Cell damage within the sinusoidal lining of human liver grafts during transplantation is an early event that is critical in ischemia-reperfusion injury and probably plays a key role in primary liver dysfunction after transplantation. No simple biochemical marker for sinusoidal injury is currently av
Creatine kinase BB: A response marker in liver and other organs
✍ Scribed by Stephen D. H. Malnick; Daniel D. Bass; Alvin M. Kaye; Michel Vaubourdolle; Jacqueline Giboudeau; Olivier Chazouillères; Raoul Poupon
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 130 KB
- Volume
- 19
- Category
- Article
- ISSN
- 0270-9139
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✦ Synopsis
We were interested to see the recent paper by Vauboudolle et al. (11, which adds the liver to the growing list of organs in which creatine kinase-BB (CK-BB) has proved a useful response marker.
CK-BB is the major component of the estrogeninduced protein in the rat uterus (2). The immature rat uterus responds to estrogen administration by increased synthesis of mRNA for CK-BB within 30 min (3). The response to estrogen is present within the entire female reproductive tract (4). CK-BB activity also increases in response to a variety of hormones and growth factors. These include estrogens (2-41, vitamin D metabolites, steroid hormones, parathyroid hormone, human growth hormone, prolactin luteinizing hormon+releasing hormone prostaglandm E, and dibutyryl CAMP (5). In the rat, growth hormone and glucocorticoids have been shown to have an additive effect that increases CK-BB activity in the liver (6). In addition, both rat hdney stimulated to undergo hypertrophy by unilateral nephrectomy and rat liver after partial hepatectomy show an increase in CK-BB activity (Somjen D, et al., Unpublished results, 1989).
Vaubourdolle et al. ( 1) have shown that CK-BB is released from damaged sinusoidal cells after an ischemic insult. It would be very interesting to examine CK-BB activity in serum and in the liver for a longer period than 30 min after reperfusion. One might expect a subsequent increase in CK-BB activity. Interestingly, an increase in CK-BB activity has been shown in fetal rat kidney and cerebellum after ischemia (7). It is proposed that the CK response could serve as a metabolic marker €or ischemia, representing part of a compensatory mechanism to overcome the energetic gap after an ischemic insult. Furthermore, it is possible to examine noninvasively by magnetic resonance spectroscopy changes in the concentration of creatine phosphate and ATP, which reflect the CK activity (8).
In summary, CK-BB may be stimulated by any agent or situation involving modulation of energy regeneration. We believe that CK-BB may serve as a response marker in liver as it already does for brain (9).
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