Case Of Drug-induced Lupus Erythematosus Research Articles

Pearls for the diagnosis and possible pathophysiological mechanisms of valproic acid-induced lupus erythematosus: A literature review.

Background: Drug-induced lupus erythematosus (DILE) accounts for 10-15% of systemic lupus erythematosus (SLE) cases, with more than 100 pharmaceutical agents implicated in its development. Depending on the offending drug, clinical and serological manifestations present great variability and, thus, DILE may be overlooked in clinical practice. Valproic acid (VPA) - induced lupus erythematosus has not been analytically reported in the literature, rendering the recognition of such cases even more difficult.Objective: The aim of this study was to analyze VPA - induced lupus features and to discuss possible pathophysiological mechanisms.Materials and Methods: This literature review was conducted in PubMed and Embase databases in June 2021, in search of DILE cases induced by VPA. We found 164 manuscripts, out of which 140 articles regarding other adverse effects or drugs were discarded. Finally, 15 cases fulfilled the eligibility criteria to be included in this review.Results: Although SLE is more common in females, VPA-induced lupus presented a male predilection. Patients developed DILE within the first three months of treatment with VPA at a percentage of 50%, whereas four patients from one to five years after VPA initiation. DILE frequently presented with mild symptoms. In most patients, serositis manifested with polyarthritis, pleural effusion or pericarditis. Notably, one patient presented with Rowell's syndrome, a rare subtype of lupus erythematosus with erythema multiforme and speckled pattern of antinuclear antibodies (ANAs). Central nervous system, renal and skin involvement was scarcely observed. Cytopenia was noted in 7 patients. Immunological findings included positive ANAs in the vast majority of the patients (86.7%), positive anti-histone antibodies in five, positive anti-dsDNA antibodies in three and hypocomplementemia in two patients. Despite the prompt resolution of clinical symptoms after VPA discontinuation, serological abnormalities persisted up to 18 months. Apart from the discontinuation of VPA administration for the resolution of DILE, treatment included corticosteroids in 8 cases.Conclusion: Valproic acid has been implicated in several cases of DILE. Clinicians should be aware of this entity and recognize it promptly to ensure a favorable outcome. Possible pathophysiologic associations may be extrapolated, but a clearer understanding of this syndrome is to be gained by further studies.

A young woman presenting a kikuchi-fujimoto’s disease associated with induced lupus

Introduction: Kikuchi-Fujimoto’s disease (KFD) or histiocytic necrotizing lymphadenitis is a benign and self-limited disease of unknown etiology mainly affecting young women. Although the association with systemic lupus erythematosus (SLE) is well described, no case of drug-induced lupus erythematosus (DILE) associated KFD has not been reported so far. Case report: We herein report a 25-year old Caucasian woman, with no medical history and no medication except for oral estrogen-progestin contraception (levonorgestrel-ethinylestradiol), who presented with cervical lymphadenopathy, fever and arthralgia without weight loss, night sweats or skin involvement. An exhaustive infectious disease screening was negative and lymph node biopsy revealed histiocytic necrotizing lymphadenitis suggesting KFD. Autoimmune screening tests evidenced high titers of anti-histone antibodies suggesting DILE induced by estrogen-progestin medication. The patient received a short course of non-steroidal anti-inflammatory treatment for painful lymphadenitis and arthralgia. Oral levonorgestrel-ethinylestradiol contraceptive medication was stopped and KFD and DILE completely recovered with a long-term disappearance of anti-histone antibodies. Conclusion: We report the first case of KFD associated-DILE following oral levonorgestrel-ethinylestradiol medication. Even though levonorgestrel-ethinylestradiol induced lupus is well known, the association with KFD has never been reported and the physiopathology remained unknown. Keywords: Kikuchi-Fujimoto disease, Lupus, Levonorgestrel-ethinylestradiol

A young woman presenting a kikuchi-fujimoto’s disease associated with induced lupus

