LETTRE
À LA
Thérapie 2013 Novembre-Décembre; 68 (6): 423–426 DOI: 10.2515/therapie/2013065
RÉDACTION
© 2013 Société Française de Pharmacologie et de Thérapeutique
Sulfasalazine-induced Aseptic Meningitis with Positive Rechallenge: a Case Report and Review of the Literature Méningite aseptique induite par la sulfasalazine avec réintroduction positive : à propos d’un cas et revue de la littérature Issam Salouage, Sihem El Aïdli, Feinène Cherif, Sarra Kastalli, Ahmed Zaiem and Riadh Daghfous National Centre of Pharmacovigilance, Tunis, Tunisia Text received March 15th, 2013; accepted September 19th, 2013 This case has been notified to the National Centre of Pharmacovigilance of Tunis (Tunisia) on September 18th, 2011 Keywords: sulfasalazine; drug adverse reaction; aseptic meningitis; ankylosing spondylarthritis; phenotype Mots clés : sulfasalazine ; effet indésirable ; méningite aseptique ; spondylarthrite ankylosante ; phénotype Abbreviations: see end of article.
1. Introduction Aseptic meningitis is characterized by serious inflammation of brain membranes (meninges). The main non infectious causes of meningitis include primary tumors of central nervous system, metastatic carcinomas, granulomatous angiitis, sarcoidosis, systemic lupus erythematosus, rheumatoid arthritis, Behçet’s syndrome or drugs.[1] Drug-induced aseptic meningitis (DIAM) is principally associated with non-steroid anti inflammatory drugs, antibiotics, intravenous immunoglobulins, monoclonal antibodies against CD3, intrathecal agents and vaccines. It was rarely reported with leflunomide, methotrexate, infliximab, or sulfasalazine.[2] We report a case of aseptic meningitis induced by sulfasalazine (Salazopirine®) with positive rechallenge in a slow acetylator phenotype patient suffering from ankilosing spondylarthritis. This case was notified to the National centre of pharmacovigilance of Tunis (Tunisia) on september 18th, 2011.
2. Case report A 34-old-woman, with no medical history or neurological troubles, was treated by paracetamol and non-steroid anti inflammatory drugs for ankilosing spondylarthritis with no improvement. So, sulfasalazine was introduced at the starting dose of 2 g daily. Paracetamol and non-steroid anti inflammatory drugs were stopped. Two weeks after starting sulfasalazine, she was admitted for fever, violent headache and vomiting. Clinical examination found a meningeal syndrome with neck stiffness and a high grade fever at 41°C. Cranial nerve examination was normal and she had no motor or sensitory defects. Blood pressure was 110/80 mmHg. Lumbar puncture was performed immediately. A clear fluid containing 102 leukocytes/mm3 with lymphocytes predominance, increased protein concentration to 0.77g/L (normal 0.28 to 0.52g/ L) and low glucose 0.55g/L (normal glycoraquia=60 to 80% of glucose plasma level, which equal to 1.87g/L) were found. Bacterial and fungal cultures of cerebrospinal fluid (CSF) were negative. Polymerase chain reaction tests for enterovirus, herpes simplex viruses, cytomegalovirus and Epstein-Barr virus were negative. Serum tests against human immunodeficiency virus, Treponema pallidum, Brucella, Coxiella burnetii as well as anti-nuclear antibodies, were also negative. Results of other routine investigations were normal. An acetylation test was performed with 100 mg of isoniazid revealed a slow acetylator phenotype. The cerebral computed tomography scan was normal. On the first day of hospitalization, sulfasalazine was withdrawn. A quick spontaneous improvement was noted and symptoms disappeared within 2 days without specific treatment. One day after, sulfasalazine was restarted at the same dose. Few hours later, she became feverish (41°C) with a severe headache. Aseptic meningitis induced by this drug was strongly suspected and sulfasalazine was definitively withdrawn. The patient recovered within 24 hours. The case was notified to the Tunisian National centre of pharmacovigilance and analyzed according to the Begaud’s method of imputation.[3] The imputation score was “likely” (I3).
