Bone Abstracts

Introduction: The creatine kinase (CK) is a dimeric enzyme, involved in energetical metabolism. It is present in many tissues, but higher concentration in skeletal and cardiac muscle.

Therefore, conditions that involve muscle tissue may increase this serum enzyme. Such enzyme elevation is usually observed in inflammatory myopathies and others autoimmune diseases.

Sometimes some elevation in CK is not fully understood out off these contexts, especially in absence of characteristical symptoms in muscle: weakness, myalgia and fatigue.

Objetive: We study patients with or without symptoms having raising ck found in laboratory tests.

Materials and methods: Were assessed patients at our rheumatology unit, with CK values greater than minimum of three timesof the normal value. Diagnostic procedures performed: interrogatiory, Exhaustive physical examination (muscle strength, muscle tone, and OTR), laboratory tests: CRP, ESR, protein electrophoresis, ANA and others auntoantibodies, according to the clinical context (Jo and MI); TSH, transaminases, EMG, muscle biopsy, and immune tagging (dystrophin, sarcoglcans, and calpain), according to appropriate procedure.

Isolated increased of the enzyme, required more intensive investigations to rule out other causes of elevations or situations that raise CK. (heart attack, rabdomiolisis, iatrogenic, toxics, endocrine: hypo/hyperthyroidism, Cushing’s diseases, hypoparathydoidism, infectious myopathy, myotonias, storage diseases, and glycogenosis (Pompe disease and McArdle disease), mitochondrial myopathy, and neuromuscular (ELA, mutations of gen cav-3).

Results: Of all patients (n 128), of both genders with CK elevations we found a dominant distribution of PM/DM (78%), among others colagen diseases(9.4%), such as RA, SEL, SSc, vasculitis, sarcoidosis, and sudeck. Also significant increases medicated patients with toxic effects (4.7%: statins, zidovudine), endocrine (3.9%): hypo/hyperthyroidism, Cushing’s diseases, hypoparathydoidism, vitamin D deficiency, and muscle dystrophy (2.3%): steinert, distrophinopathy, Nieman Pick, and amyotrophic lateral sclerosis. Patients in whom was no probable cause was found for the enzyme elevations (1.6% idiopathic).

Conclusions: There are many diseases that can generate elevations of CK, many of wich are accompanied by clear symptomatology but others less do so.

The challenge is getting to elucidate the cause of the enzymatic elevations not covered in the usual diagnostic or included within the group of idiopathic hipeckemia.