Acromegaly as an endocrine form of myopathy: case report and review of literature.

OBJECTIVE: To describe a case of muscle weakness in a patient with acromegaly and to review the pathophysiologic features of this disorder. METHODS: We present the clinical, laboratory, electromyographic, and muscle biopsy findings in our patient and review related reports in the literature. RESULTS: A 58-year-old woman with acromegaly presented with complaints of bilateral hip pain, weakness, and instability 8 months after transsphenoidal resection of a growth hormone (GH)-secreting pituitary macroadenoma. She had biochemically normal thyroid and adrenal function and no evidence of any neuropathy, inflammatory myopathy, or rheumatologic disorder to explain her symptoms. Investigations revealed increased levels of GH, insulin-like growth factor-I, serum creatine kinase (CK), and the MB fraction of CK, normal results of nerve conduction studies, and nonspecific findings on electromyography and muscle biopsy. A review of the literature revealed that although muscle weakness is a well-recognized feature of acromegaly, only a few cases similar to ours have been reported since acromegaly was first described in the late 1800s. Little is known about the natural history, best diagnostic approach, and optimal therapy for this debilitating complication. CONCLUSION: Muscle weakness in acromegaly is common and may result from a combination of the direct effect of GH excess on muscle and other metabolic derangements (hypothyroidism, hypoadrenalism, or diabetes). Mechanical factors may also contribute, such as joint laxity in conjunction with hypermobility. Affected patients may benefit from a reduction in GH levels and physiotherapy for adaptive training. Persistently increased serum CK levels in a patient with diabetes, for whom no other cause is found, should prompt an investigation for acromegaly. More research into this aspect of acromegaly is needed for enhancement of our understanding of, and therapy for, this debilitating condition.

An outbreak of trichinellosis due to consumption of bear meat infected with Trichinella nativa, in 2 northern Saskatchewan communities.

In June 2000, bear meat infected with Trichinella nativa was consumed by 78 individuals in 2 northern Saskatchewan communities. Interviews and blood collections were performed on exposed individuals at the onset of the outbreak and 7 weeks later. All exposed individuals were treated with mebendazole or albendazole, and symptomatic patients received prednisone. Confirmed cases were more likely to have consumed dried meat, rather than boiled meat (P<.001). Seventy-four percent of patients completed the recommended therapy, and 87% of patients who were followed up in August 2000 reported complete resolution of symptoms. This outbreak of trichinellosis was caused by consumption of inadequately cooked bear meat contaminated with T. nativa. Apart from clinical symptomatology, blood counts, creatine kinase levels, serology test results, and analysis of the remaining bear meat helped establish the diagnosis. Treatment with antiparasitic drugs and prednisone was beneficial in limiting the severity and duration of the illness.