Williams Hematology


Arsenic Hydride
Miscellaneous Drugs and Chemicals
Insect, Spider, and Snake Venoms
Chapter References

Arsenic, lead, copper, chlorates, and a variety of other chemicals can cause severe red cell destruction, and hemolytic anemia is a part of the clinical syndrome associated with intoxication by these substances. Arsenic may cause hemolysis by interacting with sulfhydryl groups. Lead inhibits a variety of red cell enzymes, including several enzymes of porphyrin metabolism and pyrimidine-5′-nucleotidase. The anemia that it produces is usually not primarily hemolytic in nature. Copper inhibits a number of red cell enzymes and catalyses the oxidation of intracellular GSH. Chlorates produce methemoglobin and Heinz bodies. There are many drugs that have appeared to cause hemolytic anemia, usually by unknown or poorly defined mechanisms. Animal toxins, such as those elaborated by insects, spiders, and snakes, may also cause hemolytic anemia. Hemolytic anemia is a common accompaniment of severe burns, probably as a result of direct damage to erythrocytes by heat.

Acronyms and abbreviations that appear in this chapter include: ALA, aminolevulinic acid; EDTA, ethylenediaminetetraacetic acid; GR, glutathione reductase; GSH, reduced glutathione; G-6-PD, glucose-6-phosphate dehydrogenase; NADPH, reduced nicotinamide-adenine dinucleotide phosphate.

