Linear immunoglobulin-A bullous dermatosis complicating multi-organ tuberculosis at early-stage treatment

Morice, C.; Monsel, Gentiane; Lafaurie, M.; Battistella, Maxime; Manciet, J.-R.; Bagot, M.; Petit, Antoine; Viguier, Manuelle

doi:10.1111/bjd.12286

Cited by 4 publications

(8 citation statements)

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“…Indeed, we now know that we must not rely on previous reports or retrospective studies, as data can be missed and nonhomogeneous, nor must we rely solely on a temporal relationship between a drug and an alleged reaction, as this could be misleading …”

Section: Cases Of Linear Immunoglobulin a Disease (Lad) Induced By Vamentioning

confidence: 99%

Linear immunoglobulin A disease and vancomycin: two real ancestral enemies?

et al. 2014

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While typically seen in patients with end-stage renal failure and renal transplantation, calciphylaxis has been reported in patients without end-stage renal disease (i.e. nonuraemic calciphylaxis). 3 In a systematic review of 36 cases of nonuraemic calciphylaxis, primary hyperparathyroidism (28%), malignancy (22%), alcoholic liver disease (17%) and connective tissue disease (11%) were the most common underlying aetiologies. 6 To date, the association between calciphylaxis and pancreatic cancer has not been reported. One possible link between nonuraemic calciphylaxis and pancreatic cancer is the elevation and release of pancreatic enzymes, which results in lipolysis of subcutaneous adipose tissue, formation of free fatty acids and the subsequent saponification of fat by calcium salts. 7 A number of treatment strategies have been proposed in calciphylaxis. However, to date, no controlled prospective studies comparing these various treatments have been conducted. Traditional therapies include wound care in combination with intravenous sodium thiosulfate (STS), cinacalcet, sevelamer, bisphosphonates and/or hyperbaric oxygen therapy. Intravenous STS has gained favour as a generally well tolerated, effective therapeutic option that works by dissolving vascular calcium deposits through the creation of highly soluble calcium thiosulfate complexes. 8-10 Intravenous STS is generally well tolerated and has been shown to decrease mortality when used in combination with cinacalcet and sevelamer. [8][9][10] Sevelamer and cinacalcet also help to mitigate the endocrine abnormalities seen in calciphylaxis by acting as noncalcium phosphate binders and calcimimetics, respectively. 10 Our patient was started on oral cinacalcet 30 mg twice daily and intravenous STS 25 mg three times weekly. After 2 weeks of treatment with intravenous STS followed by 4 weeks of topical STS 10% soaks and aggressive wound care, the patient experienced considerable improvement in his lower extremity pain and leg ulcers. The patient was subsequently started on gemcitabine and paclitaxel for his pancreatic cancer, but he passed away several months later owing to complications of pneumonia. In summary, we present a case of nonuraemic calciphylaxis in a white man with pancreatic cancer. To our knowledge, this is the first reported patient with pancreatic cancer-associated calciphylaxis in the setting of normal kidney and parathyroid function, who also responded favourably to intravenous and topical STS, as well as oral cinacalcet. References1 Ng AT, Peng DH. Calciphylaxis. Dermatol Ther 2011; 24:256-62.2 Ross EA. Evolution of treatment strategies for calciphylaxis. Am J Nephrol 2011; 34:460-7. 3 Mochel MC, Arakaki RY, Wang G et al. Cutaneous calciphylaxis: a retrospective histopathologic evaluation. Am J Dermatopathol 2013; 35:582-6. 4 Weenig RH, Sewell LD, Davis MDP et al. Calciphylaxis: natural history, risk factor analysis and outcome. J Am Acad Dermatol 2007; 56:569-79. 5 Harris RJ, Cropley TG. Possible role of hypercoagulability in calciphylaxis: review...

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Section: Cases Of Linear Immunoglobulin a Disease (Lad) Induced By Vamentioning

confidence: 99%

Linear immunoglobulin A disease and vancomycin: two real ancestral enemies?

et al. 2014

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“…This raises the question of the role of the underlying infectious disease itself vs . the role of only the drug itself .…”

Section: Discussionmentioning

confidence: 99%

“…Also, rifampicin and third‐generation cephalosporins are co‐administered with VCM, with the same I4 score but a lower extrinsic score, B2. Imputability and rechallenge with these drugs should be discussed case by case because they can be essential for the treatment of some diseases . However, drug reactions can be severe, sometimes life‐threatening and one should pay attention to not make the shortcut of prohibiting VCM only because of its notoriety.…”

Section: Discussionmentioning

confidence: 99%

Drug‐induced linear immunoglobulin A bullous dermatosis: A French retrospective pharmacovigilance study of 69 cases

