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Biomedical subjects

M Zeitz

Publications and source records attributed to M Zeitz.

At least 91 records · Page 5Linked to original sources
PubMed1998

Infection of an intravenous port system with Metschnikowia pulcherrima Pitt et Miller.

A patient with short bowel syndrome as a consequence of multiple intestinal resections for Crohn's disease, had a port system implanted to improve her nutritional status. One year later she presented with fever, weakness and nighttime sweating. Metschnikowia pulcherrima Pitt et Miller was grown in blood cultures from the port system. After antifungal chemotherapy using fluconazole and removal of the implant, the patient's condition improved markedly and her fever and sweating disappeared. We conclude that Metschnikowia pulcherrima can turn into a human pathogen in patients with indwelling catheters for parenteral nutrition. Chemotherapy with fluconazole and, whenever possible, removal of the implant, appear to be adequate treatment.

Adult↗
PubMed1998

Soluble CD44 and CD44v6 serum levels in patients with colorectal cancer are independent of tumor stage and tissue expression of CD44v6.

OBJECTIVES: Tissue overexpression of CD44 variants, especially CD44v6, and elevated serum concentrations of soluble CD44 variants (sCD44) have been demonstrated in patients with colorectal cancer and several other tumors. Our aim was to evaluate the clinical value of their measurement in colorectal cancer. METHODS: To examine the suitability of sCD44 and sCD44v6 as tumor markers in colorectal cancer these parameters were analyzed in serum of patients with colorectal cancer, inflammatory bowel disease, chronic renal failure, and controls. Tissue expression of CD44v6 in colorectal carcinomas was investigated by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: sCD44 and sCD44v6 levels were significantly elevated in most of the patient groups (medians, sCD44: 330-709 ng/ml; sCD44v6: 125-160 ng/ml) compared to controls (sCD44: 346 ng/ml; sCD44v6: 106.5 ng/ml). No difference was seen between colorectal cancer patients of different UICC (Union Internationale Contre le Cancer) stages and between patients with CD44v6-positive or -negative primary tumors. CONCLUSIONS: sCD44 and sCD44v6 concentrations showed no correlation to tumor burden or CD44v6 tissue expression. Sensitivity and specificity were low, compared to CEA. Therefore, in our view sCD44 and sCD44v6 measurement in screening or follow-up of patients with colorectal cancer is of very little clinical value.

Adenocarcinoma↗
PubMed1998

Increased immunoglobulin G production by short term cultured duodenal biopsy samples from HIV infected patients.

BACKGROUND: Secretory immunity is a major defence mechanism against infections at mucosal surfaces which are common in HIV infected patients. AIMS: To analyse intestinal immunoglobulin production in HIV infection in comparison with that in saliva and serum. PATIENTS AND METHODS: Immunoglobulin G (IgG), A (IgA), and M (IgM) concentrations were determined in supernatants of short term cultured duodenal biopsy samples, serum, and saliva from HIV infected patients (n = 28) and controls (n = 14) by radial immunodiffusion. RESULTS: IgG was increased in the supernatants of short term cultured biopsy samples and saliva from HIV infected patients compared with controls (p < 0.01), but IgA and IgM levels were normal. In contrast, both IgG and IgA concentrations in serum were higher in HIV infected patients than in controls (p < 0.002). No correlation was found between IgA produced by duodenal biopsy specimens and serum IgA. CONCLUSION: Abnormalities in mucosal immunoglobulin production in HIV infection were surprisingly small, indicating that specific secretory immunity rather than quantitative immunoglobulin production may be impaired. However, increased production of IgG could contribute to mucosal inflammation by complement activation. Our findings of normal mucosal IgA production and the lack of correlation between serum and mucosal IgA argues against an intestinal origin for the increased serum IgA levels in HIV infected patients.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Increased state of activation of CD4 positive T cells and elevated interferon gamma production in pouchitis.

