Hb A2-Calderdale [δ2(NA2)His→Asn; HBD: c.7C>A] and Misdiagnosis of Type 2 Diabetes Mellitus Due to Interference with Hb A1c When Using Cation Exchange High Performance Liquid Chromatography: A Case Report.

The Hb A2-Calderdale variant [δ2(NA2)His→Asn, HBD: c.7C>A] was described as a novel variant in 2014. However, a high performance liquid chromatography (HPLC) peak was never identified indicating that this fraction could be 'hiding' somewhere else in the chromatogram. In this case report, we present evidence that the physiochemical properties of Hb A2-Calderdale resemble those of Hb A1c, resulting in a coelution in variant mode on the Tosoh G8 but not the Tosoh G11. This coelution results in an overestimation of Hb A1c and can potentially cause misdiagnosis of type 2 diabetes mellitus (T2DM).

Temporary impact of blood donation on physical performance and hematologic variables in women.

BACKGROUND: No former studies have examined how blood donation influences physical performance in women, who due to menstruation may have a slower recovery of performance. Therefore, the aim of this study was to clarify how VO2peak , time trial (TT) performance, and hematologic variables are affected in 18 iron-sufficient (plasma ferritin [P-ferritin] > 30 µg/L) women after a standard 450-mL blood donation. STUDY DESIGN AND METHODS: VO2peak , TT performance, and blood variables were measured at baseline and 3, 7, 14, 21, and 28 days after blood donation in 18 iron-sufficient women. Anthropometrics were measured at baseline and Day 28. RESULTS: VO2peak was reduced by 7.5 ± 1.1% from 2973 ± 87 mL/min at baseline to 2765 ± 73 mL/min 3 days after blood donation and remained below baseline until 28 days. The TT performance was reduced by 5.2 ± 1.0% from baseline (868 ± 31 sec) to Day 3 (915 ± 29 sec), but was not different from baseline 14 days after blood donation. Blood hemoglobin (B-Hb) concentration declined by 7.6 ± 2.1% from 8.4 ± 0.1 to 7.8 ± 0.1 mmol/L at baseline and on Day 3, respectively. P-ferritin at baseline was 58 ± 7 µg/L and it decreased (55 ± 3%) to a nadir of 24 ± 3 µg/L 28 days after blood donation and remained lower at 36 ± 4 µg/L after 90 days. CONCLUSION: VO2peak and B-Hb were only recovered 28 days after a blood donation whereas TT performance was back to baseline 14 days after blood donation.

Time course for the recovery of physical performance, blood hemoglobin, and ferritin content after blood donation.

BACKGROUND: It is widely accepted that blood donation negatively affects endurance performance, but data on physical recovery after a standard blood donation are scarce. This study aimed to elucidate the temporary impact of blood donation on endurance performance, measured as peak oxygen uptake (VO2peak ) and time trial (TT) performance. STUDY DESIGN AND METHODS: VO2peak , TT performance, blood, iron, and anthropometric variables were determined before (baseline) and 3, 7, 14, and 28 days after blood donation in 19 healthy men. RESULTS: VO2peak was reduced by 6.5% from 49.7 ± 2 mL/kg/min at baseline to 46.3 ± 2 mL/kg/min on Day 3 (p < 0.001), and TT performance was reduced by 5.2% from 13:31 ± 00:42 to 14:13 ± 00:50 min:sec (p < 0.001). Both VO2peak and TT performance were back to baseline 14 days after blood donation. Blood hemoglobin (Hb) concentration declined 7.9% from 9.3 ± 0.11 mmol/L at baseline to 8.6 ± 0.1 mmol/L on Day 3 (p < 0.001) and was not different from baseline 28 days after blood donation. The hematocrit (Hct) was reduced from 43.8 ± 0.5% at baseline to 40.6 ± 0.6% on Day 3 (p < 0.001). On Day 28 Hct was 42.8 ± 0.5% and still reduced below baseline (p = 0.028). Ferritin concentration was reduced 46% from 113 ± 23 µg/L at baseline to a minimum of 61 ± 14 µg/L on Day 14 (p = 0.008). CONCLUSION: The individual recovery was variable, but physical performance was recovered 14 days after a standard blood donation, despite blood Hb concentration remaining lower than at baseline.

Glucagon does not directly stimulate pituitary secretion of ACTH, GH or copeptin.

