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| Lupus kidney disease |
1 foster optimism, properly treat the disease and establish the confidence to overcome the disease, patterns of life, pay attention to work and rest, proper rest, to prevent infection.
2 to remove a variety of incentives, including a variety of possible internal use of drugs, chronic infection foci, etc., to avoid irritating topical medications and all external stimuli.
3 Avoid sunlight and ultraviolet radiation, especially in the event of need, to add sunlight painted anti-drugs such as quinine 3% ointment, ointment compound of titanium dioxide, 15% for ammonia benzoin limp ointment, others such as cold, X-ray, etc. too much can also cause increased exposure to the disease, can not be ignored.
4. hydralazine, procainamide, penicillamine, antibiotics and sulfa drugs to reasonable effect.
5 Patients should birth control, activities of the need to avoid pregnancy, renal impairment or if system damage who should strive to make early therapeutic abortion.
a variant of lupus erythematosus that resolves within days to months after withdrawal of the culprit drug in a patient with no underlying immune system dysfunction. DILE can arise months to years after exposure to drugs prescribed to treat various medical conditions (eg, antihypertensives, antibiotics, anticonvulsants). The most common drugs that cause DILE are hydralazine, procainamide, quinidine, isoniazid, diltiazem, and minocycline (see Etiology).[1]
Drug-induced subacute cutaneous lupus erythematosus (DISCLE) is a DILE variant with predominant skin involvement, temporally related to drug exposure, and resolving after drug discontinuation.[2]
Care must be taken to correctly diagnose the symptoms of DILE and differentiate it from systemic lupus erythematosus (SLE), and DILE should be recognized clinically and serologically for prompt intervention.
Although both SLE and DILE are autoimmune disorders and can have similar clinical and laboratory features (see Table 1 below), research suggests different mechanistic pathways (see Pathophysiology). Guidelines for diagnosis and management of SLE have been established.[3] Although the pathogenesis of DILE is not completely understood, a genetic predisposition may play a role, as has been shown with certain drugs metabolized by acetylation, such as procainamide or hydralazine.[4]
Drugs such as procainamide, chlorpromazine, and quinidine cause the production of antinuclear antibodies against the histone dimer H2A-H2B. Hydralazine forms antinuclear antibodies to H1 and the H3-H4 complex.[6] Drugs that cause DILE usually take months to years before the associated symptoms occur, whereas flares of SLE due to drugs may occur within hours to days.
Most patients with DILE have 1 or more clinical symptoms of SLE, such as arthralgias, lymphadenopathy, rash, and fever, and have had no prior history of autoimmune disease. However, certain manifestations typical in persons with SLE are not usually observed in persons with DILE (see Clinical).
No specific criteria establish the diagnosis of DILE, and excluding underlying autoimmune disease is not a simple process. DILE is typically diagnosed by a process of elimination to rule out SLE (see Differentials).
Symptoms of DILE usually clear within weeks of stopping the culprit drug. Generally, no other specific treatments are known. Low doses of systemic corticosteroids may be prescribed for short periods if the symptoms are severe
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