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H Zeidler

Publications and source records attributed to H Zeidler.

At least 109 records · Page 6Linked to original sources
PubMed1998

Effects of the anti-CD2 mAb OX34 on in vivo proliferation.

In vitro studies indicate that CD2 plays an important role in the intestinal immune system with regard to T cell proliferation and T helper 2 differentiation. We asked whether anti-CD2 mAb induces T-cell proliferation in vivo. Rats received anti-CD2 mAb OX34 or control mAb over 3 days. Before exsanguination BrdU was injected. Lymphatic organs were processed for two-color immunohistology. OX34 depleted CD4+ but not CD8+ T cells in all organs. Remaining CD4+ T cells proliferated in the periarteriolar lymphocyte sheets. Surprisingly, OX34 led to strong proliferation of splenocytes in the red pulp. These cells were negative for markers of T cells, B cells, NK cells, macrophages, and myeloid cells. Taken together, the anti-CD2 mAb OX34 leads to proliferation of an as-yet-unidentified cell type in the red pulp of the spleen but not to proliferation of T cells.

Animals↗
PubMed1998

[New non-steroidal anti-rheumatic drugs: selective inhibitors of inducible cyclooxygenase].

UNLABELLED: MODE OF ACTION OF NON-STEROIDAL ANTI-INFLAMMATORY DRUGS: Non-steroidal anti-inflammatory drugs (NSAID) exert their major therapeutic and adverse effects by inhibition of prostanoid synthesis. Also the interactions with antihypertensive drugs and lithium are caused by this mechanism of action. Cyclooxygenation is a key enzymatic step in the synthesis of prostanoids. 1990 2 isoforms of the enzyme cyclooxygenase have been identified: Prostanoids synthesized by the constitutive cyclooxygenase (COX-1) are involved in physiological homeostasis. In contrast, the inducible cyclooxygenase (COX-2) produces large amounts of prostanoids, mainly contributing to the pathophysiological process of inflammation. COX-2 SELECTIVE NSAID: The discovery of the cyclooxgenase-isoenzymes ushered in a new generation of NSAID: A drug with selectivity for COX-2 would inhibit proinflammatory prostanoid synthesis while sparing physiologic prostanoid synthesis. Thus, a selective COX-2 inhibitor should be anti-inflammatory with less or no gastrointestinal or other NSAID-typical adverse effects. The experiences with currently used NSAID, which show an increasing incidence of side effects as COX-1 inhibition increases, and studies with the COX-2 selective NSAID salsalate and meloxicam, which have less adverse effects than nonselective COX inhibitors in equivalent antiphlogistic dosage, prove the concept of selective COX-2 inhibition to avoid the NSAID typical side effects. Newly developed drugs with a very high selectivity for COX-2 are now tested in clinical trials. CONCLUSION: So far the results suggest, that selective and highly selective COX-2 inhibitors have significantly fewer gastrointestinal and renal adverse effects and do not inhibit platelet aggregation.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Human b cell differentiation: dependence on interactions with monocytes and T lymphocytes via CD40, CD80 (B7.1), and the CD2-Ligands CD48 and CD58 (LFA-3).

B cell differentiation depends on cellular interactions with T lymphocytes and monocytes via adhesion molecules (AM). In order to characterize AM which are required for B cell differentiation immunoglobulin production using unseparated peripheral blood mononuclear cells (PBMC) was studied. Unstimulated human PBMC were cultured for 9 days with mAb directed at CD2/CD48, /CD58, CD59, CD5/CD72, CD11a-CD18/CD54, CD28/CD80, CD86, CD40/CD40L, or rat CD2 (control). B cell differentiation was quantified measuring IgM and in some cases IgA, IgG, and IgE production. IgM levels were significantly reduced by mAb against CD40, CD48, CD58 and CD80. The reduction was not due to isotype switching to IgA, IgG or IgE. The role of CD40, CD48, CD58 and CD80 was further investigated after depletion of different cell types. Depletion of monocytes and NK cells resulted in no detectable IgM production irrespective of added mAbs. In contrast, IgM production was still present after depletion of T cells and NK cells. Only mAb against CD80 and CD48 significantly reduced IgM production, the reduction of IgM production by anti-CD40 mAb was less than in the presence of T cells. Importantly, anti-CD58 mAb had no effect on IgM production after T cell and NK cell depletion. Taken together, the AM CD40, CD48, CD58, and CD80 are involved in Ig production of unseparated PBMCs. In this model of B cell differentiation only the AM CD58 depend on the presence of T cells while CD48 and CD80 help was found to be T cell independent.