3. Discussion Diagnosis of aseptic meningitis was supported by the meningeal syndrome, CSF findings (pleocytosis, moderate increase in protein level and sterile CSF) and negative investigations. Sulfasalazine responsibility was retained owing to a compatible delay of 2 weeks, rapid and complete resolution after drug withdrawal, absence of infectious cause and essentially a positive rechallenge. Sulfasalazine-induced aseptic meningitis is rare and there have been only six previous published reports in the literature (table I).[4-9] Sulfasalazine was used for arthritis in all cases. The daily dose varied between 500 mg and 2 000 mg (not specified in two cases).
Article publié par EDP Sciences
© Société Française de Pharmacologie et de Thérapeutique
41
74
56
60
49
34
1993 [5]
1998 [6]
2009 [7]
2009b [7]
2012c [8]
Our case
F
F
F
F
F
M
F
Rheumatoid arthritis
Spondyloarthritis
Spondyloarthritis
Rheumatoid arthritis
Unclassified oligoarthritis
2g
2g
–
–
1.5 g
0.5 g
1g
Sjogren's syndrome and polyarthritis
Rheumatoid arthritis
Dose (daily)
Medical history
3 weeks
2 months
–
2 weeks
3 weeks
11 days
3 weeks
Delay
R+
R+
R–
R–
R–
R+
R+
Rechallenge
Total resolution in the middle of the following day
CSF clear with 12 WBC, total protein=0.49g/L, glucose=0.59g/L (serum glucose=1.12g/L)
Recovery within 2 days Recovery (with hydrocortisone) Recovery within 2 days
Lymphocytic pleocytosis (18 WBC), normal protein and glucose 102 leukocytes/mm3 with lymphocytes predominance, protein=0.77g/L, glucose=0.55g/L
Recovery within 8 days
WBC 2/mm3
WBC 160/mm3 (57% polynuclear),
Recovery within 2 days
Recovery within 2 weeks (with hydrocortisone)
WBC count 0.64×109/L (mostly neutrophils), glucose 3 mmol/L, protein 3.9g/L
CSF clear, normal leucocytes
Evolution
CSF
CSF: cerebrospinal fluid; R+: positive rechallenge; R–: rechallenge not made; WBC: white blood cell Delay: time between drug intake and the onset of the symptoms a: rechallenge with meningeal syndrome and rash; b: without meningeal syndrome; c: aseptic meningitis with maculopapular eruption, facial edema and transaminitis
37
Age Sex (year)
1991a [4]
Year (ref)
Table I. Reported cases of sulfasalazine-induced aseptic meningitis.
424 Salouage et al.
Thérapie 2013 Novembre-Décembre; 68 (6)
Sulfasalazine-induced Aseptic Meningitis
The delay between drug intake and onset of symptoms varied between 11 days and 2 months. Complete resolution was within 24 hours to 2 weeks after sulfasalazine withdrawal. Positive rechallenge to sulfasalazine occurred in three patients with rapid recurrence of symptoms (between 1 and 8 hours). Clinical manifestations of DIAM are varied including predominantly headache, fever, meningismus, nausea and vomiting. Analysis of CSF is the most informative test, with pleocytosis with mononuclear predominance, normal glucose level (60 to 80% of plasma glucose level), moderately raised protein level (1 to 1,5 g/L) and essentially sterile cerebrospinal liquid.[4] Our case showed hypoglycoraquia. In the two cases reported by Chazan et al. low glucose levels were noted.[7] However, some authors think that CSF findings are not helpful in DIAM diagnosis. This diagnosis requires careful drug history with temporal relationship to drug intake, negative CSF cultures, and complete resolution of symptoms after drug withdrawal. The only confirmatory test of DIAM would be a re-challenge test.[9] Polymorphic N-acetyltransferase 2 (NAT2) is involved in the metabolism of several compounds such as sulfapyridine (the active metabolite of sulfasalazine). Caffeine test is most often used to assess the acetylation phenotype. In our case, we used isoniazid acetylation test which found slow acetylator phenotype. Thus, NAT2 phenotype was considered as a risk factor of adverse drug reactions in slow acetylators treated with isoniazid and sulfonamides and also poor tolerance to sulfasalazine. This phenotype is associated to high risk of adverse drug reactions, especially sulfamides hypersensitivity.