Antinuclear antibody lupus erythematosus

Hydantoln anticonvulsants may cause the appearance of positive L.E. cells and methemoglobinemia. Chloropromazlne has been Implicated In causing a syndrome like systemic lupus erythematosus with accompanying positive tests for L.E. cells and antinuclear antibodies (6). 

Kilbum KH, Warshaw RH. 1992. Prevalence of symptoms of systemic lupus erythematosus (SLE) and of fluorescent antinuclear antibodies associated with chronic exposure to trichloroethylene and other chemicals in well water. Environ Res 57 1-9. 

The prolonged administration often leads to the development of a positive antinuclear antibody (ANA) test, with or without symptoms of a lupus erythematosus-like syndrome. If a positive ANA titer develops, assess the benefit/risk ratio related to continued procainamide therapy. 

Lupus erythematosus Certain patients will develop a positive antinuclear antibody (ANA) test and some may show a lupus erythematosus-like syndrome similar to other drug-induced lupus, but it is not associated with hypocomplementemia and may be present without nephropathy. A positive ANA test does not mandate drug discontinuance however, a lupus erythematosus-like syndrome may develop later. Sensitivity reactions Once instituted for Wilson s disease or cystinuria, continue treatment with penicillamine on a daily basis. Interruptions for even a few days have been followed by sensitivity reactions after reinstitution of therapy. 

CNS toxicity occurs because isoniazid has structural similarities to pyridoxine (vitamin Be) and can inhibit its actions. This toxicity is dose-related and more common in slow acetylators. Manifestations include peripheral neuropathy, optic neuritis, ataxia, psychosis and seizures. The administration of pyridoxine to patients receiving INH does not interfere with the tuberculostatic action of INH but it prevents and can even reverse neuritis. Hematological effects include anaemia which is also responsive to pyridoxine. In some 20% of patients antinuclear antibodies can be detected but only in a minority of these patients drug-induced lupus erythematosus becomes manifest. 

Long-term drug use leads to increased antinuclear antibody titers in more than 80% of patients more than 30% of patients receiving long-term procainamide therapy develop a clinical lupus erythematosus-like syndrome. The symptoms may disappear within a few days of cessation of procainamide therapy, although the tests for antinuclear factor and lupus erythematosus cells may remain positive for several months. 

How an ancient Roman family name, Lupus ( wolf ), came to have a disease association is obscure (D8, pp. 515-516). The earliest known medical use of lupus appeared in a 10th-century biography of St. Martin (S24). Hundreds of years passed before several authors first recognized the varied components of SLE (BIO). The first major event of the modern study of the disease was the development of the lupus erythematosus cell test by Hargraves in 1949 (H4) it was followed by the introduction of the immunofluorescent antinuclear antibody test in 1958 (F13). The preliminary criteria for the classification of SLE were first published in 1971 (C21) and were revised in 1982 (Tl). The third revision with two changes was completed in 1997 (H12). 

Scopelitis, E., Biundo, J. J., Jr., and Alspaugh, M. A., Anti-SS-A antibody and other antinuclear antibodies in systemic lupus erythematosus. Arthritis Rheum. 23, 287-293 (1980). 

Antibodies directed to antigens that are components of cell surface receptors are often pathogenic in vivo (such as ion channel antibodies and, possibly, mGluRl antibodies) [95, 182, 183], The pathogenic relevance of antibodies to intracellular targets is much more controversial, but antinuclear antibodies are reported to be pathogenic in some diseases such as systemic lupus erythematosus [184]. 