Animals↗
PubMed1998

[Detection of Borrelia DNA in urine using polymerase chain reaction in rheumatologic laboratory diagnosis of Lyme borreliosis].

Borrelia burgdorferi specific DNA has been detected by polymerase chain reaction (PCR) in different specimens of patients with Lyme disease (LD). The aim of the present study is to evaluate PCR-diagnostic of urine specimens regarding rheumatologic diagnosis of Lyme disease. Urine specimens of 77 patients (LD, n = 34; undifferentiated arthritis (UA), n = 25; arthralgia/myalgia (AM), n = 18) and 15 controls were investigated. Flagellin gene (60 specimens) or OspA-plasmid (32 specimens) were used as targets. Sensitivity of the flagellin-nested-PCR was 27%, by OspA-nested-PCR only one positive PCR result was found. Despite of low sensitivity PCR enabled the correct diagnosis of LD in two patients classified as UA. Therefore, PCR can give valuable hints in single cases if LD is clinically suspected.

Adult↗
PubMed1998

[Reactive arthritis after cat bit: a rare manifestation of cat scratch disease--case report and overview].

Cat scratch disease (CSD) is a rarely recognized infectious disease in Germany. Only a few years ago the causative agent, Bartonella henselae, could be isolated. The typical clinical manifestations of CSD consist of skin changes at the inoculation site and a benign lymphadenopathy; other manifestations are rare. We report the case of a 47 year old woman, who developed a reactive spondylarthropathy with synovitis of finger joints, polyarthralgias of large- and medium-sized joints, and inflammatory spinal pain after a cat bite. The rheumatic manifestations resolved after 10 months by treatment with non-steroidal antirheumatic drugs. Only a few cases of rheumatic manifestations associated with CSD have been described in the literature. Because the prevalence of Bartonella henselae infection of cats is high in Europe, rheumatic manifestations might be more frequent. Diagnosis of CSD is now improved by the development of serological tests. We provide an overview of the clinical manifestations and the diagnostic criteria.

Animals↗
PubMed1998

Viability and gene expression in Chlamydia trachomatis during persistent infection of cultured human monocytes.

The principal host cell for persistently infecting synovial Chlamydia trachomatis is the macrophage. During infection of human monocytes/macrophages in culture this bacterium displays aberrant morphology and produces no new elementary bodies, reflecting the situation in synovium. Here we investigate the metabolic status of C. trachomatis (serovar K) during an extended infection of human peripheral monocytes in vitro. Using reverse transcription-polymerase chain reaction assays, we have shown that primary transcripts from the chlamydial rRNA operons are present throughout a 10-day course of infection. Other assays targeting mRNAs from chlamydial genes encoding r-proteins S5 and L5, the glycyl-tRNA synthetase, the 60-kDa cysteine-rich outer membrane protein, and the KDO transferase indicate that these messengers are also present throughout the entire 10-day period. The gene encoding the 57-kDa heat-shock protein (hsp60) is expressed by the bacterium throughout the 10-day infection of cultured monocytes, but transcript levels from the gene encoding the major outer membrane protein (omp1) appear to be attenuated. Western analyses targeting these latter proteins confirm the presence of the hsp60 gene product, and the virtual absence of major outer membrane protein, in chlamydia-infected cultured human monocytes. Thus, during extended infection of human monocytes in vitro, chlamydia are non-productive but transcriptionally active; the pattern of transcriptional activity reflects that known for persistent C. trachomatis infection in vivo in synovial tissue.

