Anti-rheumatoidal effect

Choi J, Yoon B-J, Huh K, Park K-Y, Lee K-T, Park H-J (2002) Anti-rheumatoidal effect of sulfuretin isolated from the heartwood of Rhus veniciflua in rats and mice. Nutraceuticals and Food 7 347... 

IFN- 3 reduces the induction by inflammatory cytokines of adhesion molecules and of MHC class I and II complex on endothelial cells, a process preceding attachment and transendothelial migration of T-cells. These anti-inflammatory effects of IFN- 3 exemplify antagonistic actions of type I and type IIIFN. There is, indeed, much clinical evidence for the involvement of IFN-y in inflammatory processes - through activation of iNOS and subsequent secretion of NO - leading to the establishment of autoimmune diseases as for instance in rheumatoid arthritis. 

Leflunomide is an immunomodulatory dmg inhibiting dihydroorotate dehydrogenase, an enzyme involved in de novo pyrimidine synthesis. It has also anti-inflammatory effects. Leflunomide is able to slow progression of the disease and to cause re-mission/relief of symptoms of rheumatoid arthritis and psoriatic arthritis such as joint tenderness and decreased joint and general mobility in patients. The combined use of leflunomide with methotrexate may... 

Fishman P, Bar-Yehuda S, Madi L, Rath-Wolfson L, Ochaion A, Cohen S, Baharav E (2006) The PI3K-NF-K B signal transduction pathway is involved in mediating the anti-inflammatory effect of IB-MECA in adjuvant-induced arthritis. Arthritis Res Ther 8(1) 1-9 Goldbach-Mansky R, Lipsky PE (2003) New concepts in the treatment of rheumatoid arthritis. Annu Rev Med 54 197-216... 

Finally, acetaminophen (paracetamol) products may provide some temporary analgesic effects in people with rheumatoid arthritis, but these products are not optimal because they lack anti-inflammatory effects. As discussed in Chapter 15, acetaminophen can be used to treat mild-to-moderate pain, but the lack of anti-inflammatory effects makes acetaminophen fall short of NSAIDs for conditions such as rheumatoid arthritis. Hence, patients with rheumatoid arthritis usually prefer the effects of NSAIDs to acetaminophen,110 and acetaminophen products are not typically used for the routine treatment of this disease. 

In addition to direct effects on genes regulating inflammation, glucocorticoids also inhibit the transcription factors that initiate synthesis of pro-inflammatory cytokines (e.g., interleukin-1, tumor necrosis factor), enzymes (e.g., COX-2, nitric oxide synthase), and receptor proteins (e.g., natural killer receptors).17,87,89 Glucocorticoids may also exert some of their effects via a membrane-bound receptor that regulates activity of macrophages, eosinophils, T lymphocytes, and several other types of cells involved in the inflammatory response.89 Consequently, glucocorticoids affect many aspects of inflammation, and their powerful anti-inflammatory effects in rheumatoid arthritis result from their ability to blunt various cellular and chemical components of the inflammatory response. 

Aspirin is employed for mild to moderate pain of varied origin but is not effective for severe visceral pain. Aspirin and other NSAIDs have been combined with opioid analgesics for treatment of cancer pain, where their anti-inflammatory effects act synergistically with the opioids to enhance analgesia. High-dose salicylates are effective for treatment of rheumatic fever, rheumatoid arthritis, and other inflammatory joint conditions. 

Bisphosphonates (particularly clodronate) have been shown to have anti-inflammatory effects in animal models of rheumatoid arthritis (RA), as well as in arthritis in humans. In adjuvant- and antigen-induced arthritis in rats, clodronate suppresses the inflammatory articular lesions in the inflamed joints [29], whilst in human RA, clodronate decreases the levels of interleukin (ILJ-1, tumor necrosis factor-alpha (TNFaand /1-microglobulin in the circulation [30]. In vitro, clodronate inhibits cytokine and nitric oxide (NO) release and inducible nitric oxide synthase (iNOS) expression in macrophage-like cells. 

