Serum heart type fatty acid binding protein levels are not changed in hyperthyroidism.

BACKGROUND: Heart type fatty acid binding protein (H-FABP) is a small protein and released into the circulation when myocardial damage has occurred. Previous studies have demonstrated that H-FABP is closely associated with cardiac and some endocrinologic disorders including prediabetes, metabolic syndrome, and acromegaly. Hyperthyroism is a well-known disorder associated with cardiovascular diseases. We aimed to investigate the effect of hyperthyrodism on H-FABP levels. METHODS: Forty six patients with hyperthyroidism with no known history of coronary artery disease and 40 healthy controls are involved in the study. Serum H-FABP levels are measured using sandwich enzyme-linked immunosorbent assay. RESULTS: There was no significant difference between serum H-FABP levels of patients with hyperthyroidism and controls (871±66 pg/mL, and 816±66 pg/mL, respectively P=0.56). There was no significant correlation between H-FABP, free triiodothyronine (fT3), free thyroxine (fT4), and thyroid stimulating hormone (TSH) levels in patients and controls. CONCLUSIONS: Serum H-FABP levels are not altered in patients with hyperthyroidism.

M30 does not predict the severity of hepatosteatosis, whereas adiponectin level declined with increase of ALT and the severity of hepatic steatosis.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is an emerging problem all over the world. Because NAFLD and polycystic ovary syndrome (PCOS) are both closely related with insulin resistance, it would be necessary to determine the rate of presence of NAFLD in PCOS patients. So, this study aimed to investigate the utility of M30 in PCOS patients for the diagnosis of hepatic injury. METHODS: Eighty patients with PCOS were included in the study. Ultrasonographic examination for the presence of hepatic steatosis, M30 serum level for determining the severity of ongoing apoptotic cell death in liver, and BARD index for defining the hepatic injury were performed during the study. 25-OH vitamin D and adiponectin level in sera were studied using ELISA (Enzyme-Linked ImmunoSorbent Assay). RESULTS: M30 and vitamin D levels did not change significantly with the severity of hepatic steatosis. On the other hand, M30 levels showed a positive correlation with ALT and AST levels, and M30 level suddenly increased with the presence of hepatic steatosis from 159.7 to 170 U/l, however stabilized with the increasing severity of hepatic setatosis. Adiponectin levels decreased with the increasing severity of hepatic steatosis and significantly varied between ALT greater than 40 U/l and less than 40 U/l. CONCLUSIONS: M30 level in serum increased with the appearance of hepatic steatosis and had a positive correlation with a noninvasive hepatic injury test, BARD (BMI, aspartate aminotransferase [AST]/alanine aminotransferase [ALT] ratio [AAR], diabetes mellitus [DM]) index. Adiponectin level decreased with the increasing ALT level and severity of hepatic steatosis.

Potential proteomic biomarkers in assessing liver fibrosis using SELDI-TOF MS.

BACKGROUND/AIMS: The accurate assessment of the severity of liver fibrosis is of paramount importance in determining treatment strategies, response to treatment and prognosis in patients with chronic liver disease. The aim of this study was to investigate potential proteomic biomarkers for assessing stages of hepatic fibrosis. METHODS: Serum samples of 83 patients with chronic liver disease (using METAVIR index, 17 F0, 30 F1, 6 F2, 9 F3, and 21 F4 patients) and 29 healthy controls were analyzed using surface-enhanced laser desorption/ionization time-of- flight mass spectrometry on IMAC30 ProteinChip arrays. Discriminatory peaks between groups were identified using Mann-Whitney U non-parametric test. Comparison of mild (F0, F1) and severe fibrosis (F2, F3, F4) was performed using tree classification (cross-validation) with the Biomarker Patterns Software, version 5.0 (Ciphergen Biosystems, US). RESULTS: No statistically significant discriminatory peak was evident between F0, F1 and F2 fibrosis. More than 30 peaks were found to be discriminatory between patients with cirrhosis (F4) and all other stages of liver fibrosis, including F2 and F3. Six surface-enhanced laser desorption/ionization proteomic features were found to be discriminative for mild (F0, F1) vs. advanced (F2, F3, F4) fibrosis (AUROC ≥0.8, p<0.05, Mann-Whitney test). The decision tree (m/z 4280, 10453 and 6376) yielded a sensitivity of 83.3% (30/36), a specificity of 85.1% (40/47), a positive predictive value of 81.1%, and a negative predictive value of 86.9%, with an AUROC of 0.94. CONCLUSIONS: The results of this study revealed discriminatory peaks between the protein profiles of patients with cirrhosis and other stages of liver fibrosis. Potential proteomic biomarkers can be notably determined for discriminating mild and advanced fibrosis using surface-enhanced laser desorption/ionization time-of- flight mass spectrometry.

AA amyloidosis associated with systemic lupus erythematosus: impact on clinical course and outcome.

Secondary amyloidosis (AA amyloidosis) has rarely been described in patients with systemic lupus erythematosus (SLE). We, herein, present a 56-year-old female patient, who developed AA amyloidosis following a 22-year history of SLE. She developed severe mitral regurgitation complicated with chordae tendinea rupture that led to acute congestive heart failure and went on a mitral valve replacement, where no flare symptoms of SLE were present. Three months after the operation, she presented with a nephrotic-range proteinuria, acute renal failure, and severe sepsis. She was found to have new vegetations on replaced valve and multi-organ failure caused her death. Re-evaluation of the excised mitral valve revealed AA amyloid deposition. Post-mortem biopsies from the kidney and bone marrow also revealed secondary amyloidosis.

Translocation (13;17)(q14;q25) as a novel chromosomal abnormality in acute myeloid leukemia-M4.

We report a case of AML-M4 in which G-band karyotyping revealed a previously unreported t(13;17)(q14;q25) in metaphase preparations. The breakpoints at 13q14 and 17q25 are associated with poor prognosis. The MSF and FKHR genes are located on 17q25 and 13q14, respectively. This report of AML-M4 harboring t(13;17)(q14;q25) as a unique cytogenetic abnormality provides more data on the leukomogenesis with rearrangements related with 13q14 and 17q25.