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Clinical Observation |

Presymptomatic Neuromuscular Disorders Disclosed Following Statin Treatment

Georgios Tsivgoulis, MD; Konstantinos Spengos, MD; Nikolaos Karandreas, MD; Marios Panas, MD; Athina Kladi, MS; Panagiota Manta, MD
Arch Intern Med. 2006;166(14):1519-1524. doi:10.1001/archinte.166.14.1519.
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It is well recognized that statins affect muscular tissue adversely and that their use is associated with clinically important myositis, rhabdomyolysis, mild elevation of serum creatine kinase (CK) levels, myalgias, muscle weakness, muscle cramps, and persistent myalgias or serum CK level elevations after statin treatment is discontinued. The association between statins and the disclosure of presymptomatic metabolic myopathy is another underrated phenomenon related to statin therapy that was recently recognized in rare cases. The purpose of this report is to provide additional support for this association and to report other neuromuscular disorders that have also been seen following statin intake. The present case series illustrates that statins may act as unmasking agents in asymptomatic patients with a latent neuromuscular disorder. Thus, it may be postulated that statin intake may be a sufficient insult to precipitate neuromuscular symptoms and substantially increase muscle enzymes in presymptomatic patients with an abnormal neuromuscular substrate. In conclusion, muscular symptoms or increased serum CK levels persisting after statin treatment discontinuation should alert the clinician to pursue further diagnostic evaluations for the detection of potential underlying neuromuscular diseases.

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Figure 1

. Muscle biopsy specimens and histochemical studies (original magnification for all ×500). A, Periodic acid-Schiff (PAS)-stained frozen section illustrates muscle fibers containing subsarcolemmal vacuoles (arrows) with PAS-positive material in case 2. B, Absent stain for the enzymatic activity of phosphorylase in muscle fibers of case 2; normal stain for the enzymatic activity of phosphorylase in the smooth muscle fibers of the vessel (arrows). C, Normal stain for the enzymatic activity of phosphorylase in muscle fibers of a control patient. D, Gomori trichrome stain demonstrating ragged red fibers (arrows) in case 3; the peripheral rim of red staining in some fibers represents aggregates of mitochondria. E, Succinate dehydrogenase (SDH) stain demonstrating intense activity in some fibers (ragged blue fibers) (arrows); these fibers correspond to the ragged red fibers on Gomori trichrome stain. F, Cytochrome oxidase (COX) stain demonstrating COX-negative fibers (arrows); these fibers correspond to the ragged blue fibers on SDH stain.

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Figure 2.

Atrophy of the tongue in case 4. The marked wasting of the large group of glossal muscles on each side has caused them to separate and form a longitudinal midline furrow.

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