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Diagnostic Reasoning and Clinical Problem Solving
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
In general, drug-induced aseptic meningitis and all causes of AVM are less severe and have a slower course than the rapid/severe progression of ABM. Some bacterial pathogens present less acutely with clinical features of ABM and AVE. The classic neuropathogen that displays features of both meningeal inflammation (nuchal rigidity) and mental confusion is L. monocytogenes ABM.
Drug-Induced Autoimmunity
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Robert L. Rubin, Anke Kretz-Rommel
Drugs which appear to exacerbate SLE include antibiotics, anticonvulsants, hormones, nonsteroidal anti-inflammatory drugs (NSAIDs), and dermatologic agents. Sulfonamides, tetracyclines, griseofulvin, piroxicam, and benoxaprofen are reported to be photosensitizers of varying frequency; the rash or dermatitis related to these drugs typically has a history of rapid onset and behaves as a drug hypersensitivity-type reaction that may be triggered by exposure to ultraviolet light. The majority of adverse drug reactions in previously diagnosed SLE patients are of this category.10,11 Another, possibly related category of patients are those with acute or subacute cutaneous lupus erythematosus related to photoactive medications; these patients may have systemic disease and can fulfill criteria for a diagnosis of SLE.13 Some of these drugs are also associated with typical drug-induced lupus and are included in Table 2. Drug-induced aseptic meningitis in SLE patients is occasionally associated with ibuprofen and other NSAIDs (e.g., sulindac, tolmetin, diclofenac). Hypersensitivity reactions that have been interpreted as initiating or aggravating factors in SLE are associated with hydralazine, sulfonamides, penicillin, para-aminosalacylic acid, hydrochlorothiazide, cimetidine, phenylbutazone, mesantoin and various NSAIDs. Unknown or suspected environmental chemicals such as hair dyes and permanent wave preparations are also occasionally implicated as aggravating agents in SLE and related diseases.
Aseptic meningitis after SARS-CoV-2 Pfizer/BioNTech vaccination
Published in Acta Clinica Belgica, 2022
Valérie Dupon, Stijn Arnaert, Eline Van Haute, Friedel Vulsteke, Günter Diet, Gert De Schoenmakere
The role of methylprednisolone therapy is unclear, although the alleviation of symptoms and decline of CRP after administration of corticoid therapy is remarkable. In those two cases of aseptic meningitis after Pfizer/BioNTech vaccination, CRP declined within 2 days after the first corticoid administration. Although high-dose steroids are not usually recommended for drug-induced aseptic meningitis, the alleviation of symptoms and decline of CRP after administration of corticoid therapy in our patient was remarkable, as was also seen in the first case of aseptic meningitis after the SARS-CoV-2 Pfizer/BioNTech vaccine. Corticosteroids are used as initial treatment for aseptic meningitis in patients with rheumatoid arthritis treated with anti-TNF agents. Based on limited case-based experiences, high-dose steroid is the most common initial treatment [9].
Acute aseptic meningitis during isotretinoin treatment for nodular acne solely presenting with headache: case report and brief review of the literature
Published in International Journal of Neuroscience, 2019
Ioanna Chalimou, Antonios Krilis, Garifallia G. Anastopoulou, Heike Braun, Michael Vikelis, Alexandra Makridou, Nicolaos Makris, Andreas A. Argyriou
Isotretinoin, also known as 13-cis-retinoic acid, is an orally administered medication that has demonstrated significant activity in the treatment of refractory to other treatments severe nodular acne [1]. According to an informal FDA quotation, aseptic meningitis is a quite rare adverse event of isotretinoin therapy as there are 33 reports (without any further details) of this complication in patients being treated with isotretinoin among 26,681 reports (0.1237%) of any side effect linked to this therapy [2]. In our knowledge, however, medical literature contains none detailed description of such relevant case. After obtaining written informed consent for release of personal information, we herein describe in detail the first case of aseptic meningitis during treatment with isotretinoin for nodular acne presenting with headache and discuss whether this event might be interrelated. A brief summary of the literature on drug-induced aseptic meningitis (DIAM) is also presented.
Rheumatoid granulomatous disease and pachymeningitis successfully treated with rituximab
Published in Acta Clinica Belgica, 2018
Anneleen Moeyersoons, Patrick Verschueren, Thomas Tousseyn, Ellen De Langhe
Paradoxical granulomatous reactions and pachymeningitis can be induced by anti-TNF agents. Non-necrotizing sarcoid-like granulomatosis has been described, like the supraclavicular biopsy of our patient. The median delay between anti-TNF agent introduction and granulomatosis diagnosis was 18 months [8]. Drug-induced aseptic meningitis appears to be an immune mediated hypersensitivity reaction [9]. The mechanism underlying these side effects is unknown. Marotte et al. suggest this adverse reaction to infliximab to be caused by inability of the drug to pass the blood‐brain barrier, resulting in a failure to downregulate pro-inflammatory pathways in the brain, while effectively blocking peripheral TNFα, resulting in an enhanced contribution of brain-derived TNFα or other cytokines such as interleukin 1 [10]. Similarly, leflunomide-induced aseptic meningitis has been described [11]. Both drug-induced granulomatous disease and pachymeningitis clinically and radiologically improve after discontinuation of the causative anti-TNFα drug agent with or without prednisone treatment [8]. In this case, drug-induced granulomatous reaction and meningitis cannot strictly be excluded, although we think this would be an unlikely differential diagnosis as the delay of 7 years between anti-TNF agent introduction and granulomatosis diagnosis would be unusual. Furthermore, there was no clinical or radiological improvement after discontinuation of medication. Admittedly the described median delay to recovery of sarcoid-like granulomatosis following TNF blocker discontinuation was 6 months [8].