[10,11] According to Clark, slow acetylators require a lower daily dose of sulfasalazine than fast acetylators in order to maintain remission without significant adverse drug reactions. It is therefore advisable to determine acetylation phenotype prior to sulfasalazine therapy.[12] It is also recommended to increase progressively sulfasalazine dose in slow acetylator patients. In our case, starting dose was 2 g/day. This value could contribute to high concentration of the drug. The exact pathogenetic mechanism of DIAM is still unknown and it seems depending on the type of drug involved. However, two mechanisms were suggested: i) direct meningeal irritation due to cytokine release ii) delayed hypersensitivity type reaction. The first consists on a direct irritation of meninges (attributed to a difference in lipid solubility, ionization, particle size, pH). This mechanism concerns mostly to administered intrathecally administered drugs. The second mechanism is an immunologic hypersensitivity reaction, mainly a type III response related to immune complex deposition or a type IV response involving humoral factors, most notably interleukin 6. Thus, cytokine profile helps to differentiate drug-induced aseptic meningitis from an infectious meningitis.[13] Treatment of DIAM requires immediate discontinuation of the suspected drug, once all other possible causes have been eliminated, especially those of infectious nature. A thorough medical history must be completed to determine whether an underlying
© Société Française de Pharmacologie et de Thérapeutique
425
condition could be responsible for the aseptic meningitis. Other useful information that can be obtained through medical history includes recent vaccination, recent exposure to other drugs or contrast agents, recent lumbar puncture, viral infection or an history of aseptic meningitis following drug therapy. In addition, it is important to note the time of symptom onset with regard to the beginning of the drug therapy.[1,14] The available literature for sulfasalazine-induced aseptic meningitis is limited; however more than 25 cases of trimethoprim–sulfamethoxazole association were reported. In fact, there are structural similarities between sulfapyridine and sulfamethoxazole (both are aromatic sulphonamides containing an aromatic amine group at N4 position). The cross-reactivity between sulfasalazine and sulfamethoxazole is supported by positive lymphocyte transformation tests to both medications in patients previously known to have either sulfasalazine or sulfamethoxazole allergy. We find it prudent to advise patients with hypersensitivity to sulfasalazine to avoid sulfamethoxazole. For safety reasons, we recommend adding sulfamethoxazole to the allergy passport for patients allergic to sulfasalazine.[15]
4. Conclusion Aseptic meningitis is a rare but possible adverse drug reaction that can be associated with sulfasalazine. Slow acetylator phenotype can be considered as a risk factor. A rapid recovery is usually obtained after sulfasalazine withdrawal without specific treatment. Conflicts of interests. None. Abbreviations. CSF: cultures of cerebrospinal fluid; DIAM: drug-induced aseptic meningitis; NAT2: polymorphic N-acetyltransferase 2.
References 1.
Therrien R. Possible trimethoprim/sulfamethoxazole-induced aseptic meningitis. Ann Pharmacother 2004; 38: 1863-7
2.
Hopkins S, Jolles S. Drug-induced aseptic meningitis. Expert Opin Drug Saf 2005; 4: 285-97
3.
Bégaud B, Evreux JC, Jouglard J, et al. Imputabilité des effets inattendus ou toxiques des médicaments. Actualisation de la méthode utilisée en France. Therapie 1985; 40: 111-8
4.
Merrin P, Williams IA. Meningitis associated with sulphasalazine in a patient with Sjögren's syndrome and polyarthritis. Ann Rheum Dis 1991; 50: 645-6
5.
Alloway JA, Mitchell SR. Sulfasalazine neurotoxicity: a report of aseptic meningitis and a review of the literature. J Rheumatol 1993; 20: 409-11
6.
Gerster JC, Scherrer U, Biollaz J. Méningite aseptique sur salazopyrine : une observation et revue de la littérature. Rhumatologie 1998; 50: 176-8
7.