Antibodies, Monoclonal↗
PubMed1998

Aetiological agents: their molecular biology and phagocyte-host interaction.

Inflammatory joint disease can develop following an extra-articular infection. The term reactive arthritis was coined in order to differentiate this arthritis, which is often characterized by lack of culturable organisms in the joint, from septic arthritides. Bacteria known to trigger reactive arthritis include Campylobacter, Chlamydia, Salmonella, Shigella and Yersinia. Demonstration of bacteria or bacterial macromolecules in the joint has elicited the idea that reactive arthritis is a sterile process induced and maintained by antigenic material in the synovium. Continued synthesis of antigens to maintain synovial inflammation probably requires establishment of persistent bacterial infection in the joint, or at the primary site of infection. In the case of Chlamydia trachomatis, viable, metabolically-active organisms have been demonstrated to exist for extended periods in the joints of patients with reactive arthritis. In this chapter, we review the aetiological agents, and their molecular biology and phagocyte-host interactions, that are involved in reactive arthritis and spondylarthropathy.

Arthritis, Reactive↗
PubMed1998

Undifferentiated arthritis and reactive arthritis.

The terms undifferentiated arthritis and undifferentiated characterize arthritides that do not fit into well-known clinical disease categories (e.g., seronegative rheumatoid arthritis and reactive arthritis) and that are an early stage or forme fruste of a definite rheumatic disease, an overlap syndrome between such diseases, or an unknown, etiologically undefined disease that remains to be differentiated from other types of arthritis or spondylarthritis. Undifferentiated arthritis and undifferentiated spondylarthritis share some clinical features with reactive arthritides. Recent data suggest that, at least in Chlamydia-induced reactive arthritis, the triggering bacteria persist in affected joints for some time during the course of the disease in a viable but nonreplicative state, providing an antigenic stimulus for a bacteria-specific immune reaction in the joint. The clinical manifestations of reactive arthritis include not only Reiter's syndrome or clinically suspected postinfectious arthritis but also undifferentiated oligoarthritis and spondylarthritis. The optimal treatment remains to be defined, but there is increasing data that antibiotic therapy is not as effective in cases of well-established reactive arthritis as has been suggested.

Arthritis↗
PubMed1998

Studies of persistent infection by Chlamydia trachomatis serovar K in TPA-differentiated U937 cells and the role of IFN-gamma.

Inoculation of phorbol ester-differentiated U937 cells as a model for human macrophages with Chlamydia trachomatis of the urogenital serovar K resulted in a persistent infection, with maximal growth at day 7, until day 10 post-infection. At these times inclusion bodies were present in 0.5-2% of the cells. Typical inclusion bodies containing elementary bodies and reticulate bodies were observed by electron microscopy. Furthermore, single chlamydial particles resembling atypical elementary or intermediate bodies were identified in the cytoplasm in > 80% of the host cells. IFN-gamma exerts antichlamydial activity in epithelial and fibroblastoid cells, but the infection of U937 cells by C. trachomatis was not affected by IFN-gamma. The activity of the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase (IDO) was not detected in untreated or in IFN-gamma-treated or chlamydiae-infected or mock-infected U937 cells. The presence of atypical persisting chlamydiae and the lack of IDO expression in U937 cells indicates that the development of these atypical bacteria is independent from IFN-gamma-mediated tryptophan deprivation and other IFN-gamma-mediated effects. Evaluation of persistently infected cells revealed that the expression of the chlamydial major outer-membrane protein, heat-shock protein (hsp60) and lipopolysaccharide (LPS) antigens was not significantly altered in the course of the culture. An intense staining of the LPS on the surface of the host cells was demonstrated by immunofluorescence. The data show that phorbol ester-differentiated U937 cells restrict chlamydial growth strongly but not completely through a mechanism distinct from IDO-mediated tryptophan deprivation. The mechanisms of persistence of chlamydiae in monocytes, which differ considerably from those described for other cells, require further investigation.

