Der Schmerz

, Volume 5, Supplement 1, pp S3–S12 | Cite as

Der entzündliche Gelenkschmerz

Pathobiochemie und pharmakologische Grundlagen
  • Klaus Resch
Übersichten

Zusammenfassung

Schmerz ist ein Leitsymptom entzündlicher Gelenkerkrankungen. Für seine Entstehung spielen Prostaglandine (und evtl. Leukotriene) eine wichtige Rolle. Diese Eikosanoide werden aus Arachidonsäure gebildet, die aus Membranphospholipiden freigesetzt wird. Prostaglandine setzen die Schwelle für die Konzentration anderer Moleküle herab, die Nozizeptoren erregen. Sie werden von Entzündungszellen wie Makrophagen, aber auch autochthonen Gewebszellen wie Synoviozyten sezerniert. Viele Reize könen Eikosanoidsynthese in diesen Zellen induzieren; bei entzündlichen Erkrankungen sind eine Gruppe von Proteinmediatoren am wichtigsten, die sog. inflammatorischen Zytokine, zu denen Interleukin-1, Tumor-Nekrose-Faktor und Interleukin-6 gehören. Diese werden vor allem von Makrophagen gebildet. Bei den chronisch entzündlichen Erkrankungen, wie der rheumatoiden Arthritis, wird die Aktivieriung dieser (und anderer) Entzündungszellen durch (Auto-)Immunreaktionen aufrecht erhalten; sowohl Antigen-Antikörper-Komplexe (humorale Immunreaktionen) wie auch die Sekretion von Lymphokinen wie Interferon- aus T-Lymphozyten (zelluläre Immunureaktionen) sind daran beteiligt.

Abkürzungsverzeichnis

PG

Prostaglandin

LT

Leukotrien

IL-1

Interleukin-1

IL-6

Interleukin-6

TNF

Tumor-Nekrose-Faktor

IFN-γ

Interferon-γ

HLA

Humanes-Leukozyten-Antigen

NSA

Nicht-steroidale Analgetika/Antiphologistika

Pain of the joint of inflammatory diseases pathobiochemistry and pharmacology

Abstract

Pain is the leading symptom of inflammatory joint diseases. It is immediately caused by the release of prostaglandins (and potentially leukotrienes) from cells of the inflamed tissues, which sensitizes the pain receptors. The synthesis of these mediators depends on the activation of infiltrated inflammatory cells, as well as recruitment of tissue born cells, predominantly by the inflammatory cytokines Interleukin-1 (IL-1) or tumor necrosis factor (TNF). In chronic diseases such as rheumatoid arthritis the inflammatory reaction is initialized and perpetuated by (auto)-immuno reactions. The associated chronic pain is thus the end point of a complex multi-level disease process. The hierarchy of these regulatory processes is mirrored by the pharmacological interventions. Inhibitors of the key enzyme of prostaglandin synthesis, cyclooxigenase, such as the non-steroidal anti-inflammatory drugs (NSAID) are immediately analgetic. Anti-inflammatory drugs as the glucocorticoids predominantly decrease the synthesis of cytokines, and thereby the stimuli leading to prostaglandin synthesis. Together with a decrease of the synthesis of arachidonate metabolizing enzymes this leads to correction of pain. Although not directly analgetic, immunosuppressive drugs, too, by decreasing the immune reaction dependent inflammation, contribute to pain relief.

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Copyright information

© Springer-Verlag 1991

Authors and Affiliations

  • Klaus Resch
    • 1
  1. 1.Abt. MolekularpharmakologieMedizinische Hochschule HannoverHannover 61

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