Increased S100B serum levels in dilated cardiomyopathy patients.

BACKGROUND: The S100B protein is considered a biochemical marker for brain injuries. However, our group demonstrated that the isolated rat heart releases S100B. In this study, we investigated the serum levels of S100B in dilated cardiomyopathy (DCM) patients to evaluate its levels in heart disease. METHODS AND RESULTS: We selected DCM patients, excluding any condition that could influence S100B serum levels. Control individuals were sex and age matched. Both groups were submitted to clinical evaluation and echocardiography. We measured the S100B and NT-proBNP serum levels (expressed as median [interquartile range]). NT-proBNP levels in patients group (1462 pg/mL [426-3591]) were higher than in controls (35 pg/mL [29-55]), P < .001. S100B serum levels were higher in patients group (0.051 microg/L [0.022-0.144]) than in controls (0.017 microg/L [0.003-0.036]), P = .009. Additionally, we found a positive correlation between S100B and NT-proBNP serum levels only in patients group (Spearman's coefficient r = 0.534; P = .013). CONCLUSIONS: Although we cannot rule out the influence of S100B from brain, the positive correlation between S100B and NT-proBNP levels in DCM patients points to the myocardium as the main source for the rise in S100B serum levels.

The ischemic rat heart releases S100B.

S100B is an astrocytic protein assessed in cerebrospinal fluid and serum as a biochemical marker of cerebral injuries. However, increasing evidences suggest the influence of extra cerebral sources on its serum levels. Since it was reported that the injured myocardium expresses S100B, we investigated whether the isolated heart releases this protein. The rat hearts were excised and perfused by the Langendorff technique of isolated heart perfusion. After stabilization, 10 hearts (ischemic group) were submitted to 20 minutes of ischemia and 30 minutes of reperfusion, and 5 hearts (control group) were submitted to 50 minutes of perfusion. The perfusion fluid was collected at pre-ischemia, and 0, 5, 10, 15 and 30 min after ischemia (or equivalent in controls) for S100B and cardiac troponin T (a heart injury marker) assays. In the ischemic group, S100B and troponin T levels increased significantly at time 0 min: S100B values [mug/L, median (IQ25/IQ75)] increased from < or = 0.02 (< or = 0.02/0.03) to 0.38 (0.22/0.84), while troponin T values [mug/L, median (IQ25/IQ75)] increased from 0.31 (0.15/0.45) to 2.84 (2.00/3.63). Our results point to the ischemic heart as an extra cerebral source of S100B.

Amiodarone-induced thyroid dysfunction in a tertiary center in south Brazil.

Amiodarone, used in the treatment of cardiac arrhythmias, is associated with thyroid dysfunction. No reports exist on its frequency in southern Brazil, nor studies evaluating the usefulness of clinical scores to diagnose thyroid abnormalities in these patients. This study aimed at determining the prevalence of amiodarone-induced thyroid dysfunction in a representative sample from a tertiary center, to study the conditions associated to this dysfunction and to evaluate the reliability of clinical scores of hypo and hyperthyroidism. One hundred ninety-five amiodarone users were submitted to a clinical and laboratory evaluation. Of these, 2.1% were hyperthyroid, 25.1% hypothyroid and 9.2% had only a high T4. Considering thyroid dysfunction variables researched, thyroid autoimmunity was positively associated (OR 4.8; p= 0.02), and male gender had a trend to a positive association (OR 1.86; p= 0.06). Clinical scores were highly sensitive for hyperthyroidism (100%), but not for hypothyroidism (8%). The low prevalence of amiodarone-induced hypothyroidism suggests that this specific region is iodine-sufficient. All patients receiving chronic amiodarone therapy should be checked for clinical scores for hyperthyroidism and laboratory evaluation should be performed, as a screening for thyroid dysfunction, especially if they are male or have positive microsomal antibodies.

Amiodarone-induced thyroid dysfunction in a tertiary center in south Brazil

Amiodarone, used in the treatment of cardiac arrhythmias, is associated with thyroid dysfunction. No reports exist on its frequency in southern Brazil, nor studies evaluating the usefulness of clinical scores to diagnose thyroid abnormalities in these patients. This study aimed at determining the prevalence of amiodarone-induced thyroid dysfunction in a representative sample from a tertiary center, to study the conditions associated to this dysfunction and to evaluate the reliability of clinical scores of hypo and hyperthyroidism. One hundred ninety-five amiodarone users were submitted to a clinical and laboratory evaluation. Of these, 2.1 percent were hyperthyroid, 25.1 percent hypothyroid and 9.2 percent had only a high T4. Considering thyroid dysfunction variables researched, thyroid autoimmunity was positively associated (OR 4.8; p= 0.02), and male gender had a trend to a positive association (OR 1.86; p= 0.06). Clinical scores were highly sensitive for hyperthyroidism (100 percent), but not for hypothyroidism (8 percent). The low prevalence of amiodarone-induced hypothyroidism suggests that this specific region is iodine-sufficient. All patients receiving chronic amiodarone therapy should be checked for clinical scores for hyperthyroidism and laboratory evaluation should be performed, as a screening for thyroid dysfunction, especially if they are male or have positive microsomal antibodies.