Houitte R, Abgueguen P, Masson C. Salazopyrine-induced aseptic meningitis. Joint Bone Spine 2009; 76: 216-7
Thérapie 2013 Novembre-Décembre; 68 (6)
426
Salouage et al.
8.
Tay SH, Lateef A, Cheung PP. Sulphasalazine-induced aseptic meningitis with facial and nuchal edema in a patient with spondyloarthritis. Int J Rheum Dis 2012; 15: e71-2
9.
Chazan B, Weiss A, Weiner Z, et al. Drug induced aseptic meningitis due to diclofenac. J Neurol 2003; 250: 1503-4
10. Chen M, Xia B, Chen B, et al. N-acetyltransferase 2 slow acetylator genotype associated with adverse effects of sulphasalazine in the treatment of inflammatory bowel disease. Can J Gastroenterol 2007; 21: 155-8 11. Tanigawara Y, Kita T, Aoyama N, et al. N-acetyltransferase 2 genotype-related sulfapyridine acetylation and its adverse events. Biol Pharm Bull 2002; 25: 1058-62 12. Clark DW. Genetically determined variability in acetylation and oxidation. Therapeutic implications. Drugs 1985; 29: 342-75
© Société Française de Pharmacologie et de Thérapeutique
13. Cohen JD, Jorgensen C, Sany J. Leflunomide-induced aseptic meningitis. Joint Bone Spine 2004; 71(3): 243-5 14. Jolles S, Sewell WA, Leighton C. Drug-induced aseptic meningitis: diagnosis and management. Drug Saf 2000; 22: 215-26 15. Zawodniak A, Lochmatter P, Beeler A, et al. Cross-reactivity in drug hypersensitivity reactions to sulfasalazine and sulfamethoxazole. Int Arch Allergy Immunol 2010; 153: 152-6
Correspondence and offprints: Issam Salouage, National Centre of Pharmacovigilance, 9 rue Dr Zouhaier Essafi, 1006 Tunis, Tunisia. E-mail: [email protected]
Thérapie 2013 Novembre-Décembre; 68 (6)
À LA
Thérapie 2013 Novembre-Décembre; 68 (6): 423–426 DOI: 10.2515/therapie/2013065
RÉDACTION
© 2013 Société Française de Pharmacologie et de Thérapeutique
Sulfasalazine-induced Aseptic Meningitis with Positive Rechallenge: a Case Report and Review of the Literature Méningite aseptique induite par la sulfasalazine avec réintroduction positive : à propos d’un cas et revue de la littérature Issam Salouage, Sihem El Aïdli, Feinène Cherif, Sarra Kastalli, Ahmed Zaiem and Riadh Daghfous National Centre of Pharmacovigilance, Tunis, Tunisia Text received March 15th, 2013; accepted September 19th, 2013 This case has been notified to the National Centre of Pharmacovigilance of Tunis (Tunisia) on September 18th, 2011 Keywords: sulfasalazine; drug adverse reaction; aseptic meningitis; ankylosing spondylarthritis; phenotype Mots clés : sulfasalazine ; effet indésirable ; méningite aseptique ; spondylarthrite ankylosante ; phénotype Abbreviations: see end of article.
1. Introduction Aseptic meningitis is characterized by serious inflammation of brain membranes (meninges). The main non infectious causes of meningitis include primary tumors of central nervous system, metastatic carcinomas, granulomatous angiitis, sarcoidosis, systemic lupus erythematosus, rheumatoid arthritis, Behçet’s syndrome or drugs.[1] Drug-induced aseptic meningitis (DIAM) is principally associated with non-steroid anti inflammatory drugs, antibiotics, intravenous immunoglobulins, monoclonal antibodies against CD3, intrathecal agents and vaccines. It was rarely reported with leflunomide, methotrexate, infliximab, or sulfasalazine.[2] We report a case of aseptic meningitis induced by sulfasalazine (Salazopirine®) with positive rechallenge in a slow acetylator phenotype patient suffering from ankilosing spondylarthritis. This case was notified to the National centre of pharmacovigilance of Tunis (Tunisia) on september 18th, 2011.
