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J L Trueba

Publications and source records attributed to J L Trueba.

7 recordsLinked to original sources

[Hypothyroid myopathy. Clinico-pathologic study of 20 cases].

20 patients afflicted with primary hypothyroidism were studied in order to evaluate the association of clinical or sub-clinical myopathy, detected by neurophysiological (electromyography) (EMG) or neuropathological methods (muscular biopsy with enzymatic study). 70% of the patients had muscular weakness (moderate in 30% and severe in 40%) of the scapular and pelvic muscles. 60% of the patients had muscular cramps. There was no myodema nor muscular atrophy or hypertrophy. Seric CPK was high in 70% of the cases. EMG was myopathic in 65%. All cases with weakness registered EMG alterations. The histological findings were import findings were important. The enzymatic techniques showed alterations of the fiber subtypes in 90% of the cases. The type I fibers had sarcolemmal and mitochondrial accumules in 85% and 70% had areas without oxidative activity, similar to "core". In this study, we did not find any correlation between the evolution time of hypothyroidism, hormonal levels, CPK increase, and muscular weakness. The EMG was myopathic in cases with severe weakness, however, in patients with moderate weakness it could also prove abnormal. There was no correlation between the electric myopathic pattern, CPK levels and thyroid hormones.

Adult

[Thyroid myopathy. Effect of treatment with thyroid hormones].

We studied 20 patients afflicted with primary hypothyroidism and treated with thyroid hormone replacements, with the aim of evaluating the clinical, biochemical, EMG and anatomo-pathological effects. Cramps, as well as subjective and objective proximal muscular weakness, disappeared. Seric CPK was normalized in all cases after 1-8 weeks of treatment. EMG myopathic patterns faded away in all cases. Anatomopathological changes took longer to observe; 5 cases with new biopsy showed an isolate atrophy of type II fibers, one of them after 18 months in treatment; type I fibers had mitochondrial accumula without change compared to the initial biopsy. There was a clear tendency for the destroyed fibers to become normalized and for the structures similar to the "core" to vanish.

Adult

Myotonic dystrophy associated with thyroid disease.

Two patients with hereditary, clinical, electromyographical and histological data typical of myotonic dystrophy are discussed. In both there was a thyroid disorder. The first patient had primary hypothyroidism, and the second a non-toxic multinodular goiter which necessitated total thyroidectomy. The EMG findings and the muscle histopathology of both patients are commented on and compared with the changes described in hypothyroidism. The disease processes in both patients are also discussed in relation to the muscle and metabolic changes described in myotonic dystrophy. The coexistence of these two diseases is not explicable in the light of present knowledge on the basis of a known genetic predisposition. Only two similar cases of myotonic dystrophy and hypothyroidism have been reported.

Adult