Reasons for increasing the MB fraction of creatine kinase
Last reviewed: 19.10.2021
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The presence of the BB fraction in the blood can simulate an increase in the MB fraction, up to an excess of MB-fraction activity over the total creatine kinase. CC-BB appears when the blood-brain barrier is broken (after brain operations or trauma). BB-fraction also appears with serious damage to the intestine and after childbirth (especially with caesarean section).
Increase in the activity of total creatine kinase and MB-fraction is revealed after operations or diagnostic manipulations on the heart. Radiation therapy of the breast area can also cause a slight hyperfermentation. Tachyarrhythmia or heart failure rarely cause an upsurge in creatine kinase and KK-MB activity.
Increase of the fraction of KK-MB in some cases is possible with myocarditis and myocardial dystrophies, however, it usually accounts for less than 3% of the total creatine kinase.
Damage to the skeletal muscles is accompanied by a significant increase in the activity of the MM-fraction, which can "simulate" the MB-fraction. With rhabdomyolysis, the diagnostic sensitivity of the study of the activity of creatine kinase (increased 5-fold or more) is higher than that of aldolases, AST and LDH.
Diseases and conditions accompanied by increased activity of creatine kinase and CC-MB in serum
- Physical stress and muscle trauma.
- Increased muscle mass as a result of exercise.
- Physical stress (overload).
- Surgical interventions, direct trauma, intramuscular injection.
- Acute psychosis, acute brain damage, coma (necrosis of muscles with bedsores).
- Spasms (epilepsy, tetanus), childbirth.
- Severe burns; electric shock.
- Degenerative and inflammatory lesions.
- Muscular dystrophy.
- Myositis (collagenoses, viral infections, trichinosis).
- Myocarditis.
- Toxic muscle damage.
- Acute alcohol poisoning, white fever.
- Exogenous intoxication (bromides, barbiturates, carbon monoxide).
- Tetany.
- Medications (clofibrate, bronchodilators).
- Toxic rhabdomyolysis (heroin, amphetamines).
- Malignant hyperthermia.
- Metabolic muscle damage.
- Hypothyroidism.
- Metabolic rhabdomyolysis (hypokalemia, hypophosphatemia, hyperosmolar conditions).
- Glycogenosis (type V).
- Hypoxic lesions of muscles: shock, peripheral embolism, hypothermia.