Sirs: Muscle involvement in the course of Hepatitis C Virus (HCV) infection has mainly been reported as a myositis secondary to an immunologically mediated reaction or to a direct effect of viral infection. Myositis was confirmed in these cases by the presence of perivascular infiltration of inflammatory cells in the muscle biopsy [1, 2]. However, lack of evidence for viral multiplication in muscle [3, 4] suggested a virus-triggered immune-mediated mechanism, rather than direct infection and in situ replication. On the other hand, several cases of HCV associated myopathy lacked signs of inflammation in the muscle biopsy [2, 5] suggesting other pathogenic mechanisms. A 60-year-old woman was admitted in April 2002 with a 3 year history of slowly progressive bilateral eyelid ptosis, diplopia, generalized weakness, severe distal upper limb weakness and respiratory distress after minimal exercise. Neurological examination disclosed mild neck and proximal upper limb weakness, bilateral ptosis and diplopia both in horizontal and upward gaze. Ptosis increased after sustained upward gaze. A mild impairment in the upward gaze was present mainly on the left side. Her family history was unremarkable. The patient had a post-transfusion HCV infection detected by chance ten years before the appearance of ptosis, and not treated with immunotherapy because of the benign course. Neoplastic, autoimmune, thyroidal, and rheumatologic diseases were excluded by appropriate tests. Repetitive stimulation (right ulnar nerveabductor digiti minimi muscle and facial nerve-nasalis muscle) did not show a decremental response. Acetylcholine receptor antibodies were absent. Ptosis did not improve after edrophonium chloride intravenous injection. Chest computed tomography (CT), spirometry, electrocardiography and echocardiography, brain and orbit, CT and magnetic resonance imaging were normal. Immunoglobulin G and immunoglobulin M cryoglobulins were detected (cryocrit value: 2 %). Electroneurography was completely normal. Automatic interference pattern analysis was consistent with a myopathic dysfunction. The patient had an abnormal turns/amplitude ratio demonstrated by scores below the sexand age-specific reference range in frontal muscle, left biceps brachii and quadriceps. The same muscles showed rapid recruitment of short duration and low amplitude motor unit potentials. Fibrillations and fasciculations were absent. A biopsy taken from the left deltoid muscle revealed moderate fiber atrophy, marked variation of fiber size with round or angular shape, type 2 myofiber predominance with increased nuclear centralization. Perivascular inflammation, necrosis, and ragged red fibers were absent. Mitochondrial enzyme activities showed decreased decylbenzoquinol cytochrome c reductase activity (complex III deficiency) (51.1 nmol/min mg, normal values: 70–150) while citrate synthase activity was normal (153 nmol/min mg, normal value: 80–210). Mitochondrial complex I, II IV and V activities were normal. The ultrastructural study showed increased subsarcolemmal accumulation of glycogen, and mitochondria with altered shape and concentric cristae. To verify these findings a LETTER TO THE EDITORS