Antigens, Bacterial↗
PubMed1998

[18F]fluoride PET indicates reduced bone formation in severe glucocorticoid-induced osteoporosis.

A 61-year-old female patient presenting with mixed connective tissue disease (Sharp syndrome), underwent a long-term high dose glucocorticoid treatment because of multiple organ manifestations. Under steroid therapy she developed severe osteoporosis resulting in multiple fractures. A dynamic [18F]fluoride PET study in this patient revealed reduced fluoride influx in non-fractured vertebrae. This finding corresponds to pathogenetic concepts which propose an inhibition of bone formation as major cause of glucocorticoid-induced osteoporosis. In the light of the presented case it seems to be promising to evaluate the diagnostic benefit of [18F]fluoride PET in osteoporosis.

Esophagus↗
PubMed1997

[Risk of ulcer and its prophylaxis in therapy with non-steroidal antirheumatic drugs].

Nonsteroidal antiinflammatory drugs (NSAIDs) are among the most frequently prescribed drugs in western countries. The high incidence of adverse gastrointestinal effects which are potentially life-threatening require steps for prevention. The use of NSAIDs should be restricted to patients with inflammatory rheumatic diseases. If NSAIDs are indicated it is important to identify patients who are at high risk to develop serious gastrointestinal side effects. These patients should receive Misoprostol at a dose of 2 to 3 x 200 micrograms per day. Up to date Misoprostol is the only drug with proven efficacy with respect to the prevention of gastroduodenal ulcer and its complications. NSAIDs inhibit the key enzyme of prostaglandin synthesis, the cyclooxygenase. Recently published data show that 2 isoenzymes of the cyclooxygenase exists. Cyclooxygenase-1 is primarily involved in the maintenance of organ function whereas cyclooxygenase-2 is expressed in inflamed tissue. Specific cyclooxygease-2 inhibitors have been developed. Clinical trials have to prove if the concept of a selective cyclooxygenase-2 inhibition with high antiinflammatory potency but lack of gastrointestinal side effects holds true in humans.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1997

Ultrastructural and molecular analyses of the persistence of Chlamydia trachomatis (serovar K) in human monocytes.

Previous studies have suggested that monocytes may play a role in the dissemination of Chlamydia trachomatis, and in establishment of persistent infection with this bacterium. Infection of cultured human peripheral blood monocytes with C. trachomatis serovar K produced persistent, nonproductive infection. Transmission electron microscopy of such infected cultures revealed single or multiple Chlamydia in monocyte inclusions over a culture period of 10 days. Those inclusions were aberrant, and normal reticulate bodies within the inclusions were not observed. Immunoelectron microscopy showed the chlamydial major outer membrane protein and lipopolysaccharide to be associated with the bacterial plasma membrane. Lipopolysaccharide was also identified in the monocyte cytoplasm. Molecular analyses of primary chlamydial rRNA transcripts demonstrated that the organism is viable and metabolically active within monocyte inclusions. However, attempts to overcome chlamydial growth arrest by incubation of Chlamydia-infected monocytes with tryptophan, and antibodies against alpha interferon, gamma interferon, or tumor necrosis factor, were all ineffective, suggesting that known mechanisms of growth inhibition do not hold in human monocytes. These observations indicate that infection of human peripheral blood monocytes with C. trachomatis may be involved in the genesis/maintenance of extra-urogenital inflammation, since non-culturable, metabolically active bacteria persist in those cells.

Antibodies, Blocking↗
PubMed1997

[Hepatitis C virus in rheumatic diseases].

