Plasmapheresis in the treatment of multi-drug intoxication involving levothyroxine sodium and calcium channel blockers: a case report.

Plasmapheresis, a procedure used to remove large molecular weight, protein-bound molecules from a patient's blood, has been shown to be useful in some cases of drug overdose. Levothyroxine sodium intoxication may result from the intentional or accidental ingestion of excessive amounts of the hormone, which can trigger a thyroid storm. However, case reports about the extremely large dose of 15,000 µg of thyroxine intoxication are extremely rare, and even combined with calcium channel blockers (CCBs) poisonings. We present a case of an intentional poisoning with high doses of thyroxine, diltiazem and amlodipine successfully treated with plasma exchange. A 40-year-old woman was admitted showing unconsciousness and sustained hypotension with high levels of thyroid hormones (THs). It was discovered that she had secretly ingested at least 15,000 µg of levothyroxine sodium and CCBs with unknown amounts of diltiazem and amlodipine. Following plasmapheresis, the levels of TH declined dramatically after each of the 4 sessions, with hemodynamics gradually stabilizing and mental state improving. The early and timely use of plasmapheresis appears to be a vital therapeutic tool for the management of acute and severe forms of l-thyroxine and CCB intoxication. Its use can prevent thyroid storm and reverse the disturbances in the patient's hemodynamic status.

Hypomethylation of Interleukin-6 Promoter is Associated with the Risk of Coronary Heart Disease.

BACKGROUND: Interleukin-6 (IL-6) is implicated in the pathogenesis of coronary heart disease (CHD), and IL-6 expression has associated with reduced DNA methylation of its gene promoter. However, there are no data on IL-6 promoter methylation and the risk of CHD. OBJECTIVE: To examine whether IL-6 promoter methylation measured in blood leukocyte DNA is associated with CHD risk. METHODS: A total of 212 cases with CHD and 218 controls were enrolled. Methylation at two CpG sites in IL-6 promoter was measured by bisulfite pyrosequencing, and the mean IL-6 methylation was calculated by averaging the methylation measures of the two CpGs. RESULTS: Mean methylation level in IL-6 promoter in CHD cases was significantly lower than that in controls (p = 0.023). Logistic regression analysis showed that IL-6 methylation was inversely associated with the risk of CHD. The odds ratios (ORs) of CHD for subjects in the second and first (lowest) tertile of IL-6 methylation were 1.87 (95% CI = 1.10­3.20) and 2.01 (95% CI = 1.19-3.38) (ptrend = 0.013), respectively, compared to subjects in the third (highest) tertile. The IL-6 hypomethylation-related risk estimates tended to be stronger for acute myocardial infarction (ptrend = 0.006). CpG position-specific analysis showed that hypomethylation of position 1 conferred a more pronounced increase in CHD risk than that of position 2. CONCLUSION: These findings suggest that DNA hypomethylation of IL-6 promoter is associated with the increased risk for CHD, especially for acute myocardial infarction. The two distinct CpGs in IL-6 may contribute differently to the development of CHD.

Hypomethylation of Interleukin-6 Promoter is Associated with the Risk of Coronary Heart Disease / Hipometilação do Promotor de Interleucina-6 Associada com Risco de Doença Arterial Coronariana

Abstract Background: Interleukin-6 (IL-6) is implicated in the pathogenesis of coronary heart disease (CHD), and IL-6 expression has associated with reduced DNA methylation of its gene promoter. However, there are no data on IL-6 promoter methylation and the risk of CHD. Objective: To examine whether IL-6 promoter methylation measured in blood leukocyte DNA is associated with CHD risk. Methods: A total of 212 cases with CHD and 218 controls were enrolled. Methylation at two CpG sites in IL-6 promoter was measured by bisulfite pyrosequencing, and the mean IL-6 methylation was calculated by averaging the methylation measures of the two CpGs. Results: Mean methylation level in IL-6 promoter in CHD cases was significantly lower than that in controls (p = 0.023). Logistic regression analysis showed that IL-6 methylation was inversely associated with the risk of CHD. The odds ratios (ORs) of CHD for subjects in the second and first (lowest) tertile of IL-6 methylation were 1.87 (95% CI = 1.10‑3.20) and 2.01 (95% CI = 1.19-3.38) (ptrend = 0.013), respectively, compared to subjects in the third (highest) tertile. The IL-6 hypomethylation-related risk estimates tended to be stronger for acute myocardial infarction (ptrend = 0.006). CpG position-specific analysis showed that hypomethylation of position 1 conferred a more pronounced increase in CHD risk than that of position 2. Conclusion: These findings suggest that DNA hypomethylation of IL-6 promoter is associated with the increased risk for CHD, especially for acute myocardial infarction. The two distinct CpGs in IL-6 may contribute differently to the development of CHD.

