Search PubMed⌕ Search

Biomedical subjects

H Schulze-Koops

Publications and source records attributed to H Schulze-Koops.

At least 19 recordsLinked to original sources
PubMed2006

[Superior vena cava syndrome: Catheter association as a rare cause].

HISTORY AND FINDINGS: A 78 year-old-woman was admitted with a swollen face, edema of the lower eyelids and dyspnea. The past medical history revealed an ovarian carcinoma treated with polychemotherapy. Half a year before the patient had been investigated for similar clinical symptoms but no underlying cause had been detected. The histology of an enlarged axillary lymph node did not show a malignancy. The symptoms persisted after angioedema-inducing drugs had been discontinued. INVESTIGATIONS: Initial CT scan, magnetic-resonance tomography as well as positron emission tomography failed to explain the clinical findings. Also, testing of serological, immunological and endocrinological tests as well as the differential blood count did not reveal a likely cause of the clinical symptoms. However, 4 weeks later, a repeat CT scan showed a stenosis of the superior vena cava (SVC) establishing the diagnosis of an SVC syndrome. TREATMENT AND COURSE: The port catheter tipp was localized horizontal to the vena cava superior and was touching the vein wall. Removal of the catheter and subsequent balloon dilatation of the stenosis immediately lead to a reduction of the eyelid swelling. CONCLUSIONS: Hence, in a case of an SVC-syndrome, complete stenosis caused by an implanted venous access system should be considered though it is rare.

Aged↗
PubMed2006

Plasmapheresis therapy in an elderly patient with rapidly progressive Henoch-Schönlein purpura with disseminated organ involvement.

Henoch-Schönlein purpura (HSP) frequently occurs in children below the age of 15 years and is rare with increasing age. Prognosis and therapy largely depend on the clinical presentation. The disease may be preceded by an upper respiratory tract infection, and drugs have also been implicated in the pathogenesis of the disease. Most children recover from the illness, whereas 40% of adults have persistent hematuria and 10% develop chronic renal failure. Recent studies strongly suggest that adults with HSP should be monitored for prolonged periods and treated aggressively. Here, we present a case of a patient with HSP who developed multiorgan failure requiring assistance in breathing and dialysis, and also sustained gastrointestinal bleeding despite aggressive immunosuppressive therapy. In analogy to published data in children with severe HSP, the patient was treated by plasma exchange in combination with low dose oral cyclophosphamide, while high dose steroids were reduced over time. The patient could be discharged 70 days after admission. One year after discharge, the patient is doing well without any signs of activity of HSP and completely unremarkable renal function. The maintenance daily dose of steroids is 7.5 mg.

Cyclophosphamide↗
PubMed2006

[Diagnostic and prognostic significance of antibodies against citrullinated peptides].

Antibodies against citrullinated peptides are highly specific for rheumatoid arthritis. With second generation ELISA-kits, CCP-antibodies have a specificity of > 96 % and a sensitivity of 68 %. CCP-antibodies can be detected several years before the onset of clinical symptoms. They are, thus, ideally suited for the differential diagnosis between early forms of rheumatoid arthritis and other inflammatory arthritides. As CCP-antibodies are associated with aggressive and treatment resistant courses of rheumatoid arthritis, their high predictive value can be useful in therapeutic strategy decisions in order to verify early treatment with disease modifying drugs or biologicals in line with modern treatment approaches to start aggressive therapy early to prevent bone erosions. In contrast to their role in differential diagnosis and prediction of aggressive disease, however, CCP-antibodies are of no value in monitoring treatment as they do not change essentially over prolonged periods of time.

Arthritis, Rheumatoid↗
PubMed2006

T cell activation as starter and motor of rheumatic inflammation.

Rheumatic inflammation is driven by sustained specific immunity against self-antigens, resulting in local inflammation and cellular infiltration and, subsequently, in tissue damage. Although the specific autoantigen(s) eliciting the detrimental immune reactions in rheumatic diseases have rarely been defined, it has become clear that the mechanisms resulting in the destruction of tissue and the loss of organ function during the course of the diseases are essentially the same as in protective immunity against invasive microorganisms. Of fundamental importance in initiating, controlling, and driving these specific immune responses are CD4 T cells. Currently available data provide compelling evidence for a major role of CD4 T cells in the initiation and perpetuation of chronic rheumatic inflammation. Consequently, T cell-directed therapies have been employed with substantial clinical success in the treatment of rheumatic diseases. Here, we review current knowledge based on which CD4 T cells can be implicated as the motor of rheumatic inflammation.

Animals↗
PubMed2006

Paraneoplastic syndrome, infection or arthritis: Difficulties in diagnosis.

Many different diseases have overlapping clinical symptoms. A major challenge in daily clinical practice is to differentiate between diseases associated with systemic inflammation, such as neoplasia, infection and autoimmune disease. We report on a 46-year-old Caucasian male with a 3-month history of rheumatoid arthritis presenting with dramatic weight loss and dysphagia. Computer tomography revealed multiple lesions in the liver and the spleen, strongly suggesting malignant disease of unknown origin. Surprisingly, on biopsy, the liver lesions drained pus. Workup revealed that the abscesses resulted from gastric perforation, which was the consequence of NSAR therapy for rheumatoid arthritis. Antibiotic therapy was initiated, abscesses diminished and dysfunctional deglutition improved. This unique case demonstrates in a dramatic way the difficulties in daily clinical practice to differentiate between paraneoplasia, infection and autoimmune disease and the potentially life-threatening consequences of their therapy.

