Debilidad muscular proximal progresiva de inicio subagudo en un paciente anciano: descripción de un caso / Progressive proximal muscle weakness with subacute onset in an elderly patient: a case report

Introducción: Las estatinas son de los medicamentos más recetados. Aunque las estatinas generalmente se toleran bien, pueden provocar efectos secundarios musculoesqueléticos. La miopatía autoinmune necrotizante inducida por estatinas (SINAM) es una afección rara y la prevalencia sólo es de 1 de cada 100.000 personas. Este trastorno se caracteriza por debilidad muscular simétrica progresiva y grave, elevación marcada de la creatincinasa y síntomas persistentes a pesar de la interrupción de la estatina. La electromiografía suele mostrar un patrón de miopatía irritable inespecífico, indistinguible de otras miopatías inflamatorias. La biopsia muscular muestra la presencia de fibras necróticas, fibras en regeneración sin células inflamatorias significativas y una regulación positiva difusa o focal de la expresión del complejo mayor de histocompatibilidad de clase I. Los anticuerpos anti-3-hidroxi-3-metilglutaril-coenzima A (anti-HMG-CoA) reductasa representan un rasgo serológico característico de la SINAM.Caso clínico: Presentamos a un paciente que desarrolló debilidad muscular progresiva después de tomar simvastatina durante los últimos siete años. En la presentación inicial, su nivel de creatincinasa fue de 2.954 U/L y los anticuerpos anti-HMG-CoA reductasa fueron positivos. La biopsia mostró rasgos miopáticos profundos con numerosas fibras necróticas, algunas fibras en regeneración e infiltrado de células inflamatorias perimisial, combinado con una sobreexpresión difusa del complejo mayor de histocompatibilidad de clase I. Se le diagnosticó SINAM, se suspendió la estatina y se inició una dosis alta de corticoides sistémicos, inmunoglobulina intravenosa y metotrexato. Después de tres meses de seguimiento, tuvo una mejora significativa en la fuerza muscular y el nivel de creatincinasa volvió a la normalidad.(AU)

Introduction: Statins are some of the most widely prescribed medications. Although statins are generally well tolerated, they can lead to musculoskeletal side effects. Statin-induced necrotizing autoimmune myositis (SINAM) is a rare condition and the prevalence is only 1 per 100,000 people. This disorder is characterized by progressive and severe symmetric muscle weakness, marked elevation of creatine kinase and persistent symptoms despite statin discontinuation. Electromyography commonly shows a nonspecific irritable myopathy pattern indistinguishable from other inflammatory myopathies. Muscle biopsy shows the presence of necrotic fibers, regenerating fibers without significant inflammatory cells and diffuse or focal upregulation of major histocompatibility complex class I expression. The anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR) antibodies represent a characteristic serological feature of SINAM. Case report: We present a patient who developed progressive muscle weakness after taking simvastatin for the last seven years. At initial presentation, her creatine kinase level was 2,954 U/L and anti-HMGCR antibodies were positive. The biopsy showed a profound myopathic features with numerous necrotic fibers, some regenerating fibers and perimysial inflammatory cell infiltrate, combined with a diffuse overexpression of major histocompatibility complex class I products. She was diagnosed with SINAM, statin was suspended and a high dose of systemic corticosteroids, intravenous immunoglobulin therapy and methotrexate was started. At three-month follow-up, she had significant improvement in muscle strength and creatine kinase level returned to normal...(AU)

Bilateral Sub-deltoid Bursitis in a Patient Receiving Infliximab for Crohn's Disease.

BACKGROUND: Infiximab has been shown to be effective in inducing and maintaining remission of intestinal bowel diseases. Infiximab has been associated with many adverse events. Articular manifestations are commonly reported, but they are of variable clinical expression and aetiology. Among them, inflammatory bursitis has rarely been described. OBJECTIVE: Herein a case of inflammatory bursitis in a patient with Crohn's disease after switching to biosimilar infliximab is reported. CASE REPORT: A 41-year-old man with Crohn's disease evolving from 3 years was referred to infliximab therapy at a dose of 5mg/kg because of an aggressive resistant perineal fistula. After 14 infusions of infliximab, the treatment was switched to infliximab biosimilar using the same dose and frequency of administration. Forty-eight hours after the second infusion, he developed an acute onset of muscle pain and stiffness on both of his shoulders. A musculoskeletal ultrasound was performed and revealed a hypoechoic widening of both subacromial bursae. It was more severe on the left side. DISCUSSION: The diagnosis of non-infective sub-acromial bursitis secondary to infliximab infusion was made as the patient's symptoms resolved rapidly without any antibiotics. Infliximab was definitively stopped and adalimumab was introduced. CONCLUSION: Musculoskeletal side effects of infliximab infusion are uncommonly reported. Among them, bursitis has been reported in only a few cases. Ultrasonography can help early diagnosis of bursitis. The time of occurring of this reaction regarding infliximab infusion, screening of Antibodies to Infliximab (ATI) and clinical outcome after drug discontinuation are the main helpful arguments.