Pyruvate kinase (PK) plays a crucial role in glycolysis by catalyzing the conversion of phosphoenolpyruvate and ADP into ATP and pyruvate. It is considered one of the key rate-limiting enzymes in this metabolic pathway. There are two main isoforms of PK: M-type and L-type. The M-type includes subtypes M1 and M2, with M1 primarily found in heart muscle, skeletal muscle, and brain tissue, while M2 is more common in the brain and liver. The L-type is predominantly present in the liver, kidneys, and red blood cells. When heart muscle cells die, PK is released into the bloodstream, making it a useful biomarker for diagnosing myocardial infarction.
The normal serum PK activity level is approximately (28.3 ± 12.8) U/L, measured using the pyruvate kinase method. Clinically, PK has several important applications. Following an acute myocardial infarction, PK activity begins to rise within 2 hours, peaks at 22–24 hours (about three times the baseline), and reaches its highest point on the second day (up to four times the control value). The levels gradually return to normal after 48–72 hours. This makes PK a more specific indicator for acute myocardial infarction compared to other enzymes like CK. However, some studies suggest that PK is less sensitive than CK but more specific. Due to its short duration of elevation, it is often used alongside other markers for better diagnostic accuracy. Some experts consider PK as a simple, fast, and reliable marker for detecting acute myocardial infarction.
In addition to cardiac conditions, elevated serum PK activity has been observed in various malignancies, including cervical cancer, lymphosarcoma, myeloid leukemia, and Hodgkin’s disease. In patients with myogenic disorders such as Duchenne muscular dystrophy, Becker muscular dystrophy, limb-girdle muscular dystrophy, and facioscapulohumeral muscular dystrophy, serum PK activity can increase dramatically—up to 1–25 times the normal level—with a positive detection rate exceeding 90%. In contrast, in neurogenic conditions like spinal muscular atrophy or amyotrophic lateral sclerosis, serum PK levels are typically within the normal range. This distinction helps in differentiating between myopathic and neurogenic muscle diseases.
In hematological disorders, red blood cell PK activity is significantly reduced in patients with congenital non-spherocytic hemolytic anemia. Similarly, in conditions like acute leukemia, erythroleukemia, aplastic anemia, ineffective anemia, paroxysmal nocturnal hemoglobinuria, and congenital hypoplasia, red cell PK activity may drop to as low as 50% of the control value.
For researchers and clinicians, tools such as ELISA kits, SOD kits, IgG and IgM kits, Western blot tests, immunohistochemistry, radioimmunoassay, GIBCO, and AMRESCO-Shanghai Xinfan provide essential support in analyzing these biochemical markers.
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