Many drugs and a variety of toxins have been associated with red cell destruction. Hemolysis that results when certain drugs are administered to patients deficient in glucose-6-phosphate dehydrogenase or with unstable hemoglobins is discussed in Chap. 45 and Chap. 48. Immune mechanisms may also play a role in drug- or toxin-induced hemolytic anemias. Such hemolytic anemias are discussed in Chap. 57. Microangiopathic hemolytic anemias (Chap. 51) may also be caused by drugs such as mitomycin.
The present chapter deals with drugs, toxins, and other physical agents that can cause red cell destruction by other mechanisms, or by mechanisms that are not understood at present.
The inhalation of arsine gas (arsenic hydride, AsH3) is a well-recognized cause of hemolytic anemia.1,2 Arsine is formed during many industrial processes. Most commonly it results from the reaction of nascent hydrogen, generated by the action of acid on metal, with arsenic compounds. The arsenic is usually present as a contaminant of either the acid or the metal, so that the contact with arsenic compounds may not be apparent from the history. Exposure to sufficient amounts of the gas will lead to severe anemia, jaundice, and hemoglobinuria. The mechanism of hemolysis is not clearly understood, although the well-known reactions of arsenic compounds with sulfhydryl groups in the cell membrane may play an important role.
Lead poisoning (plumbism) has been recognized since antiquity. The ingestion of beverages containing lead leached from highly soluble lead glazes or earthenware containers has been blamed for the decline and fall of the Roman aristocracy and is even now an occasional cause of lead intoxication.3 The distillation of alcohol in leaded flasks is another rare cause of plumbism in certain areas, although the practice was prohibited in 1723 by the Massachusetts Bay Colony after it was noticed that consumption of rum so distilled resulted in abdominal pain known as the “dry gripes.”3 Among the earliest published descriptions of lead poisoning is a letter written in 1786 by Benjamin Franklin4,5 who had learned as a printer that working over small furnaces of melted metal or drying racks of wet type in front of a fire might cause pain in the hands. Today, lead intoxication in children generally results from ingestion of flaking lead paint or from chewing lead-painted articles. In adults, it occurs primarily as the result of inhalation of lead compounds used or produced in industrial processes6 as in battery manufacture,7 but poisoning may occur as a result of leaching from pottery or dishes that come in contact with food.8,9 Restoring tapestries and producing pottery and tiles10,11 have also caused lead poisoning. Most patients with lead poisoning manifest some degree of anemia, although anemia is only rarely the predominant clinical manifestation.12 However, examination of the blood often provides the key diagnostic clue, and thus the hematologic findings are of special interest. Modest shortening of red cell life-span is a relatively constant feature of the disorder.13,14 In vitro treatment of red cells with lead produces measurable membrane damage: lead interferes with the cation pump,15,16 possibly in inhibiting membrane ATPase.17,18 It is not at all clear, however, that the hemolysis observed in lead poisoning is due to these changes. In some children with lead poisoning, an electrophoretically fast moving hemoglobin indistinguishable from hemoglobin A3 comprises approximately 15 percent of the total pigment.19
The anemia of lead intoxication is not usually due primarily to hemolysis. Lead apparently interferes with the normal production of erythrocytes, probably through a combination of mechanisms. Heme synthesis is markedly abnormal in patients with lead poisoning. Several enzymes of heme synthesis are inhibited, including d-aminolevulinic acid (ALA) synthetase, ALA dehydrase, heme synthetase, porphyrinogen deaminase, uroporphyrinogen decarboxylase, and coproporphyrinogen oxidase.12,13 ALA dehydrase has been considered particularly sensitive to inhibition, showing decreased activity in erythrocytes at blood lead levels in the upper portions of the normal range,17 but its sensitivity at low blood lead levels has been questioned.20 Increased amounts of d-aminolevulinic acid and coproporphyrin are found in the urine,21 and the free protoporphyrin levels22 of the erythrocytes are strikingly increased, presumably as a result of inhibition of the heme biosynthetic enzymes. Marked inhibition of the enzyme pyrimidine 5′-nucleotidase is also observed.23,24 In the absence of this enzyme, pyrimidine nucleotides accumulate in the red cells and normal depolymerization of reticulocyte ribosomal RNA does not occur. In hereditary pyrimidine 5′-nucleotidase deficiency, basophilic stippling of erythrocytes is a characteristic finding (Chap. 45), and it has been suggested that inhibition of pyrimidine-5′-nucleotidase by lead may be responsible for the basophilic stippling of erythrocytes that occurs in plumbism (see below). Inhibition of activity of the hexose monophosphate shunt has been documented.25 Synthesis of a- and b-globin chains seems to be defective in lead poisoning,26 and this may play a contributory role in the anemia of lead poisoning.
Remarkably complete observations of the acute hematologic changes occurring after the intravenous injection of lead in an attempt to treat malignant disease were published in 1928.27 Distortion of red cells was observed both in blood films and in wet preparations made immediately after infusion of lead. This was characterized by a “folding” that made the cells appear as semicircles, clumping, and the presence of “bite cells.” The anemia of chronic lead poisoning is usually mild in the adult but is frequently more severe in children. A relatively close relationship exists between blood lead levels and the hematocrit.28 The red cells are normocytic and slightly hypochromic. The hypochromia may be due to coexisting iron deficiency.29 Basophilic stippling of the erythrocytes may be fine or coarse, and the number of granules seen in each cell may be quite variable. When blood is collected in ethylenediaminetetraacetic acid (EDTA; “purple top” tube), as is commonly done, the stippling may disappear.30 Young polychromatophilic cells are most likely to be stippled. Electron microscopic studies31 have demonstrated that the basophilic granules represent abnormally aggregated ribosomes. In the marrow, ringed sideroblasts (Chap. 22) are frequently found. Iron-laden mitochondria are present31 but do not appear to contribute to the basophilic stippling that is observed on light microscopy. It may be presumed that iron entering the developing erythroblast fails to be incorporated into heme at a normal rate, either because of lead-induced impairment of heme synthesis or because of the direct effect of lead on mitochondria.
Meso 2,3-dimercaptosuccinic acid, an orally administered chelating agent has been used to treat lead poisoning.32,33
Hemolysis has also resulted from ingestion of copper sulfate in suicide attempts and from accumulation of toxic amounts from hemodialysis fluid contaminated by copper pipes.34,35 Hemolysis in Wilson disease has been attributed to the elevated plasma copper levels characteristic of that disorder,36,37 and 38 and hemolytic anemia may be the presenting symptom.39,40 The pathogenesis of this hemolytic anemia may be related to oxidation of intracellular GSH, hemoglobin, and NADPH and inhibition of glucose-6-phosphate dehydrogenase (G-6-PD) by copper.41 However, the amount of copper required to inhibit G-6-PD is large, and copper in much lower concentrations inhibits pyruvate kinase,42 hexokinase, phosphogluconate dehydrogenase, phosphofructokinase, and phosphoglycerate kinase.43 Plasma exchange has been used successfully to treat the hemolytic anemia of Wilson disease.44
Sodium and potassium chlorate are oxidative drugs which have been known to produce methemoglobinemia, Heinz bodies, and hemolytic anemia. While it might be presumed that the mechanism of hemolysis is similar to that resulting from other oxidative drugs, no cases have been observed in patients deficient in G-6-PD. The rare instances of chlorate poisoning that have been reported usually resulted from prescription errors in which sodium chlorate was dispensed instead of sodium chloride.45 Hemolytic anemia with Heinz body formation has also occurred in patients undergoing dialysis when the tap water used contained a substantial amount of chloramines. Oxidative damage of the red cells of these patients was demonstrated by the presence of Heinz bodies, a positive ascorbate-cyanide test, and methemoglobinemia.46,47 Leaching of formaldehyde from plastic used in a water filter employed for hemodialysis is also a cause of hemolytic anemia. It was suggested that the effect of the low levels of formaldehyde found in the water were not mediated through its fixative effect but rather by inducing metabolic changes in the red cells.48
There are also isolated reports of hemolytic anemia occurring after the administration of a variety of other substances, listed in Table 53-1.


