1.Adalimumab-associated intracranial Neisseria meningitidis infection
Adverse Drug Reactions Journal 2025;27(8):505-507
A 39-year-old male patient with ankylosing spondylitis received adalimumab 40 mg subcutaneously every 2 weeks plus sulfasalazine enteric-coated tablets 0.75 g orally twice daily. Two weeks after the therapy initiation, he received his second adalimumab injection and discontinued sulfasalazine because of skin rashes. Meanwhile, cetirizine 10 mg once daily was given as anti-allergic treatment for 3 days. Six days later, he developed fever and persistent holocranial dull pain. The next day the headache worsened, with one episode of vomiting gastric contents. Cranial magnetic resonance imaging revealed findings consistent with infectious leptomeningeal lesions, and cerebrospinal fluid analysis suggested intracranial infection. Empirical anti-infection therapy with ceftriaxone and ganciclovir, as well as intracranial pressure reduction therapy with 20% mannitol was initiated. Two days later, next-generation sequencing of cerebrospinal fluid identified Neisseria meningitidis as the highly probable pathogen. The therapy regimen was adjusted to ceftriaxone, acyclovir and dexamethasone. After 12 days of treatments, the patient achieved full clinical recovery from meningitis.
2.Adalimumab-associated intracranial Neisseria meningitidis infection
Adverse Drug Reactions Journal 2025;27(8):505-507
A 39-year-old male patient with ankylosing spondylitis received adalimumab 40 mg subcutaneously every 2 weeks plus sulfasalazine enteric-coated tablets 0.75 g orally twice daily. Two weeks after the therapy initiation, he received his second adalimumab injection and discontinued sulfasalazine because of skin rashes. Meanwhile, cetirizine 10 mg once daily was given as anti-allergic treatment for 3 days. Six days later, he developed fever and persistent holocranial dull pain. The next day the headache worsened, with one episode of vomiting gastric contents. Cranial magnetic resonance imaging revealed findings consistent with infectious leptomeningeal lesions, and cerebrospinal fluid analysis suggested intracranial infection. Empirical anti-infection therapy with ceftriaxone and ganciclovir, as well as intracranial pressure reduction therapy with 20% mannitol was initiated. Two days later, next-generation sequencing of cerebrospinal fluid identified Neisseria meningitidis as the highly probable pathogen. The therapy regimen was adjusted to ceftriaxone, acyclovir and dexamethasone. After 12 days of treatments, the patient achieved full clinical recovery from meningitis.

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