BACKGROUND: Immunoregulatory abnormalities of T cells might be of importance in the pathogenesis of pouchitis after ileoanal pouch anastomosis (IAP). AIMS: To characterise T cell subsets, their state of activation, and production of cytokines in inflamed and non-inflamed pouches in patients with ulcerative colitis (UC) and familial adenomatous polyposis (FAP). The influence of T cell activation on mucosal transformation was also studied. PATIENTS: Mucosal biopsy specimens were taken from 42 patients with IAP (33 with UC and nine with FAP). METHODS: Mononuclear cells were isolated by standard techniques and characterised by three colour flow cytometry. Interferon gamma (IFN-gamma) production was studied using the ELISPOT technique. RESULTS: In patients with UC with pouchitis there was a significant increase in the CD4:CD8 ratio, expression of activation markers on CD3+ cells, and number of IFNgamma producing mononuclear cells compared with patients with UC without pouchitis (CD4:CD8 ratio 1.3 (range 0.7-2.7) versus 0.6 (0. 1-1.0), p=0.012). In addition, a positive correlation between increased crypt depth and the number of CD4+ cells (r=0.57) was shown. CONCLUSION: The observed increase in activated mucosal CD4+ T cells and IFN-gamma production might lead to mucosal destruction and crypt hyperplasia as seen in pouchitis.

Adult↗
PubMed1998

Secretory immunity in HIV infection.

Secretory IgA plays a crucial role in the defense of pathogens at mucosal surfaces. As CD4+ T cells are lost early in the mucosa of human immunodeficiency virus (HIV)-infected patients and as CD4+ T cells play an essential role in the regulation of specific IgA responses to pathogenic agents at mucosal sides, it could be expected that this first line of defense is impaired in HIV-infected patients. Therefore, several studies were undertaken to characterize the humoral immune response at mucosal surfaces. However, the results obtained so far are in part contradictory. For intestinal IgA, reduced, increased and no changes compared to controls were described. The different results may be due to different methods applied. In most studies an abnormal predominance of HIV-specific IgG over IgA response was found in the intestine of HIV-infected patients. Studies on cytomegalovirus-specific intestinal antibodies indicate a complete lack of a specific intestinal IgA response. However, in cryptosporidiosis of HIV-infected patients, diarrhea persists despite a secretory IgA response indicating that other factors are also important for the clearance of this pathogen.

Cryptosporidiosis↗
PubMed1998

Mucosal HIV infection.

The gastrointestinal tract is not only a major site of clinical manifestations of the acquired immune deficiency syndrome but also an important compartment for HIV infection at all stages of the disease. In intestinal biopsies HIV has been detected so far mainly in mononuclear cells of the lamina propria but also in epithelial cells. Primary and permanent epithelial cell lines can be productively infected by HIV in vitro and epithelial cell monolayers can rapidly transport HIV by transcytosis. Both phenomena are most effective for cell-associated virus and do not require CD4 expression but seem to involve the interaction of gp120 with galactosyl ceramide. In vivo, productive HIV infection of epithelial cells appears to be rare if it occurs at all. Mucosal HIV infection is highly active at all stages of HIV infection and the gastrointestinal tract is probably a major source of HIV in the body. Highest mucosal HIV production is found rather early in HIV disease and is associated with histological abnormalities and gastrointestinal symptoms. The excessive production of HIV in the intestine appears to be due to transcriptional or translational upregulation and local variations in HIV production correlate with local cytokine levels.

Galactosylceramides↗
PubMed1998

Mucosal immunodeficiency in HIV/SIV infection.

The gastrointestinal tract is one of the major target organs for secondary infections and malignancies in HIV infection in humans indicating disturbed local immunologic defense mechanisms. Immunohistology and flow cytometric studies have demonstrated a more pronounced loss of CD4+ T cells in the intestinal mucosa compared to the peripheral blood in humans infected with HIV. In parallel, activated CD8+ T cells in the lamina propria are increased in this compartment. In SIV-infected nonhuman primates a very early loss of CD4+ T cells in the intestinal mucosa compared to the peripheral blood occurs already at 2 weeks after infection. Depletion and functional impairment of mucosal CD4+ T lymphocytes with consecutive altered cytokine secretion in HIV/SIV infection may explain the breakdown of the mucosal immune barrier leading to secondary opportunistic or nonopportunistic infections and secondary malignancies. In addition, due to the interrelation between the mucosal immune system and epithelium, these changes might be responsible for the partial small intestinal mucosal atrophy and maturational defects in enterocytes observed in HIV-infected patients.

