Minocycline
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Lactic acidosis (first report) in a patient with mitochondrial myopathy: case report An 18-year-old woman developed severe lactic acidosis while receiving minocycline for acne [dosage and duration of treatment to reaction onset not stated]; she was later found to have mitochondrial myopathy. The girl, whose only medications were minocycline and sertraline, presented to an emergency department with progressive weakness and muscle pain, and advancing dyspnoea. Fatigue, muscular discomfort and cramps had begun after an episode of infectious mononucleosis about 4 months earlier. Dyspnoea started 2 days before presentation, associated with an episode of chest pressure, and had progressed to near syncope over the next few hours; her muscle symptoms has also worsened and she had become unable to walk unassisted. She had also experienced migraines with nausea, vomiting and photophobia during the previous few weeks, and some mild hearing loss. On examination, her pulse rate was 137 and her respiratory rate was 30. Her hearing was intact, but neurological examination revealed weak neck flexors (3+/5) and extensors (4+/5), muscle wasting on her hands, mild facial weakness, upper and lower extremity strength of 5-/5 distally, hip flexion of 5-/5 and knee flexion of 4+/5 (bilateral); her reflexes were 3/4. She had a lactic acid level of 102 mg/dL, and arterial blood gas analysis revealed the following: pH 7.21, pO2 128, pCO2 14 and bicarbonate 9 mEq/L. Laboratory findings were: sodium 139 mEq/L, potassium 4.4 mEq/L, chloride 109 mEq/L, Co2 < 10 mEq/L, anion gap (calculated) 20 mEq/L and creatinine kinase 1.70 U/L. Brain MRI findings were suggestive of an incidental pineal cyst. Idiopathic lactic acidosis was diagnosed and she was hospitalised. The woman was hydrated and, the next day, she had a pH of 7.29, a pCO2 of 28 and a lactic acid level of 11 mg/dL. Her mother then revealed a family history of mitochondrial disorders; leucocyte mitochondrial DNA analysis disclosed a heteroplasmy for the G8363A mutation in tRNA (Lys). Exercise tests were consistent with mitochondrial myopathy. As an outpatient, she was treated with ubidecarenone, riboflavin [vitamin B2], bicarbonate and a low carbohydrate diet, and was advised to avoid minocycline or doxycycline in the future. She did not experience further acute decompressions during the following year. Author comment: "Since the patient had a symptomatic tRNA mutation and hence disturbed mitochondrial DNA expression, we hypothesize that the combination of minocycline plus general and oxidative stress from her bout of mononucleosis initiated her presentation of mitochondrial myopathy and lactic acidosis. Specifically the minocycline may have altered our patients respiratory chain complexes via ribosomal and cytochrome c release inhibition." Zoraster RM, et al. Severe lactic acidosis secondary to minocycline in a teenager with infectious mononucleosis and mitochondrial myopathy. Clinical Neurology 801117463 and Neurosurgery 110: 627-630, No. 6, Jun 2008 - USA
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