Pyruvate kinase (PK) plays a critical role in glycolysis by catalyzing the conversion of phosphoenolpyruvate and ADP into ATP and pyruvate. As one of the key rate-limiting enzymes in this metabolic pathway, PK exists in multiple isoforms, including M-type and L-type. The M-type further divides into M1 and M2 subtypes. M1 is predominantly found in the heart, skeletal muscle, and brain, while M2 is more common in the brain and liver. The L-type is mainly present in the liver, kidneys, and red blood cells. During myocardial necrosis, PK is released into the bloodstream, making it a useful biomarker for diagnosing myocardial infarction.
The normal serum PK level is typically around (28.3 ± 12.8) U/L, as measured by the pyruvate kinase method. Clinically, increased PK activity is a significant indicator of acute myocardial infarction. It begins to rise within 2 hours after an infarct, peaks at 22–24 hours (about three times the control value), and reaches its highest point on the second day (up to four times the control). The levels gradually return to normal after 48–72 hours. Compared to other markers like CK, PK is considered more specific for myocardial infarction, though less sensitive. Due to its short-lived elevation, it is often used in conjunction with other diagnostic tools. Some researchers consider PK a fast, simple, and reliable marker for acute myocardial infarction.
In addition to cardiac conditions, elevated serum PK activity has been observed in various malignancies such as cervical cancer, lymphosarcoma, myeloid leukemia, and Hodgkin’s disease. In muscular disorders—such as Duchenne and Becker muscular dystrophy, limb-girdle muscular dystrophy, and facioscapulohumeral muscular dystrophy—serum PK activity can increase dramatically, up to 25 times the normal level, with a positive detection rate exceeding 90%. In contrast, neurogenic diseases like spinal muscular atrophy or amyotrophic lateral sclerosis usually show normal PK levels. This distinction makes PK testing valuable in differentiating between myogenic and neurogenic myopathies.
In hematological conditions, red blood cell PK activity is significantly reduced in patients with congenital non-spherocytic hemolytic anemia. Similar decreases are seen in other blood disorders, including acute leukemia, erythroleukemia, aplastic anemia, ineffective anemia, paroxysmal nocturnal hemoglobinuria, and congenital hypoplasia. In these cases, PK activity may drop to as low as 50% of the control value.
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