Copper
Judy A. Driskell, Ira Wolinsky in Sports Nutrition, 2005
The human body contains about 1.6 mg of Cu/kg of body weight with variable distributions in various organs and blood. Examples of Cu concentrations in various tissues include kidney, 12 mg/kg; liver, 6 mg/kg; brain, 5 mg/kg; heart, 5 mg/kg; bone, 4 mg/kg; and muscle 0.9 mg/kg. Bone contains 40% of body Cu, the highest percentage of any other organ; muscle is second at about 23%. These organs also make up the greatest percentages of the body mass. Blood contains about 6% of total body Cu. The Cu concentration of RBC is approximately 16.1 ± 2.0 µmol/L of packed cells and plasma has an average concentration of 16.5± 2.5 µmol/L for men and 18.3 ± 2.5 µmol/L for women. The normal range of red blood cell (RBC) Cu for both men and women is 12.5 to 23.6 µmol/L, whereas the normal range for plasma Cu is 8.8 to 17.5 µmol/L for men and 10.8 to 26.6 µmol/L for women. However, plasma values consistently as low as 8.8 µmol/L might be considered a sign of low Cu status.
The respiratory system
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella in Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Anemia causes a decrease in the oxygen content of the blood and, therefore, a decrease in the supply of oxygen to the tissues. It is characterized by a low hematocrit that may be caused by several pathological conditions, such as a decreased rate of erythropoiesis (red blood cell production), excessive loss of erythrocytes or a deficiency of normal hemoglobin in the erythrocytes. Although there is a decrease in the oxygen content of the blood, it is important to note that anemia has no effect on the PO2 of the blood or on the oxyhemoglobin dissociation curve (see Figure 8.8). Arterial PO2 is determined only by the amount of oxygen dissolved in the blood, which is unaffected. Furthermore, the affinity of hemoglobin for oxygen has not changed. What has changed is the amount of hemoglobin in the blood. If there is less hemoglobin available to bind with oxygen, then there is less oxygen in the blood.
Introduction to Myeloproliferative Neoplasms
Wojciech Gorczyca in Atlas of Differential Diagnosis in Neoplastic Hematopathology, 2014
A simplified approach to the diagnosis of PV is presented in Figure 26.7. The differential diagnosis of erythrocytosis includes PV, reactive (secondary) erythrocytosis, and congenital polycythemia. The causes for secondary polycythemia include chronic lung disease and other diseases leading to hypoxia, smoking, living in high altitude, certain tumors (meningioma, pheochromocytoma, leiomyoma, hepatocellular carcinoma, renal cell carcinoma, etc.), postrenal transplant, and use of androgen preparations, while congenital polycythemia is associated with high oxygen affinity hemoglobin (Hb) variants, 2,3-bisphosphoglycerate (2,3-BPG) deficiency, von Hippel–Lindau (VHL) mutations, and erythropoietin receptor (EPOR) mutations [86–90]. Idiopathic erythrocytosis, characterized by an increase of red blood cell mass without an identified cause (no evidence of PV, secondary acquired polycythemias, and various congenital primary and secondary polycythemias), is rarely diagnosed and requires exclusion of early PV and unrecognized secondary or congenital polycythemia [88]. In cases negative for JAK2 V617F and exon 12 mutation when BM examination excludes PV, and clinical and laboratory data do not support acquired erythrocytosis, congenital erythrocytosis should be considered. In these cases, measurement of p50 (oxygen tension at which Hb is 50% saturated) EPOR and VHL mutation analysis and 2,3-BPG measurement should be considered [5,89–91].
