic hepatitis B. As hepatitis B virus (HBV) is considered as a major factor controlling liver inflammation, we assessed whether a particular T lymphocyte subset could be preferentially detected in the liver in accordance with viral replication. Liver-derived lymphocytes and peripheral blood lymphocytes were analysed by flow cytometry in 21 patients with histologically confirmed chronic hepatitis B without cirrhosis. Viral replication was quantified by hybridization of serum HBV DNA. Eleven patients exhibited an active viral replication with serum HBV DNA ranging from 10 to 388 pg/ml at the time of the liver biopsy, whereas 10 patients had no detectable serum HBV DNA. In patients exhibiting viral replication, CD4+/CD8+ ratios of liver-derived lymphocytes were significantly higher (P < 0.05) than those obtained in patients without viral replication. In contrast, the percentage of T cells expressing the gamma/delta receptor and that of CD2+/CD57+ cells were similar in both groups of patients. Furthermore, in patients exhibiting viral replication, CD4+CD8+ ratios of liver-derived lymphocytes correlated with serum HBV DNA levels (P < 0.001). No relationship between CD4+/CD8+ ratio of liver-derived and peripheral blood lymphocytes was observed. Our data indicate that, in patients with chronic hepatitis B, the CD4+/CD8+ ratio of liver-derived lymphocytes correlates with viral replication. This suggests that in situ helper/inducer CD4+ T lymphocytes may positively regulate the cytotoxic T cell activity in patients with HBV-related chronic hepatitis.