Animals↗
PubMed1998

[Necessary diagnosis before and reliable examinations after surgical interventions in chronic inflammatory bowel diseases].

The primary diagnosis of chronic inflammatory bowel disease (Crohn's disease, ulcerative colitis) is performed by standardized procedures in specialized Gastroenterology Departments or Ambulances. For the assessment of disease activity the clinical presentation of the patient is most important. This is also true for the indication for surgical interventions. In certain instances laboratory markers, endoscopic and histologic examinations, ultrasound, X-ray, and cross-sectional imaging like computed tomography (CT) or magnetic resonance imaging (MRI) give important additional informations. Depending on the clinical situation surgeons and gastroenterologists decide on the most useful technical examinations for planning the operative strategy. After surgery, diagnostic procedures focus on disease progression and complications. Disturbances of intestinal function as consequence of the operation have also to be considered in the routine diagnostic program.

Colitis, Ulcerative↗
PubMed1998

[Diclofenac-associated acute cholestatis hepatitis].

Diclofenac is an anti-inflammatory analgesic which is widely used in the therapy of inflammatory joint pain. Diclofenac hepatotoxicity ranges from asymptomatic elevation of transaminase activity to significant liver disease. 31 cases of diclofenac-induced hepatitis with five associated deaths have been already reported in the English, French and Spanish literature. We report the case of a 64-year-old patient who was admitted to the hospital with an icteric hepatitis of sudden onset. The only drug that was taken before admission was diclofenac in a daily dose of 150-200 mg because of a spondylodiscitis. Work-up of the patient included ERCP, laparoscopy and liver biopsy and excluded other reasons of a cholestatic hepatitis. Discontinuation of diclofenac resulted in normalization of transaminase activity and bilirubin concentration within four months. The frequent use of diclofenac and the possibility of fatal liver damage highlights the need that diclofenac-toxicity should be considered in the differential diagnosis of acute cholestatic hepatitis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

[Complications related to surgery in ulcerative colitis, pouchitis, special sequelae--internal medicine viewpoint].

There are indications that pouchitis after ileal pouch-anal anastomosis is a remanifestation of the underlying disease--ulcerative colitis--under different conditions. A small group (approximately 5-10% of the patients) develops chronic severe pouchitis with total villus atrophy. It has recently been shown that even high-grade dysplastic epithelial changes and DNA aneuploidy occur in chronic pouchitis. Thus, surveillance programs might be necessary for these patients. Pouchitis is a clinical model to study the pathogenesis of chronic destructive mucosal inflammation systematically.

Chronic Disease↗
PubMed1997

Abnormal predominance of IgG in HIV-specific antibodies produced by short-term cultured duodenal biopsy specimens from HIV-infected patients.

The aim of our study was to analyze HIV-specific humoral immunity in the intestinal mucosa at different stages of HIV infection in comparison with serum and saliva. Duodenal biopsy specimens from 30 AIDS patients and 9 HIV-infected patients without AIDS were cultured for 48 hours. Culture supernatants, as well as simultaneously obtained serum and saliva samples, were adjusted to the same immunoglobulin concentrations and tested for HIV-specific IgG and IgA by Western blot. The HIV antigen pattern differed clearly between IgA and IgG but was similar for each isotype independent of its origin (i.e., serum, saliva, or biopsy specimen supernatants). Short-term cultured duodenal biopsy specimens from HIV-infected patients at all stages produced predominantly IgG, which was broadly reactive with HIV antigens. Lower titers of HIV-specific IgA, which recognized few antigens, were found, mostly the glycoprotein gp160. At later stages of the disease compared with earlier stages, the reaction pattern of mucosal IgA from saliva and biopsy supernatants was even more restricted; secretory component was frequently absent. The abnormal predominance of HIV-specific IgG over IgA in mucosal secretions may result from abnormal antibody production in the mucosa rather than from serum leakage. Mucosal inflammation induced by HIV-IgG immune complexes and insufficient immune exclusion by secretory IgA may not only lead to increased mucosal HIV replication but may also contribute to gastrointestinal disease in HIV-infected patients.