Resumo Fundamento: Interleucina-6 (IL-6) está implicada na patogênese de doença arterial coronariana (DAC), sendo sua expressão associada com redução da metilação de DNA do promotor do seu gene. Entretanto, não há dados sobre metilação do promotor de IL-6 e risco de DAC. Objetivo: Verificar se a metilação do promotor de IL-6 medida no DNA de leucócitos sanguíneos acha-se associada com risco de DAC. Métodos: este estudo arrolou 212 casos com DAC e 218 controles. Metilação em dois sítios de CpG no promotor de IL-6 foi medida por pirosequenciamento de bissulfito, sendo a metilação média de IL-6 calculada pela média das medidas de metilação dos dois CpGs. Resultados: A média do nível de metilação no promotor de IL-6 nos casos de DAC foi significativamente mais baixa do que nos controles (p = 0,023). Análise de regressão logística mostrou associação inversa entre metilação de IL-6 e risco de DAC. As razões de chance (OR) de DAC para indivíduos no segundo e no primeiro (mais baixo) tercis de metilação de IL-6 foram 1,87 (IC 95%: 1,10-3,20) e 2,01 (IC 95%: 1,19-3,38) (ptrend = 0,013), respectivamente, comparadas à de indivíduos no terceiro (mais alto) tercil. As estimativas de risco relacionado à hipometilação de IL-6 tenderam a ser mais fortes para infarto agudo do miocárdio (ptrend = 0,006). Análise com especificidade de posição de CpG mostrou que hipometilação na posição 1 conferiu maior elevação no risco de DAC do que na posição 2. Conclusão: Tais achados sugerem que a hipometilação de DNA do promotor de IL-6 está associada com elevado risco de DAC, especialmente para infarto agudo do miocárdio. Os dois CpGs distintos no promotor de IL-6 podem contribuir de modo diferente para o desenvolvimento de DAC.

Proteomic characteristics of circulating microparticles in patients with newly-diagnosed type 2 diabetes.

OBJECTIVE: This study aimed to evaluate the proteomic characteristics of plasma microparticles (MPs) from patients with newly diagnosed type 2 diabetes (T2DM). METHODS: The subjects comprised eight male T2DM patients recruited between December 2013 and March 2014, as well as eight age and sex-matched healthy controls enrolled during the same period. Plasma microparticles (MPs) were extracted from the blood of each subject, and subjected to proteomics analysis using label-free methods. Bioinformatic analyses were performed using specialized software. RESULTS: 3,148 unique peptides and 496 proteins were identified, among these, 46 proteins were differentially expressed between the two groups. Among these 46 candidates, 20 proteins had higher expression in T2DM group compared with the control group, whereas 3 proteins displayed lower expression. There were 17 proteins only detected in T2DM group, and 6 proteins only detected in the control group. Gene ontology (GO) analysis revealed significant differences between the two groups in some functional nodes, including neutrophil accumulation, chemokine production, platelet activation, and blood coagulation. Pathway analysis showed that proteins involved in platelet activation, cell adhesion, focal adhesion, and extracellular matrix-receptor interaction were differentially expressed between the 2 groups. Network analysis indicated that ubiquitin was the protein with the highest degree of connectivity. CONCLUSIONS: Blood MPs from T2DM patients are enriched in proteins involved in platelet activation, cell adhesion, and inflammation. Therefore, MPs in T2DM patients might be associated with hypercoagulable state in diabetic patients and the development of diabetic complications.

Clinical features of ischemic hepatitis caused by shock with four different types: a retrospective study of 328 cases.