Antirheumatic Agents↗
PubMed2005

[T-lymphocytes--do they control rheumatic immune responses?].

T cells, in particular CD4(+) T cells, have been implicated in mediating many aspects of rheumatoid inflammation. In rheumatoid arthritis (RA), CD4(+) T cells display various functional abnormalities in the synovium as well as in the peripheral circulation. Current evidence suggests, however, that the role of CD4(+) T cells in the development of rheumatoid inflammation exceeds that of activated pro-inflammatory effector T cells that drive the chronic autoimmune response. Subsets of CD4(+) T cells with regulatory capacity, such as CD25(+) Tregs, have been identified in mice and man, and recent observations suggest that in RA, the function of these regulatory T cells is severely impaired. Thus, in RA, defective regulatory immune mechanisms might allow the breakdown of peripheral tolerance, following which the detrimental CD4(+) T-cell-driven immune response evolves and proceeds to chronic inflammation. Here, we review the functional abnormalities and the contribution of different T-cell subsets to rheumatoid inflammation.

Animals↗
PubMed2001

Antigen-independent Th2 cell differentiation by stimulation of CD28: regulation via IL-4 gene expression and mitogen-activated protein kinase activation.

To delineate the molecular mechanisms regulating Th2 cell differentiation, CD28-mediated generation of Th2 effectors was analyzed. In the absence of TCR ligation CD28 stimulation induced Th2 differentiation of memory but not of naive CD4(+) T cells, whereas costimulation via CD28 and the TCR enhanced Th2 differentiation from naive T cells but suppressed it from memory T cells. Stimulation of T cells via the CD28 pathway, therefore, provided critical signals facilitating Th2 cell differentiation. By comparing the responses to CD28 stimulation in memory and naive T cells and by using specific inhibitors, signaling pathways were defined that contributed to Th2 differentiation. CD28-induced Th2 differentiation required IL-4 stimulation and the activation of the mitogen-activated protein kinases p38 and extracellular signal-regulated kinases 1/2. CD28 engagement directly initiated IL-4 gene transcription in memory T cells and induced activation of phosphatidylinositol 3-kinase, p38, and c-Jun NH(2)-terminal kinase/stress-activated protein kinase pathways. Extracellular signal-regulated kinase phosphorylation that was necessary for Th2 differentiation, however, required stimulation by IL-2. These results indicate that optimal TCR-independent generation of Th2 effectors requires coordinate signaling via the CD28 and IL-2 pathways. TCR-independent generation of Th2 effectors might provide a mechanism to control Th1-dominated cellular inflammation.

Adult↗
PubMed2001

The balance of Th1/Th2 cytokines in rheumatoid arthritis.

It has been suggested that rheumatoid inflammation is mediated by activated pro-inflammatory T helper type I cells. In contrast, immunomodulatory T helper type 2 cells and their cytokines, in particular interleukin-4, are rarely found. This chapter reviews the concept of the Th1/Th2 dichotomy and summarizes the functions of the signature cytokines of the T helper subsets. We discuss current knowledge of the immunopathogenesis of rheumatoid arthritis and its related animal model, collagen induced arthritis, with regard to the Th1/Th2 paradigm. The accumulating evidence for a T helper type 1 driven inflammation and the implications for future therapy are delineated.

Animals↗
PubMed2001

Treatment of rheumatoid arthritis in the third millennium.

Immense progress has been made in recent years in the management of patients with autoimmune diseases, such as rheumatoid arthritis (RA). This progress is largely owed to the advances in our understanding of cellular and molecular mechanisms involved in the pathogenesis of inflammation and autoimmunity and the substantially improved knowledge of molecular biology. In this editorial review, we delineate recent developments in the treatment of RA with a focus on biological therapeutics. we outline the concerns and open questions risen by the current studies and we portray future expectations based on the recent observations from those trials with biological treatment interventions.

Antibodies, Monoclonal↗
PubMed2000

Rheumatoid synovial CD4+ T cells exhibit a reduced capacity to differentiate into IL-4-producing T-helper-2 effector cells.

CD4+ memory T cells (Tm) from rheumatoid arthritis peripheral blood (RAPB) or peripheral blood from normal donors produced IL-2, whereas fewer cells secreted IFN-gamma or IL-4 after a brief stimulation. RAPB Tm contained significantly more IFN-gamma producers than normal cells. Many rheumatoid arthritis (RA) synovial Tm produced IFN-gamma alone (40%) and fewer cells produced IL-2 or IL-4. An in vitro model was employed to generate polarized T-helper (Th) effectors. Normal and RAPB Tm differentiated into both IFN-gamma- and IL-4-producing effectors. RA synovial fluid (RASF) Tm demonstrated defective responsiveness, exhibiting diminished differentiation of IL-4 effectors, whereas RA synovial tissue (RAST) Tm exhibited defective generation of IFN-gamma and IL-4 producers.

Adult↗