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We evaluated whether anserine, a methylated analog of the dipeptide carnosine, is present in the cardiac and skeletal muscles of humans and whether the CARNMT1 gene, which encodes the anserine synthesizing enzyme carnosine-N-methyltransferase, is expressed in human skeletal muscle. We found that anserine is present at low concentrations (low micromolar range) in both cardiac and skeletal muscles, and that anserine content in skeletal muscle is ~15 times higher than in cardiac muscle (cardiac muscle: 10.1 ± 13.4 µmol·kg-1 of dry muscle, n = 12; skeletal muscle: 158.1 ± 68.5 µmol·kg-1 of dry muscle, n = 11, p < 0.0001). Anserine content in the heart was highly variable between individuals, ranging from 1.4 to 45.4 µmol·kg-1 of dry muscle, but anserine content was not associated with sex, age, or body mass. We also showed that CARNMT1 gene is poorly expressed in skeletal muscle (n = 10). This is the first study to demonstrate that anserine is present in the ventricle of the human heart. The presence of anserine in human heart and the confirmation of its expression in human skeletal muscle open new avenues of investigation on the specific and differential physiological functions of histidine dipeptides in striated muscles.

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Resumen: La sinovitis villonodular pigmentada extraarticular, también llamada tumor de células gigantes de la vaina tendinosa, es frecuente en la mano, siendo extremadamente rara su localización en la rodilla. Se presenta el caso de un paciente con una bursitis villonodular pigmentada de la bursa de la pata de ganso sin afectación intraarticular. Extra-articular pigmented villonodular synovitis, also called giant cell tumor of the tendon sheath, is common in the hand, being extremely rare in the knee. We present the case of a patient with a pigmented villonodular bursitis of the pes anserine bursa without intraarticular involvement.

Abstract: Extra-articular pigmented villonodular synovitis, also called giant cell tumor of the tendon seath, is common in the hand, being extremely rare in the knee. We present the case of a patient with a pigmented villonodular bursitis of the pes anserine bursa without intraarticular involvement.

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Dor no joelho é uma condição comum na clínica diária e a patologia anserina, também conhecida como pata de ganso, tem sido considerada uma das principais causas. O diagnóstico tem sido realizado de maneira eminentemente clínica, o que tem gerado equívocos. Os pacientes queixam-se tipicamente de dor na parte medial do joelho, com sensibilidade na porção ínferomedial. Estudos de imagem têm sido realizados para esclarecer se tais pacientes possuem bursite, tendinite ou ambos os distúrbios na região conhecida como pata de ganso. Entretanto, o defeito estrutural responsável pelos sintomas permanece desconhecido, motivo pelo qual preferimos intitular como "Síndrome Anserina". O diabetes mellitus é um fator predisponente bem reconhecido. O sobrepeso e a osteoartrite de joelho parecem ser fatores adicionais de risco, contudo, seus papéis na gênese da moléstia ainda não são bem entendidos. O tratamento atual inclui anti-inflamatório, fisioterapia e infiltração de corticoide, com evolução muito variável, que oscila entre 10 dias e 36 meses. A falta de conhecimento sobre a etiofisiopatologia e dados epidemiológicos exige futuros estudos para esse frequente e intrigante distúrbio.

Knee pain is a common complaint in clinical practice, and pes anserinus tendino-bursitis syndrome (PATB) has been frequently diagnosed based only on clinical features that may cause equivocal interpretations. Patients complain of characteristic spontaneous medial knee pain with tenderness in the inferomedial aspect of the joint. Studies with different imaging modalities have been undertaken during the last years to identify whether these patients suffer from bursitis, tendinitis, or both. Nevertheless, little is known regarding the structural defect responsible for this disturbance. Due to these problems and some controversies, we suggest the term "anserine syndrome" for this condition. Diabetes Mellitus is a known predisposing factor for this syndrome. Overweight and osteoarthritis seem to represent additional risk factors; however, their role in the pathophysiology of the disease is not yet understood. Treatment includes non-steroidal anti-inflammatory drugs, physiotherapy, and injections of corticosteroid, with highly variable responses, from 10 days to 36 months to achieve recovery. The lack of knowledge about its epidemiological, etiological, and pathophysiological aspects requires future studies for this common and intriguing disorder.

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