Albeit the pathogenesis of CMP is not entirely
implicated. Furthermore, variability of the cellular and humoral immune
arrangement are universally experimental, and myocardial inflammation is one of
the commonest devices in CMP 1, 2. Our data make several contributions to the
pathophysiology of MIF  and its role in
unique immune responses, and its disparities in levels are concerned as
dominant role in many disease states. CMP may afford a cruel of early
identification, genotype-based therapy, and even avoidance of the disease
6,15,16. We considered correlations of MIF genotypes with clinical and
laboratory findings of the disease and established that other serum
electrolytes levels were higher in patients with MIF GC genotype than the other
genotypes. On another hand, the valvular damage in rheumatic heart diseases
(RHD) is triggered by recurrent rheumatic insults 17. The role of MIF’s in
the early stages of the disease has up till now to be measured. Over the
disease course, the valves become thickened and, ultimately, stenosed. It had
been reported that MIF able to clear certain pathogens and apoptotic cells 17,
18, which allows to protect cardiomyocytes and delay valvular damage 17.
Contrariwise, recurrent rheumatic offenses in the incidence of MIF may surge
inflammatory cell enrollment and certify proinflammatory mediators,
consequently improving regional inflammation and destructive cardiac tissue 4,
19-20. Polymorphism of the human MIF gene (-173) has been testified, and this
polymorphism would readily overstate hosts to reformed vulnerability to or
severity of inflammatory or infectious disease 4 Cardiac patients with -173 C
allele had amplified ranks of MIF, and it also had been associated with severe
clinical manifestations and poor outcome of inflammatory disease 4, 18.
Clearly, MIF dissimilarities impact disease brutality and development;
accordingly, future clinical studies need to analyze data that include disease
stage and other clinical data. However, it was studied that no association was
found between the distributions of 
genotyping of MIF -173 G/C polymorphism and other inflammatory diseases 15.
Nevertheless, Donn et al., offered that MIF -173 C allele was associated with
juvenile idiopathic arthritis 21. However, Berdeli et al., showed that the
MIF -173 C allele was a poor outcome interpreter in juvenile rheumatoid
arthritis 7. Moreover, MIF-173 C allele had an expressively larger number of
joints in patients with juvenile idiopathic arthritis with active arthritis and
was related with an unfortunate response to glucocorticoids 22. Nevertheless,
it has been shown that MIF plays an important role in heart disease 23 For
example, Miller et al., demonstrated that adenosine monophosphate-activated
protein kinase (AMPK) activation was excited by the release of MIF out from
ischemic cardiomyocytes which endorsed glucose uptake, and thus guarded the
heart against ischemia-reperfusion injury. Accordingly, AMPK and stress
suppression play a protective role in myocardial infarction (MI) 23-26. In
the present study, five patients with dilated CMP  had detected with homozygosity for MIF-173 C
allele. It has been revealed that it has an important component in the
pathogenesis of dilated CMP with higher MIF level and cardiac inflammation
2,15,27,28. Therefore, we proposed that CC genotype in our patients may be
moderately responsible from inflammation in dilated CMP, and MIF polymorphism
may promote to MIF release from cardiomyocytes in patients with CMP. However,
we could not find any noteworthy affiliation between MIF genotypes and other
electrolytes and cardiac functions. In addition, our present study showed that
plasma sodium levels were developed in patients with MIF CC genotype than the
other genotypes this result was well-matched with others who reported that
plasma brain natriuretic peptide (BNP) concentrations were amended in numerous
forms of heart disease with impaired left ventricular systolic function with
cardiomyopathy 19, 29. Yet, we could not settle whether CC genotype of MIF
has any effect on BNP with this study. However, in patients with recognized
disease, lower expression alleles are associated with concentrated end-stage
organ involvement 17.  In addition,
other reported that MIF alleles with higher gene expression (173C and 794
extended alleles) are associated with a lower risk of systemic lupus
eyrthromatus SLE 30,31.

This study is the first to investigate the MIF gene
polymorphisms in Egyptian people with CMP. We suggested that GG genotype of MIF
(-173) gene may be a risk factor for CMP patients. Conversely, further studies
with larger samples are desirable to report the meticulous role of this
polymorphism in CMP and to explore whether modulation of MIF might have a
stimulus on perturbation on atherosclerotic disease in this high-risk
population tact.

Limitations, and future scope

Some limitations of this study should be mentioned.
Firstly, this study was only focused on CMP patients in Egypt. Our findings
still need to be certified in a larger population. Secondly, plasma levels of
MIF and other cardiac markers were not measured in this study. Therefore, we
cannot precisely determine the prospective mechanism and practical consequence
of MIF gene polymorphism on the risk of CMP with DM. Finally, increased MIF
plasma levels are features of CMP. We believe these data provide new
perspectives on the pathophysiology of CMP and DM. Obtaining this information
would facilitate identification and development of new therapeutic targets in
patients with cardiac dysfunction and associated with an abnormal increase in
blood sugar levels.