Hemolytic anemia produced by phenazopyridine is often associated with “bite cells” and “blister cells.”67 When large amounts of distilled water gain access to the systemic circulation, either by intravenous injection or when used as an irrigating solution during surgery, hemolysis will occur.68 Severe hemolysis may also result from water inhalation in near-drowning.69
Hemolytic anemia has been observed in astronauts exposed to 100 percent oxygen; a reduction of red cell volume also occurs when the O2 tension is maintained at normal atmospheric levels, and this is believed to be due in some unknown way to weightlessness.70 In at least one patient, hyperbaric oxygenation was associated with acute hemolysis.71 It was suggested that hemolysis in this instance may have been due to abnormal peroxidation of lipids in the erythrocytes, but evidence supporting this view was indirect and equivocal.
Bee72 and wasp73,74 and 75 stings have been associated with severe hemolysis, and spider or scorpion bites have occasionally been followed by hemolytic anemia and hemoglobinuria.76,77,78,79,80 and 81 The spiders usually thought to be responsible are Loxosceles loeta and Loxosceles reclusus. It is unknown why some patients suffer hemolysis after insect bites whereas others do not. Although snake venom may cause hemolysis in vitro by converting lecithin to lysolecithin (see Chap. 27), hemolysis does not often result from snake bites,82 and when it does occur, it may represent microangiopathic hemolytic anemia associated with coagulation abnormalities induced by the venom.83
It has been known for over a hundred years that heating blood to temperatures above 47°C (117°F) rapidly produces visible damage to erythrocytes. The sequence of events has been defined in detail.84 Cells damaged by heating not only show morphologic changes and increases in osmotic and mechanical fragility but are also removed rapidly after reinjection into the circulation.85 These observations explain the severe hemolytic anemia which occurs in patients with extensive burns. Spherocytosis and increased osmotic fragility are found in many patients, and blood films may show fragmentation, budding, spherocytosis, and severe microspherocytosis. These changes are particularly evident if films are made promptly after the burn occurs. Gross hemoglobinemia was observed in 11 of 40 patients with second- and third-degree burns involving 15 to 65 percent of the body surface.86 It seems likely that the acute hemolytic anemia occurring within the 24 h following a burn is due to the direct effect of heat on circulating erythrocytes. Hemolysis occurring more than 24 h after the burn may sometimes be due to the infusion of isoagglutinins (particularly anti-A) in pooled plasma, when this has been administered to the patient as part of treatment,87 or be the result of infection or coagulation disorders that are common complications of extensive burn injury.
Although reduced red cell survival is a part of the complex series of events occurring after administration of large doses of total body radiation,88 erythrocytes appear to be very resistant to the direct effects of radiation.89 Such shortened red cell survival as may occur after radiation is probably related largely to red cell loss through internal bleeding and to various secondary events such as infection.