Glucagon is best known for its contribution to glucose regulation through activation of the glucagon receptor (GCGR), primarily located in the liver. However, glucagon's impact on other organs may also contribute to its potent effects in health and disease. Given that glucagon-based medicine is entering the arena of anti-obesity drugs, elucidating extrahepatic actions of glucagon are of increased importance. It has been reported that glucagon may stimulate secretion of arginine-vasopressin (AVP)/copeptin, growth hormone (GH) and adrenocorticotrophic hormone (ACTH) from the pituitary gland. Nevertheless, the mechanisms and whether GCGR is present in human pituitary are unknown. In this study we found that intravenous administration of 0.2 mg glucagon to 14 healthy subjects was not associated with increases in plasma concentrations of copeptin, GH, ACTH or cortisol over a 120-min period. GCGR immunoreactivity was present in the anterior pituitary but not in cells containing GH or ACTH. Collectively, glucagon may not directly stimulate secretion of GH, ACTH or AVP/copeptin in humans but may instead be involved in yet unidentified pituitary functions.

Pneumatic tube validation: Reducing the need for donor samples by integrating a vial-embedded data logger.

BACKGROUND: The most common way to validate a pneumatic tube system is to compare pneumatic tube system-transported blood samples to blood samples carried by hand. The importance of measuring the forces inside the pneumatic tube system has also been emphasized. The aim of this study was to define a validation protocol using a mini data logger (VitalVial, Motryx Inc., Canada) to reduce the need for donor samples in pneumatic tube system validation. METHODS: As an indicator of the total vibration, the blood samples are exposed to under pneumatic tube system transportation; the area under the curve was determined by a VitalVial for all hospital Tempus600 lines using a five-day validation protocol. Only the three lines with the highest area under the curves were clinically validated by analysing potassium, lactate dehydrogenase and aspartate aminotransferase. A month after pneumatic tube system commissioning, a follow-up on laboratory data was performed. RESULTS: Mean area under the curve of the six lines ranged between 347 and 581. The variability of the area under the curve was between 1.51 and 11.55%. In the laboratory data follow-up, an increase in lactate dehydrogenase haemolysis was seen from the three lines with the highest area under the curve and the emergency department, which was not detected in the clinical validation. When the Tempus600 system was in commission, a higher mean area under the curve was measured. CONCLUSION: A three-day validation protocol using VitalVials is enough to determine the stability of a Tempus600 system and can greatly reduce the need for donor samples. When in commission, the stability of the pneumatic tube system should be verified and lactate dehydrogenase haemolysis should be routinely checked.

Localization of Vasoactive Intestinal Polypeptide Receptor 1 (VPAC1) in Hypothalamic Neuroendocrine Oxytocin Neurons; A Potential Role in Circadian Prolactin Secretion.

Prolactin (PRL) is a versatile hormone and serves a broad variety of physiological functions besides lactation. The release of PRL from lactotrophs in the pituitary has in rodents been shown to be released with a circadian pattern depending on the physiological state of the animal. The circadian release of PRL seems to be complex involving tonic inhibition by dopamine (DA) neurons on lactotrophs and one or even several releasing factors. Because of the circadian releasing pattern of PRL, neurons in the suprachiasmatic nucleus (SCN), "the brain clock," and especially the neurons expressing neuropeptide vasoactive intestinal polypeptide (VIP), have been suggested to be involved in the circadian regulation of PRL. In the present study, we used fluorescence immunohistochemistry, in situ hybridization histochemistry, confocal microscopy, three-dimensional reconstruction, and highly specific antibodies to visualize the occurrence of VIP receptors 1 and 2 (VPAC1 and VPAC2) in mouse brain hypothalamic sections stained in combination with VIP, oxytocin (OXT), arginine vasopressin (AVP), and DA (tyrosine hydroxylase, TH). We demonstrated that VIP fibers most likely originating from the ventral part of the SCN project to OXT neurons in the magnocellular part of the paraventricular nucleus (PVN). In the PVN, VIP fibers were found in close apposition to OXT neuron exclusively expressing the VPAC1 receptor. Furthermore, we demonstrate that neither OXT neurons nor TH or AVP neurons were expressing the VPAC2 receptor. VPAC1 receptor expression was also found on blood vessels but not in neurons expressing AVP or TH. These findings suggest that VIP signaling from the SCN does not directly target DA neurons involved in PRL secretion. Furthermore, the findings support the notion that VIP from neurons in the SCN could regulate circadian release of OXT in the posterior pituitary or modulate OXT neurons as a releasing factor involved in the circadian regulation of PRL from pituitary lactotrophs.