Meningococcal vaccine group C conjugate
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Meningococcal vaccine group C conjugate Macrophagic myofascitis and tibiotarsal arthritis due to aluminium hydroxide excipient: case report
A 15-year-old girl developed tibiotarsal arthritis and macrophagic myofascitis (MMF) due to aluminium hydroxide excipient in Meningococcal vaccine group C conjugate vaccine. The girl presented to our department with a history of bilateral tibiotarsal arthritis, distal myalgia in both forearms and intermittent fever, six months after Meningococcal vaccine group C conjugate [Meningococcal group C vaccine; dosage not stated] with aluminium hydroxide as excipient in the deltoid muscle. Laboratory parameters revealed an increased erythrocyte sedimentation rate and mild anaemia. Anti-nuclear antibodies were positive and rheumatoid factor was twice the upper limit value. She had elevated C3 and β2-mycroglobulin levels. The clinical presentation and laboratory parameters were suggestive of an undifferentiated connective tissue disease (UCTD). The girl started receiving treatment with prednisolone and complete resolution of laboratory and symptomatic abnormalities were achieved. Three years after vaccination, she presented again with oedema, functional disability, myalgia and asthenia predominantly in the right forearm. The MRI of the right forearm showed signs of inflammation in her superficial and deep flexor forearm muscles consistent with myositis. A muscle biopsy revealed extensive fibrosis and an inflammatory process involving the perimysium, endomysium and fascia along with macrophages towels. The findings confirmed a final diagnosis of macrophagic myofasciitis (MMF). Prednisolone was restarted and resolution of inflammatory signs and improvement of symptoms were noted. Physical rehabilitation was initiated along with azathioprine introduction and tapering of prednisolone. She developed leucopenia, neutropenia and headache. She also experienced pain recurrence and weaning of prednisolone was found to be impossible. Despite the initial improvement, she had clinically detectable inflammation in the right forearm with local thickening. After nine months of therapy with no significant improvement, azathioprine was switched to methotrexate. Afterwards, significant improvement of the right forearm thickening was noted. Eighteen months later, recurrence of MMF was noted. The laboratory parameters and MRI inflammation was controlled with increased dose of prednisolone. After two years of significant symptomatic control with methotrexate and low dose prednisolone, a relapse of MMF with fever, pain, increased ESR, skin and muscular thickening of the contralateral forearm was noted. She was initiated on treatment with mycophenolate mofetil and achieved a sustained improvement. She developed concurrent neutropenia. The dose of mycophenolate mofetil was decreased. One year later, methotrexate was switched to tacrolimus along with continued mycophenolate mofetil therapy. Afterwards, it was finally possible to wean prednisolone. She had normal muscle strength and mild muscular pain on myc
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