Estimation of the hemoglobin glycation rate constant

In a previous study, a method of obtaining mean erythrocyte age ($$M_{RBC}$$ M RBC ) from HbA1c and average plasma glucose (AG) was proposed. However, the true value of the hemoglobin glycation constant ($$k_g$$ k g dL/mg/day), required for this model has yet to be well characterized. Another study also proposed a method of deriving $$M_{RBC}$$ M RBC from erythrocyte creatine (EC). Utilizing these formulae, this study aimed to determine a more accurate estimate of $$k_g$$ k g . One hundred and seven subjects including 31 patients with hemolytic anemia and 76 subjects without anemia were included in this study. EC and HbA1c data were analyzed, and $$M_{RBC}$$ M RBC using HbA1c, AG and the newly-derived constant, $$k_g$$ k g were compared to $$M_{RBC}$$ M RBC using traditional $$^{51}\hbox {Cr}$$ 51 Cr in three patients whose data were taken from previous case studies. A value of $$7.0\times 10^{-6}$$ 7.0 × 10 - 6 dL/mg/day was determined for $$k_g$$ k g . $$M_{RBC}$$ M RBC using HbA1c, AG and $$k_g$$ k g were found to no be significantly different (paired t-test, $$p=0.45$$ p = 0.45 ) to $$M_{RBC}$$ M RBC using traditional $$^{51}\hbox {Cr}$$ 51 Cr . $$k_g$$ k g enables the estimation of $$M_{RBC}$$ M RBC from HbA1c and AG.

Estimation of the Hemoglobin Glycation Rate Constant

AimIn a previous study, a method of obtaining mean erythrocyte age (MRBC) from HbA1c and average plasma glucose (AG) was proposed. However, the true value of the hemoglobin glycation constant (kgdL/mg/day), required for this model has yet to be well characterized. Another study also proposed a method of derivingMRBCfrom erythrocyte creatine (EC). Utilizing these formulae, this study aimed to determine a more accurate estimate ofkg.Methods107 subjects including 31 patients with hemolytic anemia and 76 subjects without anemia were included in this study. EC and HbA1c data were analyzed, andMRBCusing HbA1c, AG and the newly-derived constant,kgwere compared toMRBCusing traditional51Cr in three patients whose data were taken from previous case studies.ResultA value of 7.0 × 10−6dL/mg/day was determined forkg.MRBCusing HbA1c, AG andkgwere found to no be significantly different (pairedt-test,p= 0.45) toMRBCusing traditional51Cr.Conclusionskgenables the estimation ofMRBCfrom HbA1c and AG.

A Novel Method for Calculating Mean Erythrocyte Age Using Erythrocyte Creatine

BackgroundsErythrocyte creatine (EC) decreases reflecting erythrocyte age.MethodsWe developed an EC model, which showed a bi- or mono-exponential relationship between mean erythrocyte age (MRBC) andEC. We reanalyzed the previously published data of 21 patients with hemolytic anemia which includedECand51Cr half-life.ResultsMRBCand logeECshowed excellent significant linearity (r= −0.9475,p <0.001), showing that it can be treated as a mono-exponential relationship within the studied range (EC: 1.45 – 11.76µmol/g Hb). We established an equation to obtainMRBC(days) fromEC(µmol/g Hb),MRBC= −22.84 logeEC+ 65.83.ConclusionThis equation allows calculation ofMRBCbased on EC which has practical applications such as the diagnosis of anemia.

Modelling primaquine-induced haemolysis in G6PD deficiency

Primaquine is the only drug available to prevent relapse in vivax malaria. The main adverse effect of primaquine is erythrocyte age and dose-dependent acute haemolytic anaemia in individuals with glucose-6-phosphate dehydrogenase deficiency (G6PDd). As testing for G6PDd is often unavailable, this limits the use of primaquine for radical cure. A compartmental model of the dynamics of red blood cell production and destruction was designed to characterise primaquine-induced haemolysis using a holistic Bayesian analysis of all published data and was used to predict a safer alternative to the currently recommended once weekly 0.75 mg/kg regimen for G6PDd. The model suggests that a step-wise increase in daily administered primaquine dose would be relatively safe in G6PDd. If this is confirmed, then were this regimen to be recommended for radical cure patients would not require testing for G6PDd in areas where G6PDd Viangchan or milder variants are prevalent.

Overexpression of Erythrocyte Glutathione S-Transferase in Uremia and Dialysis

Background: Overexpression of glutathione S-transferase (GST; EC 2.5.1.18) has been documented in the erythrocytes of patients with chronic renal failure, and this event may well be of relevance from a clinical standpoint. In fact, it could serve as a marker of uremic toxicity overall, which can contribute to impair the function and survival of the erythrocytes. However, the biochemical details of this phenomenon are poorly understood. Methods: In this study, we characterized the expression of GST in erythrocytes of 118 uremic patients under different clinical conditions. The mechanisms responsible for the regulation of protein expression and enzyme activity were investigated in light of different dialysis approaches, oxidative stress, uremic toxins, erythrocyte age, and erythropoietin (EPO) supplementation. Results: Mean GST activity in uremic patients was highly overexpressed with respect to controls, and this phenomenon was exclusively attributable to an increased expression of GST. Overexpression of GST did not appear to be dependent on oxidative stress and was not influenced by vitamin E supplementation. In the same manner, both erythrocyte age and EPO supplementation apparently did not interfere with the GST concentrations, which were the same in controls and patients. Preliminary experiments suggested that high-molecular weight or protein-bound toxins could play some role in the overexpression of GST. Conclusions: GST expression may be a useful marker for the individual accumulation of uremic toxins as well as of the efficiency of new dialysis strategies in removing them.