Adult↗
PubMed1997

[New therapeutic possibilities in chronic inflammatory bowel diseases].

New therapeutic measures in inflammatory bowel diseases (IBD) are either based on actual data on disease pathogenesis or on new pharmaceutic preparations of known drugs. An overshooting immune response with T cell activation in the local gut associated immune system seems to be central in the etiopathogenesis of IBD. Modulation of the antigenic load in the gut lumen by parenteral or enteral nutrition or antibiotic treatment can alter disease activity. Immunosuppressive drugs are able to decrease the overshooting immune response. Azathioprin has its clear value in chronic active steroid dependent disease courses of Crohn's disease. According to recent studies, Methotrexate seems to be active as well, however, more studies are necessary. Several studies were not able to prove that Cyclosporine is of value in the treatment of Crohn's disease. Newer preparations of aminosalicylates have shown effectiveness in both active disease and prolongation of remission in Crohn's disease in high doses. Local release formulations of steroids with high first-pass-effect as Budesonide will have their indication in subgroups of IBD patients. However, systemic steroid application is still the gold standard in active disease.

Aminosalicylic Acids↗
PubMed1997

The number and proportion of Vgamma9 Vdelta2 T cells rise significantly in the peripheral blood of patients after the onset of acute Coxiella burnetii infection.

We conducted serial studies on peripheral blood lymphocytes from four patients with acute Coxiella burnetii infection. These studies revealed that the proportion of gammadelta T cells in these patients significantly increased after the onset of disease (mean, 16%; range, 13%-30%) as compared with that in five healthy controls (mean, 4%; range, 0.5%-7%; P < .0055) and that in five controls with pneumonia (mean, 2%; range, 1%-3%; P < .0014). Most of the gammadelta T cells from these patients expressed the Vgamma9 Vdelta2 gene product. During the acute phase of disease, most gammadelta T cells expressed the activation marker human leukocyte antigen DR but not CD25. During this phase, gammadelta T cell activation was higher than alphabeta T cell activation. Our findings indicate that gammadelta T cells are predominantly involved in the acute immune response to C. burnetii.

Acute Disease↗
PubMed1997

Mucosal abnormalities in microsporidiosis.

OBJECTIVE: To determine the prevalence of microsporidiosis in HIV-infected patients with and without diarrhoea and to characterize alterations in mucosal architecture and brush border enzyme activities in patients with microsporidiosis. PATIENTS: A total of 259 HIV-infected patients undergoing oesophago-gastroduodenoscopy because of diarrhoea (n = 123) or other symptoms (n = 136) were studied. METHODS: Patients were evaluated for the presence of microsporidia by electron microscopy of duodenal biopsies. Brush border enzyme activities were measured by histochemistry and mucosal architecture was determined by three-dimensional morphometry in biopsies from patients with microsporidiosis and compared with biopsies from a subgroup of HIV-infected patients with or without other enteropathogens. RESULTS: Enterocytozoon bieneusi was detected in 17 patients and Encephalitozoon intestinalis was detected in two patients. Microsporidiosis was significantly more frequent in patients with chronic diarrhoea (19.1%; P < 0.0001) or in patients with acute diarrhoea (7.2%; P = 0.04) than in patients without diarrhoea (1.5%). Microsporidiosis was associated with lactase deficiency (P = 0.03) and a reduced activity of alkaline phosphatase (P = 0.028) and alpha-glucosidase (P = 0.025) at the basal part of the villus compared with brush border enzymes in patients without enteropathogens. Patients with microsporidia had reduced villus height (P = 0.043) and a villus surface reduced by 40% (P = 0.004) compared with patients with enteropathogens other than microsporidia. CONCLUSIONS: Our study confirms the association between microsporidia and diarrhoea. The pathophysiologic mechanism by which microsporidia cause diarrhoea appears in part to be malabsorption, caused by a reduction of absorptive mucosal surface and impairment of enterocyte function.

