OBJECTIVETo study the clinical significance of changes of serum myocardial enzymes in patients with acute carbon monoxide poisoning.

METHODSTo determine the dynamic changes of the activity of myocardial enzymes and ECG in 62 patients with acute CO poisoning.

RESULTSIn patients with acute CO poisoning 5 kinds of myocardial enzymes begin to increase within 24 hours, the activities of aspartate aminotransferase (AST), creatine phosphokinase (CPK), lactic dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH), CPK isoenzyme (CK-MB) were (20.2 +/- 12.3), (151.6 +/- 91.8), (146.8 +/- 50.4), (154.8 +/- 47.7), (13.8 +/- 8.1) U/L respectively, while those in control group were (12.1 +/- 6.7), (90.6 +/- 17.3), (118.7 +/- 13.5), (89.9 +/- 27.9), (5.9 +/- 3.3) U/L respectively. There was significant difference between two groups (P < 0.01); 3 d later, the activities of 5 enzymes were still increased [(21.3 +/- 12.3), (105.8 +/- 51.4), (144.8 +/- 51.4), (159.8 +/- 35.4), (16.2 +/- 9.1) U/L respectively]. 7 and 12 d later, the activities of alpha-HBDH and CK-MB were still higher than those of control (P < 0.01). LDH(1) and LDH(2) increased to peak value in 24 h after poisoning (35.3 +/- 5.8), (43.8 +/- 5.7) U/L vs (24.8 +/- 3.9), (36.9 +/- 4.3) U/L, P < 0.01. The abnormal rate of serum LDH(1) was 78.7%, LDH(2) 58.3%, LDH 45.2%, CK-MB 37.1%, alpha-HBDH 33.6% and the abnormal rate of ECG was less than 10%.

CONCLUSIONAcute carbon monoxide poisoning may cause myocardial injury. Determination of serum myocardial enzymes may contribute to showing myocardial injury, early diagnosis and treatment, results of treatment and prognosis.

Adult ; Carbon Monoxide Poisoning ; blood ; enzymology ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; Female ; Humans ; Hydroxybutyrate Dehydrogenase ; blood ; Isoenzymes ; blood ; L-Lactate Dehydrogenase ; blood ; Male ; Middle Aged ; Myocardium ; enzymology

BACKGROUNDRecent studies have identified signal transducer and activator of transcription 4 (STAT4) as a susceptibility gene for systemic lupus erythematosus (SLE) in different populations. In order to examine whether the allele distribution of the single nucleotide polymorphism (SNP) in gene STAT4 rs7574865 in patients with SLE is different from those of healthy controls in Chinese Northern Han population, we investigated whether the variants of STAT4 rs7574865 were associated with any specific clinical features of SLE.

METHODSWe genotyped SNPs in STAT4 rs7574865 in 252 patients with SLE and 497 healthy controls. All subjects were from the Northern part of Chinese Han population. The genotypes in rs7574865 were determined by polymerase chain reaction (PCR) and consequence direct sequencing of PCR products in the DNA samples.

RESULTSThere was a significant difference in distribution of the SNPs in rs7574865 between the SLE patients and healthy controls. Compared with healthy controls, there was a significant correlation between TT genotypes in rs7574865 and the risk of SLE when GG genotype was used as a reference genotype after adjusting for gender and age. The frequency of T allele in the SLE patients was strongly significantly higher than that of healthy controls. Furthermore, there was a significant difference in the distribution of SNP in rs7574865 between male and female SLE patients, when compared with healthy controls. The frequency of T allele in rs7574865 in male patients was significantly higher than that of male healthy controls or female patients. There was no significant correlation between the frequencies of T allele in STAT4 rs7574865 and the clinical features of SLE.

CONCLUSIONSThe SNP rs7574865 in STAT4 is strongly associated with risk of SLE in the Chinese Northern Han population. The TT genotype and T allele in STAT4 rs7574869 are susceptibility factors for SLE, especially for male SLE patients.

Adult ; Asian Continental Ancestry Group ; genetics ; Female ; Genetic Predisposition to Disease ; genetics ; Genotype ; Humans ; Linkage Disequilibrium ; genetics ; Lupus Erythematosus, Systemic ; genetics ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; genetics ; STAT4 Transcription Factor ; genetics ; Young Adult