After adjustment for age, gender, and serum ACE levels, a significant association between the carriage of at least one C allele of the COX2.3050G>C polymorphism and systemic sarcoidosis was observed (odds ratio [OR]: 2.3; 95% confidence interval [CI]: 1.03-5.12, p = 0.031).
Raised angiotensin converting enzyme levels, interstitial lung disease on CT chest, and non caseating granulomas on skin biopsy clinched the diagnosis of sarcoidosis.
In this study, we developed a new method for genotyping the I/D polymorphism in ACE and established genotype-specific reference intervals in order to improve the diagnostic accuracy and the value for treatment of sarcoidosis.
The aim of this study was to determine sensitivity of (18)F-FDG PET, genotype-corrected ACE and sIL-2R in active sarcoidosis as well as their correlation.
ACE insertion/deletion (I/D) gene polymorphism has been reported to have an association with SACE levels in sarcoidosis, but no evidence of an association between angiotensin II receptor gene polymorphism and SACE in this disease has been found.
In 105 sarcoidosis patients (69 female, 36 male, mean age: 41+/-1 years) and in 80 sex- and age-matched control subjects, genotyping for the ACE gene I/D polymorphism was performed by PCR and restriction enzyme digestion.
ACE and sIL2-R serum levels were significantly higher in M. tuberculosis positive sarcoidosis independent of the HLA-DRB1 specificity, but did not differ between acute and chronic disease course alone.
These results indicate that the ACE gene I/D polymorphism might be a risk factor for sarcoidosis susceptibility in the Slovene population and imply the possible role of population origin in the modulation of the influence of ACE gene variability in the pathophysiology of sarcoidosis.
In conclusion, the present authors recommend the use of new, genotype-specific reference values for serum angiotensin-converting enzyme levels, especially to improve the sensitivity and specificity of tests for angiotensin-converting enzyme in the follow-up of sarcoidosis.
ACE genotyping was performed in 72 consecutive patients with sarcoidosis and 199 controls (96 normal healthy individuals and 103 tuberculosis patients taken as disease controls).
Angiotensin converting enzyme deletion genotype has been linked to hypertension and sarcoidosis and has been reported to regulate liver fibrosis in HCV-mediated liver disease.
We earlier reported that ACE and its enzymatic product, angiotensin II (A-II), might play a role in maintaining macrophage/T lymphocyte alveolitis by enhancing an accessory function of macrophages in chronic active cases with sarcoidosis.
To find potential factors which may have a deleterious influence on arterial performance, different subgroups of sarcoidosis, such as sarcoidosis with or without cortisone therapy, pulmonary sarcoidosis in early and advanced stages, pulmonary sarcoidosis alone or combined with extrapulmonary sarcoidosis, and sarcoidosis with or without elevated blood levels of angiotensin converting enzyme (ACE)/soluble interleukin 2 receptor (sIL-2R) were investigated.
A boy was diagnosed as having juvenile sarcoidosis because he presented with cervical and pulmonary lymphadenopathy with epitheloid cells and granuloma formation and high angiotensin converting enzyme.Later, a liver abscess was diagnosed.
This study has the aim to evaluate the association of CHITO activity, ACE, hs-CRP or a combination of these biomarkers and to construct a clinical algorithm to differentiate between sarcoidosis activity/remission status.