A comprehensive review discusses the therapeutic management of RA (Turesson and Matteson, 2004). Epidemiological studies link extra-articular rheumatoid arthritis manifestations with premature mortality and support aggressive anti rheumatoid therapies for those patients. Cyclophosphamide is favored in patients with systemic rheumatoid vasculitis and methotrexate in those cases with other manifestations of extra-articular rheumatoid arthritis (Turesson and Matteson, 2004). Cyclophosphamide and TNFa inhibitors such as infliximab have some positive success in treatment resistant vasculitis associated with RA (Unger et al., 2003). However, TNFa inhibitors have also been associated with the opposite effect, an induction of extra articular rheumatoid arthritis so their use should be used only in specific cases when close monitoring is in place. 

A few patients with chronic inflammatory iilncs.scs such as asthma, rheumatoid arthritis, and lupus develop resistance to the anti-inflammatory effects of the glucocorticoids. The... 

Use Pain and anti-inflammatory effects with patients with rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, acute gout, bursitis, and tendonitis. Ophthalmic Prophylaxis/treatment of ocular inflammation Half-life 2 hours Onset IM/IV 10 minutes (dose dependent) PO 20-40 minutes Peaks Duration 1-2 hours 4—6 hours... 

Unlike rheumatoid arthritis, there is no systemic disease associated with osteoarthritis. Treatment of osteoarthritis is with NSAIDs for their analgesic and anti-inflammatory effects. Corticosteroids are not recommended and disease-modifying drugs are not effective in osteoarthritis. 

Compound G25671, like phenylbutazone, exerts an anti-inflammatory effect in rheumatoid arthritis - . It differs from phenylbutazone, however,... 

Collagenase production and release are partly responsible for the joint destruction that characterises human rheumatoid arthritis. Triterpenes from the lupane and a-amyrin groups have been studied in vitro to examine their effects on the release of the arthritic joint degradative enzyme collagenase using the rat osteosarcoma. This test and the rat synovial granuloma of adjuvant arthritis are similar both models are based on connective tissue tumours with bone-invasive properties. The pentacyclic triterpenes assayed have been shown to possess general antiproteolytic effects that can explain the anti-arthritic effects in adjuvant arthritis in rats [71,103]. 

Acetaminophen (paracetamol JV-acetyl-p-aminophenoF, TYLENOL, others) is an effective alternative to aspirin as an analgesic-antipyretic agent however, its anti-inflammatory effects are much weaker. While it is indicated for pain relief in patients with noninflammatory osteoarthritis, it is not a suitable substitute for aspirin or other NSAIDs in chronic inflammatory conditions such as rheumatoid arthritis. Acetaminophen is well tolerated and has a low incidence of GI side effects. It is available without a prescription. Acute overdosage can cause severe hepatic damage, and the number of accidental or deliberate poisonings with acetaminophen continues to grow. Chronic use of less than 2 g/day is not typically associated with hepatic dysfunction. 

Oral antimicrobial agents sometimes have beneficial effects in inflammatory bowel disease. However, in the absence of any evidence pointing toward a definite microbial cause for the colitis in this patient, a drug that decreases inflammation is indicated. Sulfasalazine has significant anti-inflammatory action, and its oral use results in symptomatic improvement in 50-75% of patients. The drug is also used for its anti-inflammatory effects in rheumatoid arthritis. The answer is (D). 

Improve anti-inflammatory effectiveness Lower the risk of gastrointestinal toxicity Reduce the cost of treatment of rheumatoid arthritis Selectively decrease thromboxane A without effects on other eicosanoids... 

It is used mainly for its anti-inflammatory effect in the treatment of rheumatoid arthritis. Being practically insoluble in water it is more gradually released and subsequently absorbed than the other water-soluble gold compounds. 

It is not known exactly how methotrexate produces its effects in rheumatoid arthritis, but one theory is that it possibly increases levels of adenosine by blocking a step in purine biosynthesis, leading to accumulation of adenosine, which results in anti-inflammatory effects. It also inhibits the enzyme 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) trans-formylase, raising levels of AICAR, which in turn increases adenosine levels. It may also contribute to the phosphorylation of adenosine nucleotides creating an accumulation of adenosine in tissues. Caffeine is an adenosine receptor antagonist and therefore could reverse the effects of methotrexate. 

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