Idiopathic Lupus Erythematosus Research Articles

A Rare Case of Antithyroid Drug-Induced Lupus Erythematosus, Graves' Disease, and Primary Infertility

Background: Drug-induced lupus erythematosus (DILE) is a rare autoimmune disorder that mimics idiopathic lupus erythematosus, triggered by certain medications. This case report presents a patient with DILE induced by methimazole, a commonly used antithyroid drug, along with Graves' disease and primary infertility. Case presentation: A 41-year-old woman presented with palpitations, a history of Graves' disease treated with methimazole, and primary infertility. She developed lupus-like symptoms including fever, joint pain, and skin rash. Examination revealed tachycardia, tenderness of the right and left knee joints and limited range of motion. Laboratory investigations confirmed hyperthyroidism and autoimmune features consistent with DILE. Conclusion: This case highlights the rare occurrence of DILE induced by methimazole, emphasizing the importance of recognizing and managing this condition in patients receiving antithyroid drugs.

ЛЕКАРСТВЕННО-ИНДУЦИРОВАННАЯ КРАСНАЯ ВОЛЧАНКА

Medicinal or drug-induced lupus erythematosus (DIL) is an autoimmune phenomenon, which is clinically and morphologically similar to idiopathic lupus erythematosus, that occurs in patients during the long-term use of drugs, the list of which currently includes more than 100 items. To date, the pathogenesis of DIL has not been fully deciphered, and diagnostic criteria have not been developed, which determines the difficulties of diagnosis and determination of therapeutic approaches. At the same time, the widespread introduction of new classes of drugs, in particular, TNF inhibitors and other genetically engineered biological drugs associated with the risk of developing a systemic form of DIL, the use of proton pump inhibitors and chemotherapy drugs that induce subacute lupus erythematosus, allow predicting an increase in the prevalence of DIL, including in children, which in its turn determines the relevance of the problem of DIL in pediatric practice. This bibliographical review summarizes the current data on drugs that are potential inducers of DIL, possible mechanisms of development and clinical forms of the disease, principles of diagnosis and therapy.

POS-014 DOXAZOCINE-INDUCED LUPUS NEPHROPATHY

Drug-induced lupus (DIL) refers to an idiosyncratic side effect of numerous, apparently unrelated medications, in which symptoms overlap with those of systemic lupus erythematosus. Over 100 drugs have been linked to DIL to date and the list is growing. Like idiopathic lupus erythematosus, DIL has systemic, subacute cutaneous, and chronic cutaneous forms. We report the first case of lupus nephrothy related to Doxazocine treatment.

Drug-Induced Lupus Erythematosus

Drug-induced lupus erythematosus (DILE) refers to a condition whose clinical, histological, and immunological features are similar to those seen in idiopathic lupus erythematosus but that occurs when certain drugs are taken and resolves after their withdrawal. Over 90 drugs have been linked to DILE to date and the list is growing. Like idiopathic lupus erythematosus, DILE has systemic, subacute cutaneous, and chronic cutaneous forms. A correct diagnosis is very important, as this condition usually resolves after withdrawal of the offending drug.

Lupus eritematoso inducido por fármacos

Drug-induced lupus erythematosus (DILE) refers to a condition whose clinical, histological, and immunological features are similar to those seen in idiopathic lupus erythematosus but that occurs when certain drugs are taken and resolves after their withdrawal. Over 90 drugs have been linked to DILE to date and the list is growing. Like idiopathic lupus erythematosus, DILE has systemic, subacute cutaneous, and chronic cutaneous forms. A correct diagnosis is very important, as this condition usually resolves after withdrawal of the offending drug.

Drug‐induced lupus erythematosus with emphasis on skin manifestations and the role of anti‐TNFα agents

Drug-induced lupus erythematosus (DILE) is a lupus-like syndrome temporally related to continuous drug exposure which resolves upon drug discontinuation. There are currently no standard diagnostic criteria for DILE. Findings include skin manifestations, arthritis, serositis, anti-nuclear and anti-histone antibodies positivity. Similarly to idiopathic lupus erythematosus, DILE can be divided into systemic (SLE), subacute cutaneous (SCLE) and chronic cutaneous lupus (CCLE). Systemic DILE presents as a milder version of idiopathic SLE, and the drugs most frequently implicated are hydralazine, procainamide and quinidine. Anti-TNFα therapies are the latest class of medications found to be associated, although rarely, with a “lupus-like” syndrome, which is however clinically distinct from classical DILE. Drug-induced SCLE is the most common form of DILE. It is very similar to idiopathic SCLE in terms of clinical and serologic characteristics. The most commonly implicated drugs are antihypertensive drugs and terbinafine, but in recent years also proton pump inhibitors and chemotherapeutic agents have been associated. Drug-induced CCLE is very rare and usually caused by fluorouracil agents and NSAIDS, but some cases have induced by pantoprazole and anti-TNFα agents.