Phoon WH, Chan MO, Goh CH, et al: Five cases of arsine poisoning. Ann Acad Med Singapore 13(2, suppl):394, 1984.

Romeo L, Apostoli P, Kovacic M, Martini S, Brugnone F: Acute arsine intoxication as a consequence of metal burnishing operations. Am J Ind Med 32:211, 1997.

Klein M, Namer R, Harpur E, Corbin R: Earthenware containers as a source of fatal lead poisoning. N Engl J Med 283:669, 1970.

The Complete Works of Benjamin Franklin, edited by J Bigelow, Putnam, New York, 1888.

Andreasen NJC: Benjamin Franklin: Physicus et medicus. JAMA 236:57, 1976.

Staudinger KC, Roth VS: Occupational lead poisoning. Am Fam Physician 57:719, 1998.

Froom P, Kristal-Boneh E, Benbassat J, Ashkanazi R, Ribak J: Predictive value of determinations of zinc protoporphyrin for increased blood lead concentrations. Clin Chem 44:1283, 1998.

Autenrieth T, Schmidt T, Habscheid W: Lead poisoning caused by a Greek ceramic cup. Dtsch Med Wochenschr 123:353, 1998.

Kakosy T, Hudak A, Naray M: Lead intoxication epidemic caused by ingestion of contaminated ground paprika. J Toxicol Clin Toxicol 34:507, 1996.

Fischbein A, Wallace J, Sassa S, et al: Lead poisoning from art restoration and pottery work: unusual exposure source and household risk. J Environ Pathol Toxicol Oncol 11:7, 1992.

Vahter M, Counter SA, Laurell G, et al: Extensive lead exposure in children living in an area with production of lead-glazed tiles in the Ecuadorian Andes. Int Arch Occup Environ Health 70:282, 1997.

Harris JW, Kellermeyer RW: Acquired abnormality: Porphyrinuria, in The Red Cell, p 35. Harvard University Press, Cambridge, 1970.

Waldron HA: The anaemia of lead poisoning: A review. Br J Ind Med 23:83, 1966.

Westerman MP, Pfitzer E, Ellis LD, Jensen WN: Concentrations of lead in bone in plumbism. N Engl J Med 273:1246, 1965.

Khalil-Manesh F, Tartaglia-Erler J, Gonick HC: Experimental model of lead nephropathy. IV. Correlation between renal functional changes and hematological indices of lead toxicity. J Trace Elem Electrolytes Health Dis 8:13, 1994.

Vincent PC, Blackburn CRB: The effects of heavy metal ions on the human erythrocyte. I. Comparisons of the action of several heavy metals. Aust J Exp Biol Med Sci 36:471, 1958.

Hernberg S, Nikkanen J: Enzyme inhibition by lead under normal urban conditions. Lancet 1:63, 1970.

Hasan J, Vihko V, Hernberg S: Deficient red cell membrane Na+ + K+-ATPase in lead poisoning. Arch Environ Health 14:313, 1967.

Charache S, Weatherall DJ: Fast hemoglobin in lead poisoning. Blood 28:377, 1966.

Chalevelakis G, Bouronikou H, Yalouris AG, et al: delta-Aminolaevulinic acid dehydratase as an index of lead toxicity. Time for a reappraisal? Eur J Clin Invest 25:53, 1995.

Goldberg A: Annotation. Lead poisoning and haem biosynthesis. Br J Haematol 23:521, 1972.

McElvaine MD, Orbach HG, Binder S, et al: Evaluation of the erythrocyte protoporphyrin test as a screen for elevated blood lead levels. J Pediatr 119:548, 1991.

Paglia DE, Valentine WN, Dahlgren JG: Effects of low-level lead exposure on pyrimidine 5′-nucleotidase and other erythrocyte enzymes. J Clin Invest 56:1164, 1975.

Aly MH, Kim HC, Renner SW, et al: Hemolytic anemia associated with lead poisoning from shotgun pellets and the response to Succimer treatment. Am J Hematol 44:280, 1993.