The aim of the study was to investigate the clinical features of ischemic hepatitis due to shock with four different types (allergic shock, hypovolemic shock, septic shock, and cardiogenic shock). A total of 328 patients (200 males, 128 females, mean age, 65.84 ± 15.21 years old, range, 15-94 years) diagnosed with shock in Tongji Hospital were retrospectively investigated from Jun 2008 to Feb 2010. The parameters of liver function test, including alanine aminotransferanse (ALT), aspartate aminotransferanse (AST), lactate dehydrogenase (LDH), total bilirubin (TB), alkaline phosphatase (ALP) and γ-glutamyltransferase (γ-GT), were recorded and analyzed. Besides, the serum levels of C-reactive protein (CRP) and brain natriuretic peptide (BNP) were also measured and relevant correlation analysis was conducted. Among all the cases, 242 (73.8%) patients developed ischemic hepatitis. The mortality of shock patients combined with ischemic hepatitis was significantly higher than the total mortality (26.0% vs 23.8%, P < 0.05). The incidence of hepatic damage was highest in the septic shock (87.5%), while the lowest in thehypovolemic shock (49.4%). The sensitivity of ALT elevation was higher than that of AST. In addition, CRP was positively correlated with the levels of liver function parameters in the septic shock and BNP was positively correlated with that in the cardiogenic shock. Ischemic hepatitis is a common complication of shock, increasing the mortality of shock patients. The septic shock is the most common cause of hepatic damage in shock patients. CRP may be a useful predictor for septic shock, while BNP may be a useful predictor for cardiogenic shock.

Clinical findings in 111 cases of influenza A (H7N9) virus infection.

BACKGROUND: During the spring of 2013, a novel avian-origin influenza A (H7N9) virus emerged and spread among humans in China. Data were lacking on the clinical characteristics of the infections caused by this virus. METHODS: Using medical charts, we collected data on 111 patients with laboratory-confirmed avian-origin influenza A (H7N9) infection through May 10, 2013. RESULTS: Of the 111 patients we studied, 76.6% were admitted to an intensive care unit (ICU), and 27.0% died. The median age was 61 years, and 42.3% were 65 years of age or older; 31.5% were female. A total of 61.3% of the patients had at least one underlying medical condition. Fever and cough were the most common presenting symptoms. On admission, 108 patients (97.3%) had findings consistent with pneumonia. Bilateral ground-glass opacities and consolidation were the typical radiologic findings. Lymphocytopenia was observed in 88.3% of patients, and thrombocytopenia in 73.0%. Treatment with antiviral drugs was initiated in 108 patients (97.3%) at a median of 7 days after the onset of illness. The median times from the onset of illness and from the initiation of antiviral therapy to a negative viral test result on real-time reverse-transcriptase-polymerase-chain-reaction assay were 11 days (interquartile range, 9 to 16) and 6 days (interquartile range, 4 to 7), respectively. Multivariate analysis revealed that the presence of a coexisting medical condition was the only independent risk factor for the acute respiratory distress syndrome (ARDS) (odds ratio, 3.42; 95% confidence interval, 1.21 to 9.70; P=0.02). CONCLUSIONS: During the evaluation period, the novel H7N9 virus caused severe illness, including pneumonia and ARDS, with high rates of ICU admission and death. (Funded by the National Natural Science Foundation of China and others.).

[389A/G polymorphism of the human beta1-adrenergic receptor in patients with acute myocardial infarction].

OBJECTIVE: To investigate the relation between the 389A/G polymorphism in the human beta 1-adrenergic receptor and acute myocardial infarction (AMI). METHODS: Polymerase chain reaction amplification and restriction fragment length polymorphism analysis were used to detect the genotypes of 150 patients with AMI and 150 age- and sex- matched control subjects, and relative clinical data were obtained. A case-control study and multiple Logistic regression analysis were performed to assess the association between 389A/G polymorphism and AMI. RESULTS: The distributions of the genotypes and allele frequencies were significantly different between two groups (P< 0.01). The prevalence of the A allele was significantly higher in patients with AMI than in control subjects. In the multivariate regression analysis, the 389A/G polymorphism (OR: 2.88, 95%CI: 1.70-4.88, P< 0.01), smoking(OR: 2.72, 95%CI: 1.52-4.88, P< 0.01), hyperlipidemia (OR: 2.85, 95%CI: 1.68-4.86, P< 0.01), diabetes mellitus(OR: 2.38, 95%CI: 1.27-4.47, P< 0.01) and hypertension (OR: 2.00, 95%CI: 1.62-3.45, P< 0.05) were independent risk factors of AMI. CONCLUSION: The 389A/G polymorphism in the human beta 1-adrenergic receptor is associated with AMI and is an independent risk factor of AMI.