Antibodies from patients with drug-induced and idiopathic lupus erythematosus react with epitopes restricted to the amino and carboxyl termini of histone.

The sera of patients with systemic lupus erythematosus (SLE) and drug-induced lupus (DIL) were used to study the antigenic epitopes on nuclear histones that bind antibodies in these sera. ELISA and immunoblotting techniques showed that antibodies from both patient groups bound all classes of intact histone: H1 greater than H2B greater than H2A greater than H3 greater than H4. The different classes of histone were enzymatically or chemically cleaved to produce a series of peptide fragments which were then used to map the reactive epitopes by ELISA and immunoblotting. Ten of 11 DIL sera and 11 of 12 SLE sera bound the carboxy and amino terminal peptides. Only one sera of each group bound to the central hydrophobic polypeptide. The reactivity of DIL sera with fractionated histone polypeptides was similar to that observed with SLE sera. This observation suggests that the histone epitopes reacting with DIL sera are no less restricted than those reacting with SLE.

Antibodies to Histones in Drug-Induced and Idiopathic Lupus Erythematosus

When tissue sections are extracted with 0.1 N HCl, cellular nuclear proteins, including histones, are removed but nuclear DNA is retained. Histones can be reconstituted back to nuclear DNA in acid-extracted tissue sections so that the resulting nuclear substrate is composed only of DNA and histones and does not contain acidic nuclear protein antigens. The resulting DNA-histone tissue substrate can be used in the immunofluorescent method for specific detention of antibodies to histones. Sera from 23 patients with drug-induced lupus erythematosus (procainamide 19, isoniazid 2, nitrofurantoin 2) and 20 patients with idiopathic (not drug-induced) systemic lupus erythematosus (SLE) were studied. All 23 patients with drug-induced lupus erythematosus (LE) lost nuclear staining on acid-extracted sections. In contrast, only 12 of 20 with idiopathic SLE lost nuclear staining on acid-extracted tissues, and in the remaining 8, there was no significant fall in titer. In the drug-induced LE group, loss of nuclear staining was due to the absence of histones on the substrate because with histone-reconstituted sections, 22 of 23 again became positive for nuclear staining at titers equal to or at one doubling dilution below titers on unextracted tissues. In contrast, of the 12 idiopathic SLE sera which lost nuclear staining, only 5 regained nuclear staining on histone-reconstituted tissue sections. In idiopathic SLE, antinuclear antibodies are heterogeneous in specificities and may consist of antibodies to native DNA, histones, or nonhistone proteins. In contrast, antinuclear antibodies in drug-induced LE are less heterogeneous and mainly consist of antibodies to histones.

Hypocomplementemia in hydralazine-associated systemic lupus erythematosus

Drug-associated lupus erythematosus is said to be differentiated from idiopathic lupus erythematosus by the invariable presence of normal serum complement levels in the former. A unique patient with hydralazine-associated lupus is described in whom activation of the complement system is documented. Other unusual features of hydralazine-associated lupus are discussed.

Pericardial tamponade: A presenting manifestation of procainamide-lnduced lupus erythematosus

Procainamide, a frequently used antiarrhythmic agent, may produce a syndrome clinically indistinguishable from idiopathic lupus erythematosus. Pericarditis with or without effusion is occasionally a prominent manifestation of the disease, but cardiac tamponade is exceptional. The patient described had a clinically evident and laboratory confirmed drug-induced syndrome complicated by an unusually severe pericarditis with effusion and tamponade necessitating pericardiocentesis. Treatment with prednisone produced impressive amelioration of the pericarditis with no recurrence of the lupus erythematosus syndrome during a prolonged period of observation following cessation of corticosteroid therapy. Prompt initiation of steroid treatment in drug-induced lupus erythematosus complicated by massive pericardial effusion is strongly suggested by this experience.

Antinuclear antibody induced by procainamide. A prospective study.

Abstract Sixteen patients were followed prospectively for the possible development of the lupus syndrome while being treated for cardiac arrhythmias with conventional doses of procainamide hydrochloride. In eight antinuclear antibody developed. Two of the eight had positive slide reactions with nucleoprotein-coated latex particles. In one of these two rheumatoid factor (anti-IgG) activity in low titer also developed. Another two of the eight showed symptoms consistent with the lupus syndrome. The high percentage of patients in this study in whom antinuclear antibody developed suggests that the lupus response appearing in patients treated with procainamide is not restricted to the small proportion of the population that may have a genetic predisposition to idiopathic lupus erythematosus.