Pharmacotherapy of the rheumatoid arthritis. Dr. Erika Pintér 2016
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1 Pharmacotherapy of the rheumatoid arthritis Dr. Erika Pintér 2016
2 Polyarthritis chronica progressiva (PCP) Multifactorial, immunologic disorder that causes significant systemic effects Chronic and progressive Causes deformation of the joints Symptoms: Pain Started in MCP and PIP joints, symmetric Morning hand and joint stiffness Laboratory factors ( We, rheumatoid factor, CRP) Prevalence: 1%
3 The aims of the therapy: -Inhibition of the disease activity -improvement of the physical condition -slow-down of the development of structural damages Drug therapy: NSAID-s steroids DMARD-s disease modifying antirheumatic drugs other additional agents
4 DMARD-s 1.methotrexate 2. cyclophosphamide 3. cyclosporine 4. chloroquine 5. leflunomide 6. gold 7. sulfasalazine 8. penicillamine 9. Monoclonal antibodies (anti-tnf-α therapy) infliximab, adalimumab, etanercept NSAID-s, streroids: symptomatic, anti-inflammatory therapy. They have no any effect on the progression of the disease. DMARD-s: disease modifying antirheumatoid drugs. Long-lasting anti-inflammatory effect, clinical remission
5 1. Methotrexate First choice (60% of the patients) It is active in this condition at much lower doses than those needed in cancer chemotherapy. Mode of action (in low dose): Inhibition of aminoimidadazolecarboxamide ribonucleotide (AICAR) transformylase, and also thymidilate synthetase, which secondary effects on PMN chemotaxis. Some effects on the dihydrofolate reductase (inhibited lymphocyte and macrophage function). Kinetics: 70% oral absorption It is metabolized to a less active hydroxylated metabolite. Both compounds are polyglutamated within cell and stay for prolong period in the body. T1/2: 6-9 h but sometimes 24 h Excretion: 70% in the urine 30% in the bile Dose: mg/week Adverse effects: nausea, mucosal ulcers, dose related hepatotoxicity. The incidence of GIT and liver function abnormalities can be reduced by the use of leucovorin 24h after each weekly dose, or by daily folic acid. Contraindicated in pregnancy.
6 2. Cyclophosphamide Mode of action: Its major active metabolite is phosphoramide mustard, which cross-links DNA to prevent cell replication. It suppress T and B cell functions by 30-40%. Dose: 2 mg/kg/day orally Side effects: dose related bone marrow suppression, alopecia, haemorrhagic cystitis
7 3. Cyclosporine Mode of action: See: immunopharmacology Kinetics: new microemulsion formulations have 20-30% oral bioavailability grape fruit juice increases CS bioavailability by as much as 62% metabolisms by CYP3A Interactions!!! Dose: 3-5 mg/kg/day Toxic effects: nephrotoxicity (interactions with drugs inhibiting CYP3A (diltiazem, potassium-sparing diuretics) Serum creatinin should be monitored!
8 4.Chloroquine See: malaria Mode of action: unclear The following mechanisms have been proposed: -suppression of T cell responses to mitogens -decreased leukocyte chemotaxis -stabilization of lysosomal enzymes -decrease DNA and RNA synthesis -trapping of free radicals Kinetics: Rapid absorption 50% plasma protein binding extensively tissue-bound, particularly in melanin-containing tissue such as the eyes. T1/2: 45 days Side effects: ocular toxicity (over 250 mg/day), ophthalmologic monitoring is advised. Dyspepsia, nausea, abdominal pain, rashes, nightmares Relatively safe in pregnancy.
9 5. Leflunomide Mode of action: It undergoes rapid conversion in the intestine and plasma A A inhibits dihydroorotate dehydrogenase leading to a decrease of ribonucleotid synthesis and arrest of stimulated cells in the Gi phase of cell growth. It inhibits T cell proliferation antibody production of B cells. It increases of IL-10 receptor mrna, decreases of IL-8 receptor, type A mrna, decreases of TNF-α-dependent NF B activation Kinetics: Completely absorbed, T1/2 : 19 days, enterohepatic circulation Adverse effects: Diarrhoe 25%, elevation of liver enzymes, might alopecia, weight gain, elevated blood pressure, Contraindicated in pregnancy.
10 6. Gold compounds (only history) They were first proved to be effective in a clinical trial (1960) i.m. formulas aurothiomalate - aurothioglucose contain 50% elemental gold oral: auranoffin (29% elemental gold) Mode of action: gold alter the morphology and functional capabilities of human macrophages, monocyte chemotactic factor 1, IL-8, IL-1b, VEGF are inhibited i.m. gold: inhibited lysosomal enzyme activity, histamine release, complement system, phagocytic activity of PMN, oral gold: inhibits PGE1, LTB4 synthesis Kinetics: i.m. gold tends to concentrate synovial membrane, liver, kidney, bone marrow, spleen, lymph node T1/2 1 year Dose: i.m. 50 mg/week for 20 weeks Adverse effects: pruritic skin rashes (15-20%), eosinophilia, stomatitis, metallic taste int he mouth, thrombocytopenia, leukopenia, pancytopenia (1-10%) enterocolitis, jaundice
11 7. Sulfasalazine Mode of action: it is metabolized to sulfapyridin and 5- aminosalicylic acid. It is thought that sulfapyridin is probably the active molecule against RA. (???) (See: ulcerative colitis and Crohn s disease.) It decreases IgA and IgM rheumatoid factor production. Kinetics: 10-20% oral absorption, enterohepatic circulation intestinal bacteria liberation of 5-aminosalicylic acid (remains in the gut) sulfapyridin (is well absorbed) Adverse effects: 30% stop of treatments nausea, vomiting, headache, rash, haemolytic anaemia, methaemoglobinaemia
12 8. Penicillamine (rarely used) It is penicillin metabolite, dimethylcysteine. D-isomer is used against RA. 75% responder patients. Mode of action: inhibition of IL-1 generation and prevention of the maturation of newly synthesised collagen. The drug has a highly reactive thiol group and also has meta-chelating properties (treatment of Wilson disease) Kinetics: It is given orally, 50% is absorbed. Dosage is started low and increased only gradually to minimise unwanted effects. Side effects: Occur in 40% of patients. Anorexia, vomiting, fever, taste disturbances. Proteinuria (20% of patients). Rashes, stomatitis, dose-related thrombocytopenia, leukopenia, aplastic anaemia
13 9. TNF-a blocking agents 1. adalimumab Mode of action: is a fully human IgG1 anti-tnf monoclonal antibody. Adalimumab complexes with soluble TNF-a and prevents its interaction with p55 and p75 cell surface receptors. Kinetics: s.c., t1/2: days, dose: 40 mg every other week Side effects: macrophag-dependent infections (tuberculosis, opportunistic infections). Increases incidence of malignancies 2. infliximab See: immunopharmacology 3. etanercept See: immunopharmacology
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