HCV-infection is an important infectious disease in rheumatology. It is the cause of mixed cryoglobulinemia and other rheumatic manifestations develop frequently during HCV-infection. These comprise: Sicca-syndrome, thromboembolic events associated with anti-cardiolipin antibodies and fibromyalgia. Also associated with HCV-infection is a non-erosive polyarthritis. This synovitis often fulfills the ACR-criteria for rheumatoid arthritis, but the disease course is different with frequent remissions and non-erosive joint involvement. The following autoantibodies are associated with HCV-infection: Cryoglobulins, rheumatoid factor, antinuclear antibodies (ANA), antismooth muscle antibodies (SMA), anti-phospholipid-antibodies and anti-thyroid-antibodies. In HCV-associated sicca-syndrom, antibodies against Ro (SSA) and La (SSB) are not detected. The course of HCV-infection is often occult, without elevation of liver enzymes. We summarize the clinical and serological signs and symptoms when HCV-infection should be suspected and when HCV-testing should be performed in a rheumatological setting. The identification of HCV-infection in rheumatic patients is important to minimize the risk of aggravating hepatitis by prescription of hepatotoxic drugs and because of the availability of alpha-interferon as a potential virus eradicating agent.

Arthritis, Reactive↗
PubMed1997

Socioeconomic evaluation of rheumatoid arthritis and osteoarthritis: a literature review.

Limited resources and the need to improve the cost-effectiveness of medical procedures underlie the increasing importance of socioeconomic evaluations of health care. A search of MEDLINE was conducted to identify publications on the socioeconomic aspects of the two most important joint diseases: rheumatoid arthritis (RA) and osteoarthritis (OA). Analysis of the retrieved publications focused on three areas: (1) description of the socioeconomic effects of these diseases; (2) methodological approaches of the economic analyses; and (3) discussion from the perspective of patients, clinicians, or public health policy-makers. Of 52 publications dealing with cost data for RA and OA, 44 presented original and recently collected and developed data. Twenty-six were classified as cost analyses, three as cost-benefit analyses, and 11 as cost-effectiveness analyses (four did not fit into any of these classifications). Eight established methodological criteria were used to test for "full economic evaluation"; none of the reviewed studies fulfilled all eight, and only one study fulfilled seven. The gap between the importance of the socioeconomic effects of RA and OA and the research conducted in this field is considerable. A quality standard could be developed to serve as a guideline for further research.

Arthritis, Rheumatoid↗
PubMed1997

Treatment of hepatitis B-related polyarteritis nodosa with famciclovir and interferon alfa-2b.

BACKGROUND: The association between polyarteritis nodosa and viral hepatitis B infection is well established and still remains a therapeutic challenge. Famciclovir--a new nucleoside analog--has a broad spectrum of antiviral activity against herpes viruses and the human hepatitis B virus. CASE REPORT: A 56-year-old man with hepatitis B-related polyarteritis nodosa presented with symptoms correlating to high levels of HBV DNA. The patient did not respond to treatment with steroids (prednisolone started with 100 mg daily) and two courses of interferon alfa-2b (5 x 10(6) units 3 times per week for 6 months). Therefore, a combination therapy of interferon alfa-2b (5 x 10(6) units 3 times per week) and famciclovir (500 mg tid, orally) was started; 5 mg daily prednisolone was given at this time. Under this regimen HBV DNA rapidly declined, with a reduction of 79% after the first week (HBV DNA 53 pg/ml), and 88% after the second week (29 pg/ml), accompanied by a significant improvement in clinical symptoms. After 1 year of famciclovir treatment, HBeAg-anti-HBe seroconversion was noted; HBsAg still remained positive. Long-term famciclovir therapy has been continued at a reduced dose of 125 mg tid for 3 years now. HBV DNA values have been stable below 100 pg/ml, transaminases have normalized and clinical symptoms of polyarteritis nodosa have disappeared. CONCLUSIONS: Famciclovir has been successfully administered to a patient with hepatitis B-related polyarteritis nodosa. A reduction in viral replication and an improvement of symptoms were noted within 4 weeks of starting famciclovir. The oral nucleoside analog famciclovir is effective and well tolerated, even in long-term therapy, and might offer new treatment options in immunosuppressed patients for whom hepatitis B replication is critical for the disease process.

2-Aminopurine↗