Lachant N, Tomoda A, Tanaka KR: Inhibition of the pentose phosphate shunt by lead: A potential mechanism for hemolysis in lead poisoning. Blood 63:518, 1984.

White JM, Harvey DR: Defective synthesis of alpha and beta globin chains in lead poisoning. Nature 236:71, 1972.

Brookfield RW: Blood changes occurring during the course of treatment of malignant disease by lead, with special reference to punctate basophilia and the platelets. J Pathol 31:277, 1928.

Schwartz J, Landrigan PJ, Baker EL, Jr., Orenstein WA, von Lindern IH: Lead-induced anemia: dose-response relationships and evidence for a threshold. Am J Public Health 80:165, 1990.

Clark M, Royal J, Seeler R: Interaction of iron deficiency and lead and the hematologic findings in children with severe lead poisoning. Pediatrics 81:247, 1988.

White JM, Selhi HS: Lead and the red cell. Br J Haematol 30:133, 1975.

Jensen WN, Moreno GD, Bessis MC: An electron microscopic description of basophilic stippling in red cells. Johns Hopkins Med J 25:933, 1965.

Berlin CMJ: Lead poisoning in children. Curr Opin Pediatr 9:173, 1997.

Miller AL: Dimercaptosuccinic acid (DMSA), a non-toxic, water-soluble treatment for heavy metal toxicity. Altern Med Rev 3:199, 1998.

Klein WJ Jr, Metz EN, Price AR: Acute copper intoxication. A hazard of hemodialysis. Arch Intern Med 129:578, 1972.

Manzler AD, Schreiner AW: Copper-induced acute hemolytic anemia. A new complication of hemodialysis. Ann Intern Med 73:409, 1970.

McIntyre N, Clink HM, Levi AJ, Cumings JN, Sherlock S: Hemolytic anemia in Wilson’s disease. N Engl J Med 276:439, 1967.

Deiss A, Lee GR, Cartwright GE: Hemolytic anemia in Wilson’s disease. Ann Intern Med 73:413, 1970.

Hansen PB: Wilson’s disease presenting with severe haemolytic anaemia. Ugeskr Laeger 150:1229, 1988.

Shimono N, Ishibashi H, Ikematsu H, et al: Fulminant hepatic failure during perinatal period in a pregnant woman with Wilson’s disease. Gastroenterol Jpn 26:69, 1991.

Jain S, Nur AM, Ghosh K: Acute hemolytic anemia and biliary colic as presenting manifestations of Wilson’s disease. Am J Gastroenterol 85:476, 1990.

Fairbanks VF: Copper sulfate-induced hemolytic anemia. Arch Intern Med 120:428, 1967.

Blume KG, Hoffbauer RW, Löhr GW, Rüdiger HW: Genetische und biochemische Aspekte der Pyruvatkinase menschlicher Erythrozyten (E.C. Verh Dtsch Ges Inn Med 75:450, 1969.

Boulard M, Blume K, Beutler E: The effect of copper on red cell enzyme activities. J Clin Invest 51:459, 1972.

Kiss JE, Berman D, Van Thiel D: Effective removal of copper by plasma exchange in fulminant Wilson’s disease. Transfusion 38:327, 1998.

Jackson RC, Elder WJ, McDonnell H: Sodium-chlorate poisoning complicated by acute renal failure. Lancet 2:1381, 1961.

Eaton JW, Kolpin CF, Swofford HS, Kjellstrand CM, Jacob HS: Chlorinated urban water: A cause of dialysis-induced hemolytic anemia. Science 181:463, 1973.

Caterson RJ, Savdie E, Raik E, Coutts D, Mahony JF: Heinz-body haemolysis in haemodialysed patients caused by chloramines in Sydney tap water. Med J Aust 2:367, 1982.

Orringer EP, Mattern WD: Formaldehyde-induced hemolysis during chronic hemodialysis. N Engl J Med 294:1416, 1976.

Lubash GD, Phillips RE, Shields JD, Bonsnes RW: Acute aniline poisoning treated by hemodialysis. Arch Intern Med 114:530, 1964.

