Endocrine Abstracts

Introducing: Hypothyroidism is the most common endocrinopathy causing rhabdomyolysis. Muscle manifestations are common in hypothyroidism, but myopathy is most often limited to discrete clinical signs such as myalgias, stiffness or cramps accompanied by a simple elevation of muscle enzymes. On the other hand, rhabdomyolysis associated with hypothyroidism is a rare diagnosis to our knowledge. We report a case of severe rhabdomyolysis in the setting of profound Hashimoto’s hypothyroidism.

Observation: Mr A.I, 32 years old. Hospitalized in psychiatry for an acute psychotic attack, having as antecedent a schizophrenia since 6 years under neuroleptics in stop for 3 years. The interrogation found signs of hypothyroidism. The clinical examination showed a bradycardia, a generalized myxedema with a puffiness of the face and pre tibial myxedema, the osteotendinous reflexes sharp, a reduced mimic, the lower lips everted with a moderate bilateral ptosis, filling of the supra clavicular hollows. Goitre homogeneous. On workup: Total CPK at 28 times normal, normokalemia, moderate renal failure, deep peripheral hypothyroidism. Thyroid ultrasonography revealed a goiter with significant vascularization, positive anti-TPO antibodies. The diagnosis of Hashimoto’s thyroiditis was made. This hypothyroidism is associated with rhabdomyolysis diagnosed on a CPK level (28 times norma), in normo kalemia, as well as moderate renal failure. The patient was put on Levothyroxine with an initiation dose of 1.7 µg/kg/j.

Discussion: Muscle involvement during hypothyroidism is often frequent and early, simulating a pathology of the locomotor system. Moderate elevation of creatinine phosphokinase (CPK) during hypothyroidism is found in 80% of cases, however, cases of major CPK elevation during hypothyroid myopathy remain exceptional. Most patients with hypothyroidism who develop rhabdomyolysis have a clear precipitating factor, in which case intermittent use of neuroleptics can be suggested, although rhabdomyolysis caused by severe hypothyroidism alone has been reported in the literature. Myolysis in hypothyroidism is explained by muscle degeneration with atrophy of type II fibers and compensatory hypertrophy of type I fibers secondary to a defect in mitochondrial metabolism. Glycosaminoglycan deposition, altered contractility of actin-myosin units, and low myosin ATPase activity in skeletal muscle are also involved in the pathophysiology.

Conclusion: Rhabdomyolysis is a rare but fatal complication of hypothyroidism. Hormone replacement therapy, started gradually, allows resolution of muscle signs and normalization of muscle enzymes. A major elevation of CPK should prompt a search for hypothyroidism, although this is a rare cause, and warrants monitoring of thyroid status during any muscle lysis with elevated muscle enzymes, as recommended