Sera from patients with myocardial infarction and cardiac arrhythmias were analyzed for myoglobin concentration and the activities of total creatine kinase, creatine kinase isoenzyme-2, and lactate dehydrogenase isoenzyme-1 at the time of hospital admission and during the first few days of hospitalization. The nine patients with a final diagnosis of myocardial infarction had abnormally high values for total creatine kinase, creatine kinase-2, lactate dehydrogenase-1, and myoglobin. Myoglobin concentrations were highest on admission in six patients and on the day after admission in the other three patients. Creatine kinase-2 manifested maximum activity on the day after admission for all patients with myocardial infarction. Lactate dehydrogenase-1 did not reach maximal values until the second or third day after admission. The six patients with arrhythmias did not show any significant increases in creatine kinase-2 or lactate dehydrogenase-1. Myoglobin and total creatine kinase, however, were increased in the four patients who had received cardioversion. The specificity and diagnostic usefulness of these serum measurements are discussed.
BACKGROUND: Soluble forms of RAGE (sRAGE) have been found circulating in plasma and tissues. Evidence is accruing in human subjects linking levels of sRAGE to oxidative stress in many disorders. Because sickle cell disease (SCD) is a state of oxidative stress, we tested the hypothesis that circulating sRAGE levels may be involved in the vascular pathology of SCD. OBJECTIVES: To determine the sRAGE levels in children and adolescents with SCD and investigate their association with markers of hemolysis, iron overload, and SCD-related organ complications. SUBJECTS AND METHODS: The level of sRAGE was measured in 40 children and adolescent with SCD compared with 40 healthy controls using enzyme-linked immunosorbent assay (ELISA). RESULTS: sRAGE was significantly higher in patients compared with controls (p < 0.001) and was elevated in patients with history of stroke, acute lung syndrome, and frequency of sickling crisis or serum ferritin > 2500 (p < 0.05). Patients with high sRAGE levels are candidates for chelation. sRAGE was positively correlated with HbS% (r = 0.422, p = 0.007), LDH (r = 0.329, p = 0.038), and serum ferritin levels (r = 0.516, p = 0.001). Multivariable regression analysis proved that both HbS% and serum ferritin were significant independent factors affecting sRAGE level (p < 0.05). CONCLUSION: Our findings suggest that sRAGE may be considered as a marker for vascular dysfunction in SCD patients.
Purpose
To assess dry eye disease (DED) in thalassemic adolescents by evaluating corneal epithelial thickness (CET) and various dry eye clinical tests and correlate them to tissue iron overload.
Methods
The study included 120 Beta-thalassemia patients (11 to 18 years) and 120 matched controls. CET maps were captured using anterior segment optical coherence tomography. OSDI questionnaire was completed. Dry eye tests included Schirmer test, tear film breakup time (TBUT), and ocular surface staining (OSS) with fluorescein and lissamine green. We recorded serum ferritin level, and liver iron concentration (LIC) measured by magnetic resonance imaging.
Results
Superior and inferior CET was thinner, while map standard deviation (MSD) was higher in thalassemics compared to controls (all P<0.001). Thalassemic group also showed higher OSDI scores (P<0.001), shorter TBUT (P<0.001), and higher OSS grades (P<0.001). Both superior and inferior CET was correlated positively with TBUT, and negatively with OSS (all P < 0.001). Serum ferritin and LIC showed negative correlations with CET (superior and inferior, both P< 0.001), positive correlations with MSD, P< 0.001, as well as with TBUT (P< 0.001), OSS (P< 0.001), and OSDI scores (P< 0.001).
Conclusion
Thalassemic adolescents had thinner CET with higher thickness’ variability, shorter TBUT and more marked OSS than controls. Correlation of higher serum ferritin and hepatic iron overload with irregular epithelial thinning and more affected dry eye tests results supports our hypothesis that high tissue iron levels could play a pivotal role in DED pathogenesis in thalassemic patients.
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