CARBAMAZEPINE INDUCED SLE-A RARE AND SERIOUS ADR

<p style="line-height: 150%; margin-bottom: 0cm;" align="justify">Carbamazepine is a commonly used antiseizure medication. Carbamazepine-induced SLE (Systemic Lupus Erythematosus) is a very rare phenomenon. Drug-induced SLE is an autoimmune disease caused by long-term use of certain drugs. Carbamazepine is a drug with low risk for causing lupus symptoms. The process that leads to drug-induced SLE are not entirely understood. A very few cases are reported with carbamazepine association with SLE. Herein we report a case of 4 y old girl with SLE induced by carbamazepine showing a causality score of 8 by Naranjo ADR probability scale.</p>

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Drug-Induced Gingival Overgrowth in an 8-Year-Old Girl: A Case Report

Avicenna Journal of Dental Research ◽

10.34172/ajdr.2021.21 ◽

2021 ◽

Vol 13 (3) ◽

pp. 109-112

Author(s):

Parviz Torkzaban ◽

Amir Talaie

Keyword(s):

Systemic Lupus Erythematosus ◽

Case Report ◽

Autoimmune Disease ◽

Lupus Erythematosus ◽

Immunological Tolerance ◽

Systemic Autoimmune Disease ◽

Channel Blockers ◽

Systemic Lupus ◽

Drug Induced ◽

Gingival Overgrowth

Systemic lupus erythematosus is a systemic autoimmune disease that involves multi organs. Genetic, endocrine, immunological, and environmental factors influence the loss of immunological tolerance against self-antigens leading to the formation of pathogenic autoantibodies that cause tissue damage through multiple mechanisms. The gingival overgrowth can be caused by three factors: noninflammatory, hyperplastic reaction to the medication; chronic inflammatory hyperplasia; or a combined enlargement due to chronic inflammation and drug-induced hyperplasia. Drug-Induced Gingival Overgrowth is associated with the use of three major classes of drugs, namely anticonvulsants, calcium channel blockers, and immunosuppressants. Due to recent indications for these drugs, their use continues to grow.

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Systemic Lupus Erythematosus Presenting with Kikuchi-Fujimoto’s Disease as a Long-Term Sequela of Drug-Induced Hypersensitivity Syndrome

Dermatology ◽

10.1159/000187619 ◽

2008 ◽

Vol 218 (3) ◽

pp. 275-277 ◽

Cited By ~ 28

Author(s):

N. Aota ◽

K. Hirahara ◽

Y. Kano ◽

T. Fukuoka ◽

A. Yamada ◽

...

Keyword(s):

Systemic Lupus Erythematosus ◽

Lupus Erythematosus ◽

Hypersensitivity Syndrome ◽

Systemic Lupus ◽

Drug Induced

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Negative Double Stranded DNA and Anti-Smith Antibodies in Lupus Nephritis

Nephrology Research & Reviews ◽

10.4081/nr.2012.e13 ◽

2012 ◽

Vol 4 (2) ◽

pp. 55-57

Author(s):

Gagangeet Sandhu ◽

Anip Bansal ◽

Aditi Ranade ◽

Ritu Aggarwal ◽

Gopal Narayanswami ◽

...

Keyword(s):

Systemic Lupus Erythematosus ◽

Autoimmune Disease ◽

Lupus Nephritis ◽

Lupus Erythematosus ◽

Systemic Lupus ◽

Drug Induced ◽

Serological Screening ◽

Double Stranded Dna ◽

Dsdna Antibodies

Systemic lupus erythematosus (SLE) is an autoimmune disease in which auto-antibodies are generated against a variety of intracellular antigens. Anti-Smith (Sm) and anti-double stranded DNA (dsDNA) antibodies in particular are considered to be nephritogenic and their role and correlation with lupus nephritis (LN) has been well established. We present here a case in which the patient had diffuse proliferative full house severe LN, yet negative ds-DNA and anti-Sm antibodies. Although extremely rare, a few subsets of patients with drug-induced LN (hydralazine) have been described in the literature to have negative dsDNA and anti-Sm antibodies on serological screening. Our patient, however, had no evidence of drug induced LN. On further review, and similar to our case, we found only 6 additional well documented cases of non-drug induced severe LN with negative dsDNA antibodies.

