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Evaluate muscle wasting process. High levels are found in progressive Duchenne muscular dystrophy (MD). Elevations occur in carriers of MD, in limb-girdle dystrophy and other dystrophies, in dermatomyositis, polymyositis, and trichinosis, but not in neurogenic atrophies (eg, multiple sclerosis or in myasthenia gravis).
As muscle mass diminishes, aldolase decreases. Serum aldolase elevation is not specific for muscle disease since it is present in many tissues (see Additional Information).
In the progressive dystrophies, aldolase levels may be 10 to 15 times normal when muscle mass is relatively intact, as in early stages of the disease. When advanced muscle wasting is present, values decline. In the inflammatory myopathies (eg, dermatomyositis) serum aldolase (as well as CK) levels may be applied to monitoring the response to steroid therapy. They are of particular value in guiding tapering of steroid administration.1 No elevation is found in muscular dystrophy secondary to alteration of the nerves or nerve centers.
Aldolase is present as a tetramer composed of two of three known subunits designated A, B, and C. Of the four isoenzymes, AAAA is predominant in skeletal muscle, BBBB predominates in liver, and CCCC in brain and other tissue. A hybrid isoenzyme, AAAC is present in tissues but at a lower concentration.2 The enzymatic method determines total enzyme activity and thus is not specific for muscle aldolase.
Elevated aldolase levels may be found with hepatitis, other liver diseases, myocardial infarction, hemorrhagic pancreatitis, gangrene, delirium tremens, and in some cases of neoplasia. In cases of acute viral hepatitis, increase in serum aldolase tends to parallel ALT (SGPT) levels and is usually up to 20 times the average of normal. Normal results are usually obtained in portal cirrhosis and obstructive jaundice. A small fraction of cases of measles in young adults has been reported to have significant elevations of serum CK and aldolase.3,4 Serum aldolase and CK may be elevated in the serum of patients who have taken L-tryptophan and develop eosinophilia-myalgia syndrome.5
1. Visnapuu LA, Karlson LK, Dubinsky EH, Szer IS, Hirsch CA. Pediatric reference ranges for serum aldolase. Am J Clin Pathol. 1989 Apr; 91(4):476-477. PubMed 2929505
2. Gendler SM. Aldolase. In: Pesce AJ, Kaplan LA, eds. Methods in Clinical Chemistry. St Louis, Mo: Mosby-Year Book Inc; 1987: 872-875.
3. Leibovici L, Sharir T, Kalter-Leibovici O, Alpert G, Epstein LM. An outbreak of measles among young adults. Clinical and laboratory features in 461 patients. J Adolesc Health Care. 1988 May; 9(3):203-207. PubMed 3372286
4. Gavish D, Kleinman Y, Morag A, Chajek-Shaul T. Hepatitis and jaundice associated with measles in young adults. An analysis of 65 cases. Arch Intern Med. 1983 Apr; 143(4):674-677. PubMed 6838292
5. Kilbourne EM, Swygert LA, Philen RM, et al, Interim guidance on the eosinophilia-myalgia syndrome. Ann Intern Med. 1990 Jan 15; 112(2):85-86. PubMed 2153013
