[Draft proposal to estimate true values of serum potassium in samples from patients with myeloproliferative neoplasma].

The pseudohyperkalemia in thrombocytosis is assumed to be due to potassium released from blood cells during blood clotting as reported previously, but its mechanisms remain to be cleared. Although plasma potassium measurements with blood collection tubes containing heparin are performed in many hospitals to avoid pseudohyperkalemia, the burden on patients may come out with further blood sampling by another heparinized tube. Taken together, we investigated laboratory data possibly involved in pseudohyperkalemia in 184 samples from patients with myeloproliferative neoplasma (MPN), and studied estimation capability for true values of serum potassium, driving a correction formula by means of several laboratory data to explain the difference of measured potassium values (K-difference: serum value minus plasma value). Platelet count and mean corpuscular volume (MCV) were adopted as significant variables correlated to K-difference as a result of multiple regression analysis. A correction formula was driven by multiple regression equation with these two variables as follows: y = 0.0006 x 1+0.0004 x 2-0.177 (r= 0.885; x 1, platelet count; x 2, MPV). The correction formula was considered to be useful for estimating the true value of serum potassium in samples from patients with MPN because the corrected serum potassium value correlated highly with plasma potassium value (r = 0.885). These results propose that true values of serum potassium can be estimated by the correction of measured serum potassium values with platelet count and MCV, suggesting that not only quantitative factors but also qualitative factors may be involved in pseudohyperkalemia.

[Triglyceride (TG) and remnant lipoproteins].

Lowering low-density lipoprotein (LDL) cholesterol (LDL-C) can reduce the risk of cardiovascular disease (CVD) by approximately 30%, and the remaining 70% should be the second front of CVD risk reduction. Such residual risks include high triglyceride (TG) concentrations and low levels of high-density lipoprotein (HDL) cholesterol (HDL-C) in terms of dyslipidemia. TG-rich lipoproteins are heterogenous and composed of a variety of subfractions, all of which are not necessarily relevant to atherosclerosis and CVD risk. However, remnant lipoproteins, TG-rich lipoproteins, are atherogenic and related to CVD risk. Two different methods (RLP-C and RemL-C) have been developed to measure cholesterol levels of remnant lipoproteins. Although there is a difference in affinity to intermediate-density lipoprotein (IDL) between the two methods, they may be better qualified as biomarkers of CVD risk than TG itself. TG measurements play a certain role in the evaluation of CVD risk, but the remnant lipoprotein cholesterol measurement can provide better screening for patients at high CVD risk than TG and may be a useful examination in both quantity and quality.

[Medical safety management in the blood collection center of clinical laboratory].

Safety management is essential for providing patients with medical services. Our hospital, opened at Kashiwa in 1987, has been building up systems and taking a number of steps to reduce the blood collection related problems, including venipuncture-related infection, nerve injury, and vasovagal reflex with syncope in accordance with guidelines for the standard method of venipuncture blood collection. We also have made efforts for improving medical services, including reductions in patient waiting time and prevention of patient misidentification, medical test malpractice, and patient privacy. However, ultimately, it is of obvious significance to educate and train communication skills for humanity and friendly kindness because most of medical accidents are basically attributed to communication errors between patients and medical staff.

Mechanisms of LDL oxidation.

BACKGROUNDS: Many lines of evidence suggest that oxidized low-density lipoprotein (LDL) is implicated in the pathogenesis of atherosclerotic vascular diseases. This review summarizes a diversity of mechanisms proposed for LDL oxidation serving for the so-called "LDL oxidation hypothesis of atherogenesis". METHODS AND RESULTS: We investigated the literature and our research results related to mechanisms of LDL oxidation and its atherogenesis. LDL oxidation is catalyzed by transition metal ions and several free radicals, and LDL is also oxidized by some oxidizing enzymes. In this way, LDL can be converted to a form that is recognized specifically by and with high affinity to macrophage scavenger receptors, leading to foam cell formation, the defining characteristic of fatty streak lesions. CONCLUSIONS: Several pathways are involved in the promotion of LDL oxidation in vitro and in vivo, but it would appear that the physiologically relevant mechanisms of LDL oxidation are still imperfectly understood. The underlying mechanisms of LDL oxidation must be further explored to reveal appropriate ways for the diagnosis and treatment of atherosclerosis and its relevant diseases.

Structural and glycation site changes of albumin in diabetic patient with very high glycated albumin.

BACKGROUND: Glycated albumin (GA) has been utilized to monitor mid-term glycemic control, and reflects the status of blood glucose more rapidly and effectively than hemoglobin A(1c) (HbA(1c)). To examine the relationship between GA level and structural changes or glycation sites of albumin, we analyzed pre- and post-treatment samples from a diabetic patient with extraordinary increase of GA. METHOD: A female diabetic patient with poor glycemic control had a GA >94% and was treated with intensive insulin therapy to decrease blood glucose. We analyzed changes in fluorescence derived from tryptophan (Trp) and advanced glycation end product (AGE) of albumin isolated/purified from pre- and post-treatment samples. To determine the sites of glycation of albumin, samples were carboxymethylated and digested by Glu-C endoprotease, and peptides were analyzed using liquid chromatography/mass spectrometry. RESULTS: GA level decreased almost linearly and reflected the improved glycemic state well. Trp-related fluorescence of pre- and post-treated samples did not change while AGE-related fluorescence increased depending on GA level. Ten major glycation sites were detected in the pre-treatment sample, while 3 major glycation sites were detected in post-treated samples. CONCLUSIONS: GA level reflects the status of blood glucose more rapidly than HbA(1c). Since GA level was related to AGE-related fluorescence and number of glycation sites, it might be a good marker for not only glycemic control of diabetic patients but also structural and functional changes of albumin.