Hb Alessandria [β37(C3)Trp→Leu; HBB: c.113G>T]: a Novel Variant on the β-Globin Chain with Slightly Increased Affinity for Oxygen Detected by Capillary Electrophoresis
Published in Hemoglobin, 2022
Lara Calcagno, Maria M. Ciriello, Monica Maccarini, Massimo Mogni, Massimo Maffei, Giuseppina Barberio, Sauro Maoggi, Domenico Coviello, Giovanni Ivaldi
To further confirm the presence of a Hb variant, we also performed analysis by CE (Capillarys 3 Tera with Hemoglobin(e) kit; Sebia). The abnormal Hb was observed in zone (F), well separated from Hb A, in an amount of 39.9% and Hb A2 of 3.1% (normal range: 2.2–3.2%) (Figure 2). All procedures were conducted according to the manufacturers’ recommendations. Erythrocyte parameters were measured using an automated hematology analyzer (ADVIA 2120 Hematology System; Siemens Italia, Milan, Italy): red blood cell (RBC) count 4.76 × 1012/L (normal range: 4.20–5.40), Hb 14.1 g/dL (normal range: 12.0–16.0), mean corpuscular volume (MCV) 92.8 fL (normal range: 82.0–90.5), mean corpuscular Hb (MCH) 29.6 pg (normal range: 26.0–34.0), and packed cell volume (PCV) 0.44 L/L (normal range: 0.37–0.47). The patient appeared to be clinically normal without erythrocytosis or other hematological abnormalities.
An integrated in silico and in vivo approach to determine the effects of three commonly used surfactants sodium dodecyl sulphate, cetylpyridinium chloride and sodium laureth sulphate on growth rate and hematology in Cyprinus carpio L
Published in Toxicology Mechanisms and Methods, 2022
Ritwick Bhattacharya, Ismail Daoud, Arnab Chatterjee, Soumendranath Chatterjee, Nimai Chandra Saha
For analysis of hematological parameters, fish specimens were sampled after 15, 30, and 45 days of exposure. By the utilization of a disposable sterile syringe and a needle, blood was obtained by transfixing the heart. The collected blood sample was transferred immediately to vials containing an anticoagulant, EDTA, and was softly shaken to eschew blood hemolysis. Red blood cell (RBC) counts were calculated using a hemocytometer (Mishra et al. 1977). Briefly, blood was drawn up to 0.5 mark in RBC pipette and immediately, the diluting fluid (Hayem’s solution) was drawn up maintaining the dilution of 1:200. Pipette was shaken thoroughly and diluted blood was transfered into the counting chamber, after discarding two drops. The solution was allowed to settle for few seconds and the number of RBCs was counted in five small squares of the RBC column under high power microscope and the number of RBCs per cubic mm was calculated. Hemoglobin (Hb) content was estimated by employing the protocol of Dacie and Lewis (1984). Briefly, 20 μL of blood was diluted by adding 5 ml of diluting solution, and mixed well. After 5 minutes of standing at room temperature, the absorbance at 540 nm was measured with an Ultraviolet-Visible Spectrophotometer. The hematocrit value (Ht%) or packed cell volume (PCV) was determined by blood centrifugation (3000 rpm; 10 min) in heparinized glass capillaries, using a microhematocrit centrifuge and the reading was directly taken using a reader associated with centrifuge.
Diabetes mellitus and pernicious anemia: interrelated therapeutic triumphs discovered shortly after William Osler’s death
Published in Baylor University Medical Center Proceedings, 2020
Marvin J. Stone
In 1886, Frederick P. Henry and Osler reported a 42-year-old man with the clinical features of PA and atrophy of the stomach, confirming the previous findings of Austin Flint and Samuel Fenwick.12,14 Physical examination showed the skin to have a peculiar yellowish pallor, which by now Osler stated was almost pathognomonic of PA, along with pale mucous membranes. The red blood cell count was 790,000 per mm3 with some red cells four times normal size. The patient died 6 months later. The last red blood cell count was 315,000 per mm3. Autopsy showed the gray pallor of the skin and all organs, and bone marrow hyperplasia. The stomach showed a grossly thin mucous membrane in the fundus but was otherwise unremarkable except for pallor and small nodular projections. A prominent feature of the gastric atrophy in this patient was round cell infiltration in all the layers of the stomach that we now know to be lymphocytes that evoke cell-mediated autoimmune attack on the gastric parietal cells.11