2. Case report A 34-old-woman, with no medical history or neurological troubles, was treated by paracetamol and non-steroid anti inflammatory drugs for ankilosing spondylarthritis with no improvement. So, sulfasalazine was introduced at the starting dose of 2 g daily. Paracetamol and non-steroid anti inflammatory drugs were stopped. Two weeks after starting sulfasalazine, she was admitted for fever, violent headache and vomiting. Clinical examination found a meningeal syndrome with neck stiffness and a high grade fever at 41°C. Cranial nerve examination was normal and she had no motor or sensitory defects. Blood pressure was 110/80 mmHg. Lumbar puncture was performed immediately. A clear fluid containing 102 leukocytes/mm3 with lymphocytes predominance, increased protein concentration to 0.77g/L (normal 0.28 to 0.52g/ L) and low glucose 0.55g/L (normal glycoraquia=60 to 80% of glucose plasma level, which equal to 1.87g/L) were found. Bacterial and fungal cultures of cerebrospinal fluid (CSF) were negative. Polymerase chain reaction tests for enterovirus, herpes simplex viruses, cytomegalovirus and Epstein-Barr virus were negative. Serum tests against human immunodeficiency virus, Treponema pallidum, Brucella, Coxiella burnetii as well as anti-nuclear antibodies, were also negative. Results of other routine investigations were normal. An acetylation test was performed with 100 mg of isoniazid revealed a slow acetylator phenotype. The cerebral computed tomography scan was normal. On the first day of hospitalization, sulfasalazine was withdrawn. A quick spontaneous improvement was noted and symptoms disappeared within 2 days without specific treatment. One day after, sulfasalazine was restarted at the same dose. Few hours later, she became feverish (41°C) with a severe headache. Aseptic meningitis induced by this drug was strongly suspected and sulfasalazine was definitively withdrawn. The patient recovered within 24 hours. The case was notified to the Tunisian National centre of pharmacovigilance and analyzed according to the Begaud’s method of imputation.[3] The imputation score was “likely” (I3).
3. Discussion Diagnosis of aseptic meningitis was supported by the meningeal syndrome, CSF findings (pleocytosis, moderate increase in protein level and sterile CSF) and negative investigations. Sulfasalazine responsibility was retained owing to a compatible delay of 2 weeks, rapid and complete resolution after drug withdrawal, absence of infectious cause and essentially a positive rechallenge. Sulfasalazine-induced aseptic meningitis is rare and there have been only six previous published reports in the literature (table I).[4-9] Sulfasalazine was used for arthritis in all cases. The daily dose varied between 500 mg and 2 000 mg (not specified in two cases).
Article publié par EDP Sciences
© Société Française de Pharmacologie et de Thérapeutique
41
74
56
60
49
34
1993 [5]
1998 [6]
2009 [7]
2009b [7]
2012c [8]
Our case
F
F
F
F
F
M
F
Rheumatoid arthritis
Spondyloarthritis
Spondyloarthritis
Rheumatoid arthritis
Unclassified oligoarthritis
2g
2g
–
–
1.5 g
0.5 g
1g
Sjogren's syndrome and polyarthritis
Rheumatoid arthritis
Dose (daily)
Medical history
3 weeks
2 months
–
2 weeks
3 weeks
11 days
3 weeks
Delay
R+
R+
R–
R–
R–
R+
R+
Rechallenge
Total resolution in the middle of the following day
CSF clear with 12 WBC, total protein=0.49g/L, glucose=0.59g/L (serum glucose=1.12g/L)
Recovery within 2 days Recovery (with hydrocortisone) Recovery within 2 days
Lymphocytic pleocytosis (18 WBC), normal protein and glucose 102 leukocytes/mm3 with lymphocytes predominance, protein=0.77g/L, glucose=0.55g/L
Recovery within 8 days
WBC 2/mm3
WBC 160/mm3 (57% polynuclear),
Recovery within 2 days
Recovery within 2 weeks (with hydrocortisone)
WBC count 0.64×109/L (mostly neutrophils), glucose 3 mmol/L, protein 3.9g/L
CSF clear, normal leucocytes
Evolution
CSF
CSF: cerebrospinal fluid; R+: positive rechallenge; R–: rechallenge not made; WBC: white blood cell Delay: time between drug intake and the onset of the symptoms a: rechallenge with meningeal syndrome and rash; b: without meningeal syndrome; c: aseptic meningitis with maculopapular eruption, facial edema and transaminitis
37
Age Sex (year)
1991a [4]
Year (ref)
Table I. Reported cases of sulfasalazine-induced aseptic meningitis.