Differential diagnoses of peripheral neuropathy were entertained. Laboratory tests revealed that serum parameters for electrolytes and proteins were all within the normal range. Urine porphyrinogen and porphobilinogen levels were normal. Tests were negative for serum rheumatoid factor and antinuclear antibodies, the latter used in detection of connective tissue diseases such as systemic lupus erythematosus and polyarteritis nodosa that could present with features of peripheral neuropathy. Nerve conduction studies of the radial, ulnar, and median nerves revealed delayed conduction. Biopsies of the ulnar and radial nerves showed loss of nerve fibers and sudanophilic (indicating lipid) deposits in the Schwann cells of the neurons. Similarly, the yellowish plaques of the pharynx showed abundant macrophages filled with sudanophilic material. These deposits were not membrane-bound. 

Photo-induced annular or papulosquamous eruptions due to subacute cutaneous lupus erythematosus with positive antinuclear, anti-Ro, and anti-La antibodies have been reported with verapamil, nifedipine, and diltiazem (113). 

Although patients treated with etanercept commonly develop new antinuclear antibodies or anti-double-stranded DNA antibodies, there were no reports of cutaneous or systemic lupus erythematosus in early clinical trials. However, since then, at least eight cases have been reported, including five patients with a lupus-like syndrome, two with acute discoid lupus, and one with subacute cutaneous lupus erythematosus (26-29). All were women and they developed their first symptoms 6 weeks to 14 months after the first injection of etanercept. Antinuclear and/or anti-DNA antibodies were positive in most of them. Etanercept was withdrawn in all patients with features of systemic lupus erythematosus, and the symptoms resolved within 2-8 weeks. The skin lesions also improved with local glucocorticoids, despite continued etanercept treatment in two patients with discoid lupus or subacute cutaneous lupus erythematosus. This suggests that etanercept-induced autoantibodies are sometimes associated with clinical autoimmune disease. 

According to the authors, the patient fulfilled all the criteria for a diagnosis of drug-induced lupus-like syndrome, that is no history of lupus erythematosus before minocycline therapy, the presence of antinuclear antibodies, at least one clinical feature of lupus erythematosus, and prompt recovery after withdrawal of minocycline. She also had positive antihistone antibodies, compatible with drug-induced lupus-like syndrome. 

Concerns that PUVA therapy can cause systemic lupus erythematosus (SLE) and other connective tissue diseases, such as giant cell arteritis (SEDA-6, 147), have been raised by several reports (SED-12, 336) (30), (SEDA-15, 139) (SEDA-17, 183). There have been several studies of the incidence of serum antinuclear antibodies in patients who have received PUVA, with both... 

Exacerbation of lupus erythematosus has been reported during terbinafine therapy (55-57,61). Of 21 consecutive patients with subacute cutaneous lupus erythematosus who attended an outpatient dermatology department in Germany during 1 year, 4 had terbinafine-associated disease (62). In addition to high titers of antinuclear antibodies with a homogeneous pattern, anti-Ro(SS-A) antibodies were present in three of the four women, anti-La(SS-B) antibodies were also found. All the... 

Several cases of a reaction resembUng systemic lupus erythematosus have been described (24-26). One patient taking hydrochlorothiazide developed unequivocal antinuclear antibody (ANA) positivity, with the homogeneous pattern most commonly found in drug-induced lupus (27). It is uncertain whether thiazides cause a lupuslike syndrome or activate latent disease in predisposed individuals. 

Zonisamide-induced lupus erythematosus has been reported in a 5-year-old child taking zonisamide and etho-suximide (15). He had raised titers of antinuclear antibodies and anti-DNA antibodies and presented with fever, pericarditis, pleurisy, and arthralgia. Clinical recovery and a reduction in the anti-DNA-antibody titer promptly followed withdrawal. A lymphocyte transformation test against zonisamide was positive. 

Quinidine may be associated with a syndrome called cinchonism, which is characterized by headache, vertigo, and tinnitus. Procainamide may result in hypotension or a reversible syndrome similar to lupus erythematosus. Patients may develop positive antinuclear antibody (ANA) titers and complain of rash, arthralgia, and arthritis. Disopyramide is poorly tolerated due to its anticholinergic effects (urinary retention, dry mouth, blurred vision), and its use should be avoided in patients with congestive heart failure (CHF) due to negative inotropic effects. 

