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Atrophy of Skeletal Muscle in Patients With Cushing's Syndrome
David E. Pleasure, MD;
Gregory O. Walsh, MD;
W. King Engel, MD
Arch Neurol. 1970;22(2):118-125.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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CUSHING'S syndrome or therapy with any of the glucocorticoids may cause proximal muscular weakness.1,2 Muscle wasting is usually apparent clinically. Occasional fibers undergoing degeneration and scattered atrophic fibers have been described in muscle biopsy specimens.1,3,4 In this paper, histochemical studies of affected muscle in two patients with Cushing's syndrome are described and indicate that the grossly visible wasting can be accounted for by a diminution in diameter of practically all muscle fibers, with atrophy being more prominent in the type II (high in myofibrillar adenosine triphosphatase [ATPase] and phosphorylase) than in the type I (low in myofibrillar ATPase, high in most mitochondrial oxidative enzymes) fibers.5 There was no evidence of a myopathic process in the usual sense of necrosis, phagocytosis, cellular infiltrates, or endomysial connective tissue proliferation. The potassium content of muscle was diminished.
Report of Cases
CASE 1.—This 67-year-old woman was confined to bed during
. . . [Full Text PDF of this Article]
Author Affiliations
Bethesda, Md
From the Medical Neurology Branch, National Institute of Neurological Diseases and Stroke, Bethesda, Md.
Footnotes
Submitted for publication July 12, 1969; accepted Sept 17.
Reprint requests to Medical Neurology Branch, National Institute of Neurological Diseases and Stroke, Bethesda, Md 20014 (Dr. Engel).
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