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Letter to the Editor
Immune-mediated necrotising myopathy after treatment with adalimumab in a patient with HLA-B27 ankylosing spondylitis
Miopatía necrotizante inmunomediada tras tratamiento con adalimumab en paciente con espondilitis anquilosante HLA-B27
A. Chavarría-Mirandaa,
Corresponding author
alba-chavarria@hotmail.com

Corresponding author.
, A. Hernández Lainb, O. Toldos Gonzálezb, M.I. Pedraza Huesoa
a Servicio de Neurología, Hospital Clínico Universitario de Valladolid, Valladolid, Spain
b Servicio de Anatomía Patológica, Hospital Universitario Doce de Octubre, Madrid, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Autoimmune myopathies are rare&#44; with a prevalence of 9-14 cases per 100 000 population&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Immune-mediated necrotising myopathy &#40;IMNM&#41; is characterised by proximal muscle weakness&#44; elevated creatine kinase &#40;CK&#41; levels&#44; muscle fibre necrosis with signs of regeneration&#44; and minimal or no inflammatory infiltration in muscle biopsy&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Development of IMNM has been associated with statin use&#44;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> certain connective tissue disorders&#44; and HIV infection&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;4</span></a> According to published series&#44;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> some patients test positive for anti-HMGCR &#40;33&#37;&#41; or anti-SRP antibodies &#40;24&#37;&#41;&#44; although up to 20&#37;-30&#37; of patients are seronegative&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> We present a case of immune-mediated necrotising myopathy following treatment with adalimumab in a patient with HLA-B27 ankylosing spondylitis&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Our patient was a 55-year-old man with history of psoriasis and HLA-B27 ankylosing spondylitis of 20 years&#8217; progression&#44; who had been under treatment with adalimumab for the previous 2 years&#46; He consulted due to predominantly proximal muscle pain in the limbs&#44; starting 6 months after onset of adalimumab treatment&#46; The patient reported greater difficulty walking and climbing up and down stairs&#44; and loss of muscle mass in the arms and legs&#46; The neurological examination revealed bilateral paresis &#40;Medical Research Council grade 4&#47;5&#41; in the psoas muscle and quadriceps&#44; and muscle atrophy in the deltoid and quadriceps muscles&#46; We detected no fasciculations or any other spontaneous muscle activity&#44; and the patient did not present scapular winging&#46; Deep tendon reflexes were present and gait was normal&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Laboratory analysis revealed elevated CK levels &#40;385&#160;IU&#47;L&#41; at 7 months after treatment onset&#59; results from a complete blood count&#44; erythrocyte sedimentation rate&#44; aldolase level determination&#44; liver profile&#44; kidney profile&#44; and serology testing were all within normal ranges&#46; Due to suspicion of myopathy&#44; we performed an MRI scan of the lower limbs&#44; which showed no alterations&#44; and an electromyography study&#44; finding no signs of myopathy&#46; CK levels were determined periodically&#44; with a maximum level of 598&#160;IU&#47;L&#46; A biopsy of the quadriceps muscle revealed signs compatible with IMNM &#40;<a class="elsevierStyleCrossRefs" href="#fig0005">Figs&#46; 1 and 2</a>&#41;&#46; Tests for antinuclear&#44; anti-ENA&#44; anti-HMGCR&#44; and anti-SRP antibodies and a myositis autoantibody panel yielded negative results&#46; A chest-abdomen-pelvis CT scan ruled out underlying neoplasia&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">In view of the anatomical pathology findings&#44; we suspended adalimumab and started corticosteroid therapy&#44; initially with intravenous methylprednisolone at 500&#160;mg for 3 days&#44; followed by oral prednisone in decreasing doses until reaching a maintenance dose of 20&#160;mg&#47;day&#46; At 6 months&#44; CK levels had decreased to 120-130&#160;IU&#47;L and motor deficits had improved slightly&#44; although muscle pain persisted&#46; Azathioprine 50&#160;mg&#47;12&#160;h slightly improved pain&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Tumour necrosis factor-&#945; &#40;TNF-&#945;&#41; inhibitors are increasingly used for the treatment of autoimmune diseases&#46; Paradoxically&#44; due to their immunomodulatory effects&#44; cases have been reported of immune disorders associated with use of TNF-&#945; inhibitors&#44; including vasculitis&#44; lupus-like syndrome&#44; and interstitial lung disease&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> Case series have been published of patients receiving treatment with TNF-&#945; inhibitors and presenting onset of such immune-mediated myopathies as myositis and dermatomyositis&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7&#44;8</span></a> Despite this potential association&#44; no cases have previously been described of IMNM associated with adalimumab use&#46; In our patient&#44; the short time between onset of treatment with adalimumab and onset of symptoms and the improvement in CK levels and muscle pain after adalimumab discontinuation suggest that this drug played a role in the development of myopathy&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">The recommended treatment for IMNM is induction therapy with oral or intravenous corticosteroids&#59; an immunosuppressant may be added at onset of corticosteroid therapy or during the following month&#44; depending on symptom severity and initial response to treatment&#46; Acceptable response has been reported for such immunosuppressants as methotrexate&#44; azathioprine&#44; ciclosporin&#44; and mycophenolate mofetil&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> Combination therapy with several immunosuppressants may be necessary in 50&#37; of cases&#59; intravenous immunoglobulins or rituximab constitute an alternative for refractory cases&#44; or may even be administered during induction therapy&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> In conclusion&#44; TNF-&#945; inhibitors have been associated with the development of immune-mediated myopathy&#59; identification of the causal factor and early discontinuation of the drug are essential for disease prognosis&#46;</p></span>"
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