424 Salouage et al.
Thérapie 2013 Novembre-Décembre; 68 (6)
Sulfasalazine-induced Aseptic Meningitis
The delay between drug intake and onset of symptoms varied between 11 days and 2 months. Complete resolution was within 24 hours to 2 weeks after sulfasalazine withdrawal. Positive rechallenge to sulfasalazine occurred in three patients with rapid recurrence of symptoms (between 1 and 8 hours). Clinical manifestations of DIAM are varied including predominantly headache, fever, meningismus, nausea and vomiting. Analysis of CSF is the most informative test, with pleocytosis with mononuclear predominance, normal glucose level (60 to 80% of plasma glucose level), moderately raised protein level (1 to 1,5 g/L) and essentially sterile cerebrospinal liquid.[4] Our case showed hypoglycoraquia. In the two cases reported by Chazan et al. low glucose levels were noted.[7] However, some authors think that CSF findings are not helpful in DIAM diagnosis. This diagnosis requires careful drug history with temporal relationship to drug intake, negative CSF cultures, and complete resolution of symptoms after drug withdrawal. The only confirmatory test of DIAM would be a re-challenge test.[9] Polymorphic N-acetyltransferase 2 (NAT2) is involved in the metabolism of several compounds such as sulfapyridine (the active metabolite of sulfasalazine). Caffeine test is most often used to assess the acetylation phenotype. In our case, we used isoniazid acetylation test which found slow acetylator phenotype. Thus, NAT2 phenotype was considered as a risk factor of adverse drug reactions in slow acetylators treated with isoniazid and sulfonamides and also poor tolerance to sulfasalazine. This phenotype is associated to high risk of adverse drug reactions, especially sulfamides hypersensitivity.[10,11] According to Clark, slow acetylators require a lower daily dose of sulfasalazine than fast acetylators in order to maintain remission without significant adverse drug reactions. It is therefore advisable to determine acetylation phenotype prior to sulfasalazine therapy.[12] It is also recommended to increase progressively sulfasalazine dose in slow acetylator patients. In our case, starting dose was 2 g/day. This value could contribute to high concentration of the drug. The exact pathogenetic mechanism of DIAM is still unknown and it seems depending on the type of drug involved. However, two mechanisms were suggested: i) direct meningeal irritation due to cytokine release ii) delayed hypersensitivity type reaction. The first consists on a direct irritation of meninges (attributed to a difference in lipid solubility, ionization, particle size, pH). This mechanism concerns mostly to administered intrathecally administered drugs. The second mechanism is an immunologic hypersensitivity reaction, mainly a type III response related to immune complex deposition or a type IV response involving humoral factors, most notably interleukin 6. Thus, cytokine profile helps to differentiate drug-induced aseptic meningitis from an infectious meningitis.[13] Treatment of DIAM requires immediate discontinuation of the suspected drug, once all other possible causes have been eliminated, especially those of infectious nature. A thorough medical history must be completed to determine whether an underlying
© Société Française de Pharmacologie et de Thérapeutique
425
condition could be responsible for the aseptic meningitis. Other useful information that can be obtained through medical history includes recent vaccination, recent exposure to other drugs or contrast agents, recent lumbar puncture, viral infection or an history of aseptic meningitis following drug therapy. In addition, it is important to note the time of symptom onset with regard to the beginning of the drug therapy.[1,14] The available literature for sulfasalazine-induced aseptic meningitis is limited; however more than 25 cases of trimethoprim–sulfamethoxazole association were reported. In fact, there are structural similarities between sulfapyridine and sulfamethoxazole (both are aromatic sulphonamides containing an aromatic amine group at N4 position). The cross-reactivity between sulfasalazine and sulfamethoxazole is supported by positive lymphocyte transformation tests to both medications in patients previously known to have either sulfasalazine or sulfamethoxazole allergy. We find it prudent to advise patients with hypersensitivity to sulfasalazine to avoid sulfamethoxazole. For safety reasons, we recommend adding sulfamethoxazole to the allergy passport for patients allergic to sulfasalazine.[15]
4. Conclusion Aseptic meningitis is a rare but possible adverse drug reaction that can be associated with sulfasalazine. Slow acetylator phenotype can be considered as a risk factor. A rapid recovery is usually obtained after sulfasalazine withdrawal without specific treatment. Conflicts of interests. None. Abbreviations. CSF: cultures of cerebrospinal fluid; DIAM: drug-induced aseptic meningitis; NAT2: polymorphic N-acetyltransferase 2.
