Rheumatic Disease Drug Therapy

Rheumatic Disease Drug Therapy

Principles of management The management of rheumatological disorders should be tailored to the underlying diagnosis. Certain aspects are common to many disorders, however, the general principles are:


Non-pharmacological interventions -To educate patients about their disease -Physical and occupational therapy Local heat, ice packs, wax baths and other local external applications can induce muscle relaxation and provide temporary relief of symptoms in a range of rheumatic diseases.

Hydrotherapy induces muscle relaxation and facilitates enhanced movement in a warm, pain-relieving environment without the restraints of gravity and normal load-bearing. Various manipulative techniques may also help improve restricted movement.

pharmacological therapy

*simple analgesic drugs *NSAIDs *Topical creams * Opioid analgesics *Amitriptyline 'disease-modifying antirheumatic drug' ((DMARD *

1-SIMPLE ANALGESIA

Paracetamol (1 g 6-8-hourly) is the oral analgesic of choice because of its efficacy, lack of contraindications or drug interactions, long-term safety, low cost and availability. Paracetamol inhibits prostaglandin synthesis centrally in the brain but has little effect on peripheral production of prostaglandins

2-NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS)

These are among the top five most prescribed drugs in many countries. Oral NSAIDs are often effective for the pain and stiffness of inflammatory disease. Long-acting NSAIDs given at night are particularly helpful for marked inflammatory early morning stiffness. NSAIDs may also reduce bone pain due to secondary malignant lesions.


The major drawback of NSAIDs is gastrointestinal toxicity. Prostaglandins of the E series play a major role in gastroduodenal defence mechanisms. By depleting mucosal prostaglandin levels, aspirin and NSAIDs impair this 'cytoprotection', resulting in mucosal injury, erosions and ulceration. NSAIDs are an important aetiological factor in up to 30% of gastric ulcers.

3-CORTICOSTEROIDS IN RHEUMATOID ARTHRITIS

Systemic corticosteroids have disease-modifying activity, but their primary role is in the induction of remission in patients with early RA who are starting synthetic DMARD treatment. Various regimens have been used One strategy is to give a high dose of oral prednisolone initially (60 mg daily) and to reduce and stop this gradually over a period of 3 months as the DMARD starts to take effect.


Intra-articular corticosteroids are primarily indicated when there are one or two ‘problem joints’ with persistentsynovitis despite good general control of the disease. Although corticosteroids are very useful, they alsohave significant adverse effects., osteoporosis is probably the most important since this is a known complication of RA, even in the absence of corticosteroid therapy. Accordingly DEXA scanning followed by bone protection should be considered in any patient with RA who is expected to be on more than 7.5 mg prednisolone daily for more than 3 months

4-‘Disease-modifying antirheumatic drugs

Methotrexate (MTX) is the core DMARD in RA, and PsA. It inhibits folic acid reductase, preventing formation of tetrahydrofolate, which is necessary for DNA synthesis in leucocytes and other cells.


The most common adverse effectsnausea, vomiting and malaise within 24–48 hours . Patients who experience these can sometimesbe successfully treated with subcutaneous methotrexate.Folic acid (5 mg/week) reduces the incidenceThe most common combination is triple therapy .

The most common combination is triple therapy methotrexate, sulfasalazine and hydroxychloroquine are combined Other DMARDs can be substituted or added, along with a low-dose glucocorticoid such as prednisolone (5–10 mgdaily) if the patient fails to respond fully. If disease activity remains high (DAS28 > 5.1) despite triple therapy, however, it is usual to progress to biologic therapy. The most commonly used first-linebiologics in RA are TNF inhibitors, although several other options are available

These drugs are more effective than standard DMARDs (with a faster onset of action, greater clinical efficacy and sustained benefit) but because of their cost many countries have set restrictive guidelines for their use.
Current recommendations are that biological therapy should be initiated only in active RA (DAS28 > 5.1) when an adequate trial of at least two other DMARDs (including methotrexate) has failed.
5- Biological Treatment


1- Anti-TNF therapy (Infliximab) is the first-line biological drug in RA.Several agents are available. With the exception of infliximab, which must be prescribed with methotrexate to reduce the risk of neutralizing antibodies developing, these agents can be used as monotherapy. In clinical practice, however, most are co-prescribed with methotrexate, as this is more efficacious. The main adverse effects are serious infections and reactivation of latent tuberculosis

 2- Competitively blocks binding of IL-1 to its receptor (Anakinra)

3- Monoclonal antibody that binds CD20 antigen on B-cells surface (Rituximab)
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surgery

Synovectomy can be helpful in joints that have failed to respond adequately to systemic therapy and intra-articular injections. Jointreplacement surgery may be required but the need for this hasdiminished over recent years, resumably as the result of moreaggressive medical management. Other surgical procedures thatcan be helpful are excision of the metatarsal heads in patientswith subluxation of the MTP joints; neurosurgery in patientswith atlanto-axial subluxation; and fusion or the wrist or ankle inpatients with joint damage .