Cerebellar Nocardiosis and Myopathy from Long-Term Corticosteroids for Idiopathic Thrombocytopenia

Infection of the central nervous system with Nocardia sp. usually manifests as supratentorial abscesses. Supratentorial and cerebellar abscesses from infection with Nocardia sp. following immunosuppression with long-term corticosteroids for idiopathic thrombocytopenia (ITP) have not been reported. An 83 years-old, human immunodeficiency virus (HIV)-negative, polymorbid male with ITP for which he required corticosteroids since age 53 years developed tiredness, dyspnoea, hemoptysis, abdominal pain, and progressive gait disturbance. Imaging studies of the lung revealed an enhancing tumour in the right upper lobe with central and peripheral necrosis, multiple irregularly contoured hyperdensities over both lungs, and right-sided pleural effusions. Sputum culture grew Nocardia sp. Neurological diagnostic work-up revealed dysarthria, dysphagia, ptosis, hypoacusis, tremor, dysdiadochokinesia, proximal weakness of the lower limbs, diffuse wasting, and stocking-type sensory disturbances. The neurological deficits were attributed to an abscess in the upper cerebellar vermis, myopathy from corticosteroids, and polyneuropathy. Meropenem for 37 days and trimethoprime-sulfamethoxazole for 3 months resulted in a reduction of the pulmonary, but not the cerebral lesions. Therefore, sultamicillin was begun, but without success. Long-term therapy with corticosteroids for ITP may induce not only steroid myopathy but also immune-incompetence with the development of pulmonary and cerebral nocardiosis. Cerebral nocardiosis may not sufficiently respond to long-term antibiotic therapy why switching to alternative antibiotics or surgery may be necessary.

A Case of Steroid induced Myopathy in Patient with Iatrogenic Cushing Syndrome / 대한내분비학회지

Many endocrinologic diseases can induce muscular diseases. Myopathy caused by exogenous steroid is a common problem in patients prescribed steroids as therapy. We report a case of iatrogenic steroid myopathy in a 55-year-old female who had taken steroids under her own volition at a local pharmacy for more than 3 months due to skin rash and itching. She complained of severe proximal muscle wasting and weakness in the lower extremities and also exhibited other stigmata of Cushing's syndrome such as moon face, buffalo hump or easy bruising. Needle electromyography showed the typical pattern of myopathy. Muscle biopsy revealed intermixed numerous, markedly atrophic and angulated basophilic fibers and a few fat cells without inflammation. In addition there was marked and selective atrophy of type II fiber on ATPase staining in pH 9.4 buffer. After discontinuation of steroid treatment, she has experienced slow improvement through physical therapy, including isotonic exercise.

Effects of Growth Hormone on Steroid-induced Musculoskeletal Changes of Rats

OBJECTIVE: To evaluate the efficacy of growth hormone in reversing glucocorticoid-induced musculoskeletal changes including osteoporosis and myopathy in rats. METHOD: Experimental rats were divided into five groups and each group was composed of 10 rats. The group 1 was administered with saline, group 2 with growth hormone, group 3 with glucocorticoid, group 4 with combined dosages of growth hormone and glucocorticoid, and group 5 with glucocorticoid for 4 weeks and then growth hormone for another 4 weeks. All injections were carried out every other day for 8 weeks. The half of animals were sacrificed after 4 weeks and another half after 8 weeks in each group. The triceps surae muscle was biopsied and examined histologically for the evaluation of mean area of muscle fiber. The femur was removed and dissected for the measurement of its weight, length, and diameter. The bone mineral density of the femur was measured by a dual energy X-ray absorptiometer. RESULTS: Administration of growth hormone partially reversed the complications of steroid such as decrease in body weight, decrease in weight, length, diameter, and bone mineral density of femur, and decrease in mean area of muscle fiber. CONCLUSION: This study indicated that growth hormone could be applied for the management of steroid-induced osteoporosis and myopathy.

Effect of Physical Exercise on Experimental Steroid-Induced Myopathy

BACKGROUND: Steroid myopathy is an unexpected side effect to the prolonged therapeutic use of steroids. To treat steroid myopathy, the followings are recommended; reduction of the steroid dose, usage of a nonfluorinated steroid, and conversion to an alternate day regimen. As muscle loading is encouraged in maintaining normal muscle properties, it is also apparent that physical exercise may be useful in the prevention and treatment of steroid myopathy. METHOD: The experiment was designed to investigate the effects of exercise on steroid myopathy. Rats being treated with triamcinolone acetonide (TA) (5 mg/kg/day) for 7 days exercised on a treadmill (speed 20m/min, 30 min/day, 3 days/week) for 2 weeks. The extensor digitorum longus (EDL) and soleus were then examined histochemically and ultrastructurally. RESULTS: Rats treated with TA showed significant loss of body and muscle weight. In the TA treated group, cross-sectional areas of type II fibers of both EDL and soleus were decreased in comparison with the controls. Necrotic changes were found only in type II fibers of the soleus. Recovery from the weight loss with type II fiber atrophy was more pronounced in the exercise group than that of the sedentary group, but was not significant statistically. Ultrastructural abnormalities, that consisted of subsarcolemmal mitochondrial accumulation, mitochondrial vacuolation, increased number of mitochondria in autophagic vacuoles, and dilatation of sarcoplasmic reticulum, were seen in TA treated muscles. These injuries were significantly reduced by the exercise, however, complete recovery could not be seen. CONCLUSIONS: These results suggest that treadmill exercise for 2 weeks partially ameliorate steroid myopathy in.