Alterations in Serum Creatine Kinase and Lactate Dehydrogenase: DISCUSSION part 2

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Serum total LD was elevated in all three groups of patients and there was much overlapping between the three groups (Fig 4). This enzyme system was not capable of differentiating the groups from one another. These findings agree with our previous experimental results which suggest that LD may be only minimally elevated by acute bowel infarction but other conditions (such as myocardial infarctions or major aortic recon­struction) can cause elevations above the upper limits of normal for this enzyme.

The ratio of LD/LD/2 was quite capable of differ­entiating patients with AMI from patients with acute bowel infarctions and patients undergoing major AAS (Fig 5). The only patients who had LD,/LD2 ratios greater than 1.00 were those who had electrocardio- graphically proven AMI. None of the patients in the other two groups had this isoenzyme change in any of the serum samples evaluated. Other clinical conditions which can cause this change in LD/LD2 ratio are renal infarction and hemolysis of blood samples. These conditions can be differentiated from acute bowel infarction or myocardial infarction on a clinical basis.

The prospective evaluation of CK and LD and their isoenzymes has important implications for the differ­ential diagnosis of myocardial infarction and necrotic bowel particularly in postoperative aortic surgery patients. Clearly, elevation of the serum CK-MB isoenzyme level is not specific for myocardial infarc­tion. Necrotic bowel must also be considered. The results of this study also explain why other clinical investigators have conflicting results when they looked for CK-MB and CK-BB in the serum of patients with necrotic or ischemic bowel. The elevations in the levels of these isoenzymes were clearly evident in this study, but they were transient. If the blood samples were not taken during the relevant time period, the elevation of these enzymes can be missed. In addition, the transient character of the elevations means that failure to find these isoenzyme levels elevated does not exclude the diagnosis of necrotic bowel.
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FIGURE 4. Serum total LD

FIGURE 4. Serum total LD is presented. Bars represent standard errors of the mean. The horizontal line at 110 IU/L represents the upper limit of normal for our laboratory. Note that all three groups start off with nearly identical value for total LD. Patients having AMI and those with necrotic bowel had significantly greater values for LD by 24 hours following their event than did patients having major aortic reconstructions. These two groups could not be differentiated from one another based on measurement of this enzyme.

In summary, the findings suggest that evaluation of two isoenzyme systems can differentiate between AMI and bowel necrosis as well as the changes which attend major abdominal aortic surgery. With acute bowel infarction, serum С К and LD will be elevated but the presence of both serum CK-BB and CK-MB will suggest the diagnosis of bowel necrosis rather than myocardial necrosis. Confirmation of necrotic bowel may be obtained by analysis of LD isoenzymes which will show an LD^Da ratio less than 1.00 following the infarction. Acute myocardial infarction can be diagnosed by the presence of serum CK-MB bands along with a LD ratio LD/LDg greater than 1.00. In patients who have uncomplicated major aortic recon­struction without any evidence of ischemic necrosis, the serum total LD will be elevated but isoenzyme distributions for LD will be normal with an LD/LD2 ratio which is less 1.00. Only CK-MM, and perhaps, small traces of CK-MB will be detected in the post­operative serum of these patients.
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FIGURE 5.The LD-LD ratios for

FIGURE 5.The LD,/LD ratios for each of the groups of patients studied. All three groups had overlapping initial values. Those patients with necrotic bowel and those having major aortic reconstruction had no deviation from their initial levels at any time throughout the study period. Those patients with AMI had LD,/LD2 ratios that exceeded the 1.00 level by 16 hours following their clinical events and these elevations were maintained throughout the remainder of the study period.

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