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Blood pressure and albuminuria in a female mouse model of systemic lupus erythematosus: impact of long-term high salt consumption

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00070.2020 ◽

2020 ◽

Vol 319 (4) ◽

pp. R448-R454

Author(s):

Elena L. Dent ◽

Hanna J. Broome ◽

Jennifer M. Sasser ◽

Michael J. Ryan

Keyword(s):

Systemic Lupus Erythematosus ◽

Autoimmune Disease ◽

Renal Disease ◽

Lupus Erythematosus ◽

High Salt ◽

Systemic Lupus ◽

High Salt Diet ◽

Salt Diet ◽

Endothelin A

Hypertension and kidney involvement are common in patients with autoimmune disease. Sodium intake is linked to hypertension in both human and animal studies. Evidence suggests that dietary salt may be an important environmental factor that promotes autoimmune activity. Therefore, we hypothesized that a long-term high-salt diet would accelerate the progression of autoimmunity, hypertension, and albuminuria during systemic lupus erythematosus (SLE), an autoimmune disease that predominantly affects young women and has a high prevalence of hypertension and renal disease. To test this hypothesis, an established experimental model of SLE (female NZBWF1 mice) that develops hypertension and renal disease was used. SLE mice were fed a high-salt (4% NaCl) or normal (0.4% NaCl) diet for 24 wk beginning at 10 wk of age and ending at 34 wk of age, a time by which female NZBWF1 mice typically have hypertension and exhibit signs of renal disease. Plasma anti-dsDNA autoantibodies were measured as an indicator of active SLE disease, and urinary albumin was monitored longitudinally as a marker of renal disease. Arterial pressure was measured in conscious, freely moving mice at 34 wk of age. Urinary endothelin-1 (ET-1) excretion, renal endothelin A and B receptor protein expression, and renal mRNA expression of NOS1, NOS2, NOX2, MCP-1, TNF-α, serum- and glucocorticoid-regulated kinase 1, and interleukin-2 (IL-2) were assessed to determine the impact on gene products commonly altered by a high-salt diet. SLE mice fed a high-salt diet had increased circulating autoantibodies, but the high-salt diet did not significantly affect albuminuria or arterial pressure. Urinary ET-1 excretion was increased, whereas renal endothelin A receptor and IL-2 expression were decreased in response to a high-salt diet. These data suggest that a chronic high-salt diet may not accelerate cardiovascular and renal consequences commonly associated with SLE.

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Long-Term Treatment of the Patient with Systemic Lupus Erythematosus

Nishi Nihon Hifuka ◽

10.2336/nishinihonhifu.37.924 ◽

1975 ◽

Vol 37 (6) ◽

pp. 924-929 ◽

Cited By ~ 1

Author(s):

Hideaki YAMAURA ◽

Masaharu RIKIMARU ◽

Isamu TAKAHASHI ◽

Sadao ANAN ◽

Tomio AKIYAMA ◽

...

Keyword(s):

Systemic Lupus Erythematosus ◽

Lupus Erythematosus ◽

Term Treatment ◽

Systemic Lupus ◽

Long Term Treatment

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Acute interstitial nephritis and drug-induced systemic lupus erythematosus due to chlorthalidone and amiodarone: A case report

SAGE Open Medical Case Reports ◽

10.1177/2050313x20910029 ◽

2020 ◽

Vol 8 ◽

pp. 2050313X2091002 ◽

Cited By ~ 1

Author(s):

Umut Selamet ◽

Ramy M Hanna ◽

Anthony Sisk ◽

Lama Abdelnour ◽

Lena Ghobry ◽

...

Keyword(s):

Systemic Lupus Erythematosus ◽

Interstitial Nephritis ◽

Lupus Erythematosus ◽

Kidney Biopsy ◽

Kidney Injury ◽

Acute Interstitial Nephritis ◽

Systemic Lupus ◽

Drug Induced ◽

Systemic Manifestations

Drug-induced lupus erythematosus has features distinct from primary systemic lupus erythematosus. It can occur with a wide variety of agents that result in the generation of anti-histone or other types of antibodies. Systemic manifestations of drug-induced systemic lupus erythematosus may include renal dysfunction due to circulating immune complexes or due to other immune reactions to the culprit medication(s). Acute interstitial nephritis occurs due to DNA–drug or protein–drug complexes that trigger an allergic immune response. We report a patient who developed acute kidney injury, rash, and drug-induced systemic lupus diagnosed by serologies after starting chlorthalidone and amiodarone. A renal biopsy showed acute interstitial nephritis and not lupus-induced glomerulonephritis. It is important to note that systemic lupus erythematosus and acute interstitial nephritis can occur together, and this report highlights the role of the kidney biopsy in ascertaining the pathological diagnosis and outlining therapy in drug-induced lupus erythematosus.

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