References 1.
Therrien R. Possible trimethoprim/sulfamethoxazole-induced aseptic meningitis. Ann Pharmacother 2004; 38: 1863-7
2.
Hopkins S, Jolles S. Drug-induced aseptic meningitis. Expert Opin Drug Saf 2005; 4: 285-97
3.
Bégaud B, Evreux JC, Jouglard J, et al. Imputabilité des effets inattendus ou toxiques des médicaments. Actualisation de la méthode utilisée en France. Therapie 1985; 40: 111-8
4.
Merrin P, Williams IA. Meningitis associated with sulphasalazine in a patient with Sjögren's syndrome and polyarthritis. Ann Rheum Dis 1991; 50: 645-6
5.
Alloway JA, Mitchell SR. Sulfasalazine neurotoxicity: a report of aseptic meningitis and a review of the literature. J Rheumatol 1993; 20: 409-11
6.
Gerster JC, Scherrer U, Biollaz J. Méningite aseptique sur salazopyrine : une observation et revue de la littérature. Rhumatologie 1998; 50: 176-8
7.
Houitte R, Abgueguen P, Masson C. Salazopyrine-induced aseptic meningitis. Joint Bone Spine 2009; 76: 216-7
Thérapie 2013 Novembre-Décembre; 68 (6)
426
Salouage et al.
8.
Tay SH, Lateef A, Cheung PP. Sulphasalazine-induced aseptic meningitis with facial and nuchal edema in a patient with spondyloarthritis. Int J Rheum Dis 2012; 15: e71-2
9.
Chazan B, Weiss A, Weiner Z, et al. Drug induced aseptic meningitis due to diclofenac. J Neurol 2003; 250: 1503-4
10. Chen M, Xia B, Chen B, et al. N-acetyltransferase 2 slow acetylator genotype associated with adverse effects of sulphasalazine in the treatment of inflammatory bowel disease. Can J Gastroenterol 2007; 21: 155-8 11. Tanigawara Y, Kita T, Aoyama N, et al. N-acetyltransferase 2 genotype-related sulfapyridine acetylation and its adverse events. Biol Pharm Bull 2002; 25: 1058-62 12. Clark DW. Genetically determined variability in acetylation and oxidation. Therapeutic implications. Drugs 1985; 29: 342-75
© Société Française de Pharmacologie et de Thérapeutique
13. Cohen JD, Jorgensen C, Sany J. Leflunomide-induced aseptic meningitis. Joint Bone Spine 2004; 71(3): 243-5 14. Jolles S, Sewell WA, Leighton C. Drug-induced aseptic meningitis: diagnosis and management. Drug Saf 2000; 22: 215-26 15. Zawodniak A, Lochmatter P, Beeler A, et al. Cross-reactivity in drug hypersensitivity reactions to sulfasalazine and sulfamethoxazole. Int Arch Allergy Immunol 2010; 153: 152-6
Correspondence and offprints: Issam Salouage, National Centre of Pharmacovigilance, 9 rue Dr Zouhaier Essafi, 1006 Tunis, Tunisia. E-mail: [email protected]
Thérapie 2013 Novembre-Décembre; 68 (6)