Introduction: Kikuchi-Fujimoto’s disease (KFD) or histiocytic necrotizing lymphadenitis is a benign and self-limited disease of unknown etiology mainly affecting young women. Although the association with systemic lupus erythematosus (SLE) is well described, no case of drug-induced lupus erythematosus (DILE) associated KFD has not been reported so far. Case report: We herein report a 25-year old Caucasian woman, with no medical history and no medication except for oral estrogen-progestin contraception (levonorgestrel-ethinylestradiol), who presented with cervical lymphadenopathy, fever and arthralgia without weight loss, night sweats or skin involvement. An exhaustive infectious disease screening was negative and lymph node biopsy revealed histiocytic necrotizing lymphadenitis suggesting KFD. Autoimmune screening tests evidenced high titers of anti-histone antibodies suggesting DILE induced by estrogen-progestin medication. The patient received a short course of non-steroidal anti-inflammatory treatment for painful lymphadenitis and arthralgia. Oral levonorgestrel-ethinylestradiol contraceptive medication was stopped and KFD and DILE completely recovered with a long-term disappearance of anti-histone antibodies. Conclusion: We report the first case of KFD associated-DILE following oral levonorgestrel-ethinylestradiol medication. Even though levonorgestrel-ethinylestradiol induced lupus is well known, the association with KFD has never been reported and the physiopathology remained unknown. Keywords: Kikuchi-Fujimoto disease, Lupus, Levonorgestrel-ethinylestradiol

Development of lupus erythematosus during infliximab treatment

Infliximab is a TNFα inhibiting recombinant monoclonal antibody, which provides an efficient therapeutic opportunity in the treatment of psoriasis and other immune-mediated inflammatory diseases. It is well tolerated and improves quality of life significantly. The authors present a case of drug-induced lupus erythematosus as a possible side effect of this medication. The patient developed psoriasis 9 years ago when she was on beta-receptor blocker therapy. The symptoms deteriorated despite topical and systemic treatments and, therefore, biological therapy was introduced. In the third year of treatment drug-induced lupus erythematosus was diagnosed on the background of general symptoms. After cessation of the biologic treatment a low dose corticosteroid therapy was introduced which proved to be effective. Symptoms as well as pathological laboratory parameters showed an improvement. The authors conclude that biologicals are effective and safe in the treatment of psoriasis, nevertheless, they have risks too. To reduce side effects a meticulous follow-up of patients is essential. Any general symptom requires careful examination since they might be linked to serious side effects of the biological therapy. Orv. Hetil., 2013, 154, 590–598.

Drug-induced lupus erythematosus

Drug-induced lupus is a syndrome which share symptoms and laboratory characteristics with the idiopathic systemic lupus erythematosus (SLE). The list of medications implicated as etiologic agents in drug-induced lupus continues to grow. The terms used for this condition are lupus-like syndrome, drug-induced lupus erythematosus (DILE) and drug related lupus. More than 80 drugs have been associated with DILE. The first case of DILE was reported in 1945 and associated with sulfadiazin. In 1953 it was reported that DILE was related to the use of hydralazine. Drugs responsible for the development of DILE can divided into three groups, but the list of these drugs is quite long because new drugs are included yearly in the list. The syndrome is characterised by arthralgia, myalgia, pleurisy, rash and fever in association with antinuclear antibodies in the serum. Recognition of DILE is important because it usually reverts within a few weeks after stopping the drug.

Two cases of late-onset drug-induced lupus erythematosus caused by ticlopidine in elderly men

We have experienced two cases of drug-induced lupus erythematosus caused by ticlopidine in the last three years. Both were late-onset cases (1 and 4 years) that occurred in elderly men (76 and 81 years old). The common features were fever, arthralgia, myalgia, serositis, and the presence of anti-histone autoantibodies. Because ticlopidine is widely used in elderly people with ischemic vascular disease, ticlopidine-induced lupus should be considered when patients taking ticlopidine present lupus-like symptoms.