Garel

Ingen‐Housz‐Oro

Afriat

et al. 2019

Brit J Clinical Pharma

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AIMSLinear immunoglobin A (IgA) bullous dermatosis is a rare autoimmune dermatosis considered spontaneous or drug-induced (DILAD). We assessed all DILAD cases, determined the imputability score of drugs and highlighted suspected drugs. METHODSData for patients with DILAD were collected retrospectively from the French Pharmacovigilance network (from 1985 to 2017) and from physicians involved in the Bullous Diseases French Study Group and the French Investigators for Skin Adverse Reactions to Drugs. Drug causality was systematically determined by the French imputability method. RESULTSOf the 69 patients, 42% had mucous membrane involvement, 20% lesions mimicking toxic epidermal necrolysis (TEN), 21% eosinophil infiltrates and 10% keratinocytes necrosis. Direct immunofluorescence, in 80%, showed isolated linear IgA deposits. Vancomycin (VCM) was suspected in 39 cases (57%), 11 had TEN-like lesions, as compared with three without VCM suspected. Among the 33 patients with a single suspected drug, 85% had an intrinsic imputability score of I4. Among them, enoxaparin, minocycline and vibramycin were previously unpublished. For all patients, the suspect drug was withdrawn; 15 did not receive any treatment. First-line therapy for 31 patients was topical steroids. Among the 60 patients with British Journal of Clinical Pharmacology Br J Clin Pharmacol (2019) 85 570-579 570 available follow-up, 52 achieved remission, 10 without treatment. Four patients experienced relapse, four died and five had positive accidental rechallenges. CONCLUSIONSThere is no major clinical difference between DILAD and idiopathic linear IgA bullous dermatosis, but the former features a higher prevalence of patients mimicking TEN. VCM, suspected in more than half of the cases, might be responsible for more severe clinical presentations. We report three new putative drugs. WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT• Linear IgA bullous dermatosis (LABD) is a rare autoimmune dermatosis that may be spontaneous or drug induced.• Vancomycin (VCM) is the most frequent putative drug.• Drug-induced LABD (DILAD) may be more severe than idiopathic LABD, mimicking toxic epidermal necrolysis with Nikolsky sign and large erosions WHAT THIS STUDY ADDS• In this large series of DILAD, we systematically assessed the imputability of suspect drugs. Most of them are antibiotics with VCM as the most frequent. Eighty percent of suspect drugs had a high causality score. Three drugs had never been reported to induce DILAD before (enoxaparin, minocyclin, vibramycin). • Twenty percent of cases (especially those induced by VCM) mimicked toxic epidermal necrolysis. Data collectionFor each case, data collected from pharmacovigilance or medical files included epidemiological and clinical characteristics Drug-induced linear immunoglobulin A bullous dermatosis Br J Clin Pharmacol (2019) 85 570-579 571 Drug-induced linear immunoglobulin A bullous dermatosis Br J Clin Pharmacol (2019) 85 570-579 579

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“…One patient with untreated HIV developed LABD days after initiating treatment for multisystemic tuberculosis. The authors suspected tuberculosis as the trigger for LABD given that years earlier, the patient had been exposed to the same anti-tuberculosis medication without skin complication ( Morice et al, 2013 ). Another case report described a case of LABD in a patient who was recently diagnosed with HIV.…”

Section: Autoimmune Blistering Disorders In Hiv/aidsmentioning

confidence: 99%

“…However, the risk of AIBD cannot alone be explained by CD4 counts or immune restoration. In fact, we identified four cases in which an AIBD was diagnosed in patients with CD4 < 200 ( De et al, 2008 , Mignona et al, 2005 , Morice et al, 2013 , Splaver et al, 2000 ). Although CD4 counts normalize in HIV-positive patients on therapy, the broader milieu of immune restoration is believed to remain altered ( Zandman-Goddard and Shoenfeld, 2002 ).…”

Section: Mechanisms For Development Of Autoimmune Disorders In Hiv-inmentioning

confidence: 99%

Autoimmune blistering disorders in the setting of human immunodeficiency virus infection

Min

Damstetter²,

Chen

2018

International Journal of Women's Dermatology

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The interplay between immune dysfunction and human immunodeficiency virus (HIV) is complex. Reports of autoimmune disorders including autoimmune bullous disorders (AIBDs) have been increasing in prevalence in the HIV population since the introduction of highly active antiretroviral therapy in 1995. We offer a literature review of clinical experiences in various AIBDs with particular emphasis on therapeutic management as well as a brief overview of the mechanisms that explain the relationship between AIBD and HIV. Because immunosuppressants are first-line therapies for AIBD treatment, careful consideration is warranted when considering management in the HIV population.

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Linear immunoglobulin-A bullous dermatosis complicating multi-organ tuberculosis at early-stage treatment

Cited by 4 publications

References 8 publications

Linear immunoglobulin A disease and vancomycin: two real ancestral enemies?

Linear immunoglobulin A disease and vancomycin: two real ancestral enemies?

Drug‐induced linear immunoglobulin A bullous dermatosis: A French retrospective pharmacovigilance study of 69 cases

Autoimmune blistering disorders in the setting of human immunodeficiency virus infection

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