AIDS-Related Opportunistic Infections↗
PubMed1996

Intestinal T-cell lymphoma: a reassessment of cytomorphological and phenotypic features in relation to patterns of small bowel remodelling.

Intestinal T-cell lymphoma (ITCL) is an uncommon entity among primary gastrointestinal lymphomas. In this study we evaluated tumours from 20 patients presenting with (n = 8) or without (n = 12) a history of coeliac disease (CD). Neoplastic lesions were composed of predominantly small (n = 4), small-to-medium (n = 2), medium/mixed-to-large (n = 7) or large and anaplastic (n = 7) cells. Different patterns of tumour growth and remodelling of the small bowel wall were observed. Pattern a (n = 4) was characterized by an intramucosal spread of small tumour cells with a small growth fraction. This pattern resembles mucosal inflammation in CD. In pattern b (n = 2), ulcerated solitary or multiple tumours composed of small to medium-sized cells were observed. The adjacent or distant mucosa showed a nearly normal architecture. In pattern c (n = 7), ulcerated lesions were composed of medium-sized to large cells. Mucosal flattening occurred in all segments infiltrated by lymphoma. In pattern d (n = 7), bowel remodelling was observed along the small intestine even at sites not affected by lymphoma. The main neoplastic lesions were composed of pleomorphic large or anaplastic cells frequently expressing the CD30 molecule. Intramucosal spread of a small epitheliotropic T-cell population was observed in the vicinity or even at distant segments of the small bowel. The demonstration of clonal rearrangements of T-cell receptor genes helped to trace widespread occurrence of this small intraepithelial neoplastic component. We suggest that different features of tumour cells such as the expression of activation antigens may contribute to the remodelling of small bowel mucosa. The addition of immunophenotyping data to macroscopic and microscopic features of specimens provided evidence that this uncommon lymphoma exhibits a spectrum in cytological composition and growth patterns. However, despite the considerable heterogeneity of the cases analysed, most of them shared a characteristic immunohistochemical profile (CD3+, CD8+/-, CD103+), further substantiating the view that ITCL is the neoplastic equivalent of an intraepithelial T-cell subset of the small intestine. This phenotype and the intraepithelial accumulation of lymphoma cells observed in the surviving mucosa are clues to the diagnosis of this clinicopathological lymphoma entity characterized by a broad range of morphological expressions.

Adult↗
PubMed1996

Special features of the intestinal lymphocytic system.

The gastrointestinal lymphocytic system can be divided in two functional compartments, the organized lymphoid tissue, for example, the Peyer's patches, and the lymphocytes located diffusely in the mucosa, the lamina propria lymphocytes (LPL), and the intra-epithelial lymphocytes (IEL). Antigens enter the Peyer's patches as the afferent part of the GALT via specialized epithelial cells called M cells. After the initiation of the immune response by antigen processing and presentation to B and T cells in Peyer's patches, primed lymphocytes leave the mucosa via the thoracic duct. Finally they migrate back to the mucosa where they exert effector functions. Adhesion molecules, including integrins, especially alpha 4 beta 7 and alpha E beta 7 (HML-1) are involved in these homing and adhesion processes. LPL and LEL differ from peripheral blood lymphocytes in their expression of adhesion molecules and other surface and activation markers. Additionally, they exhibit functional features different from those of other lymphocyte compartments. In the mucosal immune system, plasma cells mainly secrete IgA, which is part of the specialized humoral defence in the gut.

Animals↗