In hemolysis

Administration of dapsone may result in hemolysis (destruction of red blood cells), nausea, vomiting, anorexia, and blurred vision. 

Assa, Y., Shany, S., Gestetner, B., Tencer, Y., Birk, Y., and Bondi, A. (1973) Interaction of alfalfa saponins with components of the erythrocyte membrane in hemolysis. Biochim. Biophys. Acta 307, 83-91. 

Glucose 6-phosphate dehydrogenase deficiency impairs the ability of an erythrocyte to form NADPH, resulting in hemolysis. 

The authors postulated that iodide toxicity had resulted in hemolysis and hemoglobinuria, which, together with acute interstitial nephritis secondary to inhibition of prostaglandin synthesis from mefenamic acid ingestion, had resulted in acute renal insufficiency. The mechanism of hemolysis resulting from toxic doses of iodine is not clear, although it may reflect inhibition of various red cell enzymes. 

The accumulation of hydrogen peroxidase affects many intracellular processes and results in hemolysis. These include the cross-linking of membrane proteins hemoglobin denaturation (manifest as Heinz body formation), which in turn affects the physical properties of the erythrocyte and lipid peroxidation, which may affect the cell membrane to cause direct hemolysis (Fig. 11-8). The resultant damage leads to a mixture of intravascular hemolysis and extravascu-lar hemolysis (by which hemolysis occurs in the reticuloendothelial system). In acute hemolytic episodes, the clinical picture is of predominantly intravascular hemolysis, while predominantly extravascular hemolysis is seen in patients with chronic hemolysis. 

Composition of electroporation buffer is an important factor affecting electroporation yields. Ionic strength of cell suspension medium needs control, which determines resistance of the cell suspension and resultant RC time constant of the field pulse. Medium supplemented with Ca and Mg in mM concentration range is found to promote efficiency of transformation and cell viability. Erythrocytes electroporated in isotonic buffer in the presence of EDTA or membrane specific drugs showed significant modification in hemolysis response to electroporation [33,34]. Use of square wave pulse removes the medium conductivity mediated effects on cell/tissue electroporation outcome. Generally, cells are pulsed in suspensions of sucrose, mannitol, or sorbitol. Electroporation as well as incubation of pulsed cells can be carried out in medium containing usual cell culture recipes. 

Ribavirin accnmnlates in erythrocytes, resnlting in hemolysis by an nnknown mechanism, perhaps related to oxidative damage to the erythrocyte membrane. Time-dependent and dose-dependent hemolytic anemia (eventnaUy associated with hyperbilirubinemia and a high reticnlocyte connt) is the only major toxic effect associated with oral or intravenons ribavirin and is reversible on withdrawal. There was a fall in hemoglobin concentrations below 10.0 g/dl in 9% of patients with hepatitis C treated with ribavirin and interferon alfa (6,7). 

The clinical manifestations of serum phosphate depletion depend on the length and degree of the deficiency. Moderate hypophosphatemia of 1.5 to 2,4 mg/dL (0.48 to 0.77 mmol/L) is usually not associated with clinical signs and symptoms (unless chronic, when osteomalacia or rickets develops). Plasma concentrations less than 1.5 mg/dL (0.48 mmol/L) may produce clinical manifestations. Because phosphate is necessary for the formation of ATP, glycolysis and cellular function are impaired by low intracellular phosphate concentrations. Muscle wealmess, acute respiratory failure, and decreased cardiac output may occur in phosphate depletion. At very low serum phosphate (<1 mg/dL or <0.32 mmol/L), rhabdomyolysis may occur. Phosphate depletion in erythrocytes decreases erythrocyte 2,3-diphosphoglycerate, which causes tissue hypoxia because of increased affinity of hemoglobin for oxygen. Severe hypophosphatemia (serum phosphate concentration <0.5 mg/dL [<0.16 mmol/L]) may result in hemolysis of the red blood cells. Mental confusion and frank coma also may be secondary to the low ATP and tissue hypoxia. If hypophosphatemia is chronic, impaired mineralization of bone produces rickets in children and osteomalacia in adults. 

Hematologic Alterations in the hematopoietic system can also occur, resulting in hemolysis, reduction in phagocytotic and granulocyte chemotactic ability, as well as defective clot retraction and thrombocytopenia. 

Complications resulting from these problems are rare nowadays. They include hyper- and hyponatremia, hyper- and hypokalemia, hypercalcemia, hypermagnesemia, air embolism, overheated dialysate resulting in hemolysis and possibly fatal hyperkalemia, and electrocution (B22). 

Mannitol (IV only) inhibits water reabsorption in the proximal convoluted tubule (PCT) (main site), the thin descending limb of the loop of Henle, and the collecting ducts. It increases urine volume, preventing anuria in hemolysis and rhabdomyolysis, and facilitates elimination of toxic drugs (e.g cisplatin). Similar osmotic actions in the ECF of other tissues —>4- intraocular and intracerebral pressure. 

A glucose-6-phosphate dehydrogenase deficiency in the red blood cell can result in hemolysis after treatment with sulfa antibiotics or antimalarials. 

In many cases the hemolysis caused by the prosthesis is mild or moderate, and is generally compensated for quite adequately by natural regeneration in the bone-marrow. Cloth covering on the valve superstructure (such as with the Starr-Edwards and Beall valves) will lead to an increase in hemolysis depending on the structure and surface characteristics of the fabric. Hemolysis, however mild, is not innocuous. It is the forerunner in one of the proposed mechanisms for platelet aggregation and coagulation, which in turn could lead to the formation of thromboemboli. 

A methylated pCD is more hydrophobie than the pCD, therefore, it forms a more stable (but soluble) eomplex with cholesterol. Its affinity to eholesterol is so strong that it extracts cholesterol from the blood eell membranes resulting in hemolysis in around 1 mg/mL eoneentration. 

On the other hand, the disease may rapidly deteriorate and resanble fulminant hepatic failure with massive jaundice, hypoalbuminemia, ascites, severe coagulation defects, hyperammonania and hepatic encephalopathy. Hepatocellular neCTOsis results in the release of large amounts of stored copper. Hypercupriania results in hemolysis and severe hemolytic anemia compUcates acute hver disease. Although Wilson disease is a rare disease, in patients presenting with fiilminant hepatic failure it is not uncommon and accounts for 6-12% of patients with fulminant hepatic failure referred for anergency hver transplantation. 

When cells are damaged, particularly in hemolysis— red blood cell (RBC) breakdown or destruction. 

While vascular prostheses are now in common use, they present several problems for long term stability (110). The first problem is the rapid adsorption of protein, triggering blood coagulation and leading to platelet adhesion. The second problem arises because of the difference in modulus and surface properties of vascular prostheses and normal blood vessels. As a result of the latter, the surfaces of the red blood cells may become abraded, resulting in hemolysis, platelet activation, and aggregation. Note that in this instance, it is not the polymer undergoing wear, but the red blood cell membranes. 

Urinary excretion of iron occurs in normal persons at a fairly constant rate with an average of about 1 mg. per day. This amount is increased for about 24 hr. after intravenous injection, but the total amount excreted represents only 1 or 2% of that injected. The inability of the body to excrete iron by this route is well illustrated in hemolytic anemia and in hemolysis induced by acetylphenylhydrazine during treatment of polycythemia when less than 0.5% of the large amount of iron liberated in the body by destruction of red cells is excreted in urine and feces. ... 

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