Drug-induced lupus erythematosus

Drug-induced lupus erythematosus (DILE) is defined as a lupus-like syndrome temporally related to continuous drug exposure which resolves after discontinuation of the offending drug. There are currently no standard diagnostic criteria for DILE and the pathomechanisms are still unclear. Similarly to idiopathic lupus, DILE can be diveded into systemic (SLE), subacute cutaneous (SCLE) and chronic cutaneous lupus (CCLE). Systemic DILE is characterized by typical lupus-like symptoms including skin signs, usually mild systemic involvement and a typical laboratory profile with positive antinuclear and anti-histone antibodies, while anti-double strand (ds) DNA and anti-extractable nuclear antigens antibodies are rare. High risk drugs include hydralazine, procainamide and isoniazid. Drug-induced SCLE is very similar to idiopathic SCLE in terms of clinical and serologic characteristic, and it is more common than the systemic form of DILE. Drugs associated with SCLE include calcium channel blockers, angiotensin-converting enzyme inhibitors, interferons, thiazide diuretics and terbinafine. Drug-induced CCLE is very rarely reported in the literature and usually refers to fluorouracile agents or non steroidal anti-inflammatory drugs. Recently, cases of DILE have been reported with anti-TNFalpha agents. These cases present with disparate clinical features including arthritis/arthralgia, skin rash, serositis, cytopenia and variable laboratory abnormalities. DILE to anti-TNFalpha agents differs in several ways to classic DILE. The incidence of rashes is higher compared to classical systemic DILE. In most cases of classic DILE visceral involvement is rare, whereas several cases of anti-TNFalpha DILE with evidence of renal disease have been reported. Low serum complement levels as well as anti-extractable nuclear antigen antibodies and anti-dsDNA antibodies are rarely present in classic DILE, whereas they are reported in half the cases of anti-TNFalpha DILE; in contrast, anti-histone antibodies are described in classic DILE more often than in anti-TNFalpha DILE. Recognition of DILE in patients receiving anti-TNFalpha therapy can be difficult due to the symptoms of their underlying disease. A temporal association (months to years) of the offending drug with characteristic or suggestive symptoms, and resolution of symptoms on drug withdrawal is the best evidence for this diagnosis of DILE.

Drug-Induced Lupus due to Anti-Tumor Necrosis Factor α Agents

To evaluate the reported cases of drug-induced lupus erythematosus (DILE) due to anti-tumor necrosis factor (TNF) alpha therapy and to compare "classic" DILE with DILE secondary to anti-TNFalpha therapy. We also add 3 case reports related to 3 different anti-TNFalpha drugs to the literature. We searched the Medline database for cases published in English and evaluated 53 cases in 27 papers purported to be TNFalpha-induced DILE. We compared the clinical and laboratory features of cases that fulfilled our criteria for TNFalpha DILE to those of DILE due to non-TNFalpha drugs as found in standard texts. We also report the clinical and laboratory findings of our 3 patients with drug-induced lupus related to anti-TNFalpha drugs, 1 each in patients treated with adalimumab, etanercept, and infliximab. Of the 53 purported cases of DILE due to anti-TNFalpha therapy, we excluded 17 with cutaneous manifestations alone and 3 with overlap syndromes and mixed connective tissue disease. In the 33 cases that met our criteria for systemic DILE, 21 cases were due to infliximab, 10 cases were due to etanercept, and only 2 cases were related to adalimumab. TNFalpha-blocker-induced DILE cases had a higher prevalence of antibodies to double-stranded DNA, rash, and hypocomplementemia than DILE due to other drugs. Fever is common in both types of DILE. Renal disease, which is rare in classic DILE, has been reported in cases of TNFalpha DILE. TNFalpha DILE has significant clinical and laboratory manifestations which distinguish it from DILE due to drugs other than anti-TNF agents and may be difficult to diagnose in patients treated for autoimmune diseases. It is appropriate to consider whether all patients who are begun on anti-TNF therapy should have pretreatment serologic evaluation for systemic lupus erythematosus.

Drug-Induced Lupus

To the Editor.— In their article, "Drug-Induced Systemic Lupus Erythematosus (222:191, 1972), Greenberg and Lutcher state, "to our knowledge, it represents the first such case described in the literature, and emphasizes the potential severity of the drug-induced lupus syndrome," and, "in reviewing the literature, we are unable to find a similar case of drug-induced lupus erythematosus in which cardiac tamponade was present." A prior case of cardiac tamponade requiring emergency pericardicentesis was described in the article entitled, "Systemic Lupus Erythematosus in Childhood" published in Pediatrics (32:257, 1963). Case 3 in that series (p 260), presumably induced by methyl phenylethylhydantoin, had an emergency pericardicentesis that was life saving, as was detailed in that report. I observed that boy for many years after the offending drug therapy was withdrawn and he remained free of signs and symptoms of systemic lupus erythematosus. The two fatalities detailed in 1963, and the near fatalities described