T-cell function is reduced in many epileptics receiving anticonvulsants, and systemic lupus erythematosus occurs in about 10% of treated individuals. Antinuclear antibodies have been reported in 55%, and low serum IgA and IgG concentrations in 25% of the patients. Other reported biochemical abnormalities include reduced serum concentrations of HDL cholesterol, urate, and urea nitrogen. 

Antinuclear antibodies are detected in 25% of patients with rheumatoid arthritis. These antibodies usually have a diffuse pattern of immunofluorescence. Tests for antibodies to double-stranded DNA (usually positive in systemic lupus erythematosus) are negative. Serum complement is usually normal, although complement concentrations of joint fluid often are depressed from consumption secondary... 

We do not currently have data pertaining to the predictive ability of antinuclear antibodies with respect to development of lupus. However, a study using serum samples from 130 active-duty personnel in the United States military who developed systemic lupus erythematosus documented the presence of antinuclear antibodies, anti-Ro antibodies, anti-La antibodies, antiphospholipid antibodies, and anti-dsDNA antibodies a mean of 1-3 years before the occurrence of symptoms (Arbuckle et al., 2003). 

Anti-TNF-a drugs have recently been approved for the treatment of a number of autoimmune diseases, including rheumatoid arthritis and Crohn disease. A number of adverse consequences, including the development of antinuclear antibodies and anti-dsDNA antibodies and the autoimmune diseases leukocytoclastic vasculitis and systemic lupus erythematosus, have been reported following treatment with anti-TNF-a drugs (Hyrich et al., 2004). 

Cat 6-Propylthiouracil Systemic lupus erythematosus antinuclear antibodies, Sm antigen lymphadenopathy, haemolytic anaemia... 

Monkey L-Canavanine (alfalfa seeds) Systemic lupus erythematosus Antinuclear antibodies... 

Systemic lupus erythematosus (SLE). A chronic, remitting-relapsing inflammatory autoimmune disease affecting multiple organ systems, such as the skin, joints, serosal membranes, kidneys, blood cells, and central nervous system. The disease is very heterogeneous in clinical expression and serological factors. Autoantibodies directed against nuclear components ( - antinuclear antibodies) are typically detected. Anti-dsDNA, anti-Sm, and antiphospholipid antibodies are used as classification criteria. 

Hydralazine. Vasodilator drug which causes systemic lupus erythematosus in a significant proportion of patients. Several predisposing factors have been identified dose (>25 mg) duration of therapy (mean 18 months) acetylator phenotype (slow) HLA type (DR4) gender (females males, 4 1). Antinuclear antibodies and antihydralazine antibodies detected in serum. Causes a Type III immune reaction. Mechanism is unclear but may involve reaction of parent drug or metabolite with protein. Interference with the complement system and interaction with nucleic acids also occur. Metabolism also may be mediated by myeloperoxidase in activated neutrophils. 

Tests were performed on Sis Lupus s blood to detect elevated levels of antinuclear antibodies (including antibodies to DNA, antibodies to histone, antibodies to ribonucleopro-teins, and antibodies to nuclear antigens). The tests were strongly positive and, in conjunction with her symptoms, led to a diagnosis of systemic lupus erythematosus (SLE). 

DNA vaccines are derived from bacterial DNA plasmid and, thus, are able to stimulate anti-DNA antibodies. If these antibodies are cross-reactive with host chromosomal DNA, they could act like autoantibodies and induce autoimmune diseases (such as systemic lupus erythematosus) characterized by the accumulation of DNA, antinuclear antibodies, and complement in various organs along with local inflammatory responses. Specific lupus-prone mouse strains exist that develop a similar disease. Repeated application of DNA vaccines to these mice did not alter the onset or the course of the disease. In normal mice, anti-DNA antibodies were induced by DNA vaccines, but these remained far below those levels... 

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