Lowenstein L, Ballew DH: Fatal acute haemolytic anaemia, thrombocytopenic purpura, nephrosis and hepatitis resulting from ingestion of a compound containing apiol. Can Med Assoc J 78:195, 1958.

Schroder C, Kruger E, Abel J: Acute poisoning caused by the herbicide dichlorprop (preparation SYS 67 PROP). Kinderarztl Prax 59:81, 1991.

Martin H, Woerner W, Rittmeister B: Hämolytische Anämie durch Inhalation von Hydroxylaminen. Klin Wochenschr 42:725, 1964.

Fisher B: The significance of Heinz bodies in anemias of obscure etiology. Am J Med Sci 143, 1955.

Nierenberg DW, Horowitz MB, Harris KM, James DH: Mineral spirits inhalation associated with hemolysis, pulmonary edema, and ventricular fibrillation. Arch Intern Med 151:1437, 1991.

Hunter D: Industrial toxicology. Q J Med 12:185, 1943.

Gasser VC: Perakute hämolytische Innenkörperanamie mit Methämoglobinamie nach Behandlung eines Säuglingsekzems mit Resorcin. Helv Paediatr Acta 9:285, 1954.

Brandes JC, Bufill JA, Pisciotta AV: Amyl nitrite-induced hemolytic anemia. Am J Med 86:252, 1989.

Pugh JI, Enderby GEH: Haemoglobinuria after intravenous myanesin. Lancet 2:387, 1947.

Poinsot J, Guillois B, Margis D, et al: Neonatal hemolytic anemia after intra-amniotic injection of methylene blue. Arch Fr Pediatr 45:657, 1988.

Sills MR, Zinkham WH: Methylene blue-induced Heinz body hemolytic anemia. Am J Dis Child 148:306, 1994.

Davidson S, Seldon M, Jones B: Omeprazole and Heinz-body haemolytic anaemia. Aust N Z J Med 27:441, 1997.

Hassan AB, Seligmann H, Bassan HM: Intravascular hemolysis induced by pentachlorophenol. BMJ 291:21, 1985.

Adams JG, Heller P, Abramson RK, Vaithianathan T: Sulfonamide-induced hemolytic anemia and hemoglobin Hasharon. Arch Intern Med 137:1449, 1977.

Greenberg MS: Heinz body hemolytic anemia. Arch Intern Med 136:153, 1976.

Kaplinsky N, Frankl O: Salicylazosulphapyridine-induced Heinz body anemia. Acta Haematol (Basel) 59:310, 1978.

Ward PCJ, Schwartz BS, White JG: Heinz-body anemia: “Bite cell” variant—A light and electron microscopic study. Am J Hematol 15:135, 1983.

Yoo D, Lessin LS: Drug-associated “bite cell” hemolytic anemia. Am J Med 92:243, 1992.

Landsteiner EK, Finch CA: Haemoglobinuria after intravenous myanesin. N Engl J Med 237:310, 1947.

Rath CE: Drowning hemoglobinuria. Blood 8:1099, 1953.

Tavassoli M: Anemia of spaceflight. Blood 60:1059, 1982.

Mengel CE, Kann HE Jr, Heyman A, Metz E: Effects of in vivo hyperoxia on erythrocytes. II. Hemolysis in a human after exposure to oxygen under high pressure. Blood 25:822, 1965.

Dacie JV: The Haemolytic Anaemias. Grune & Stratton, New York, 1967.

Monzon C, Miles J: Hemolytic anemia following a wasp sting. J Pediatr 96:1039, 1980.

Schulte KL, Kochen MM: Haemolytic anaemia in an adult after a wasp sting. Lancet 2:478, 1981.

Vachvanichsanong P, Dissaneewate P, Mitarnun W: Non-fatal acute renal failure due to wasp stings in children. Pediatr Nephrol 11:734, 1997.

Nance WE: Hemolytic anemia of necrotic arachnidism. Am J Med 31:801, 1961.

Madrigal GC, Ercolani RL, Wenzl JE: Toxicity from a bite of the brown spider (Loxosceles Reclusus): skin necrosis, hemolytic anemia, and hemoglobinuria in a nine-year-old child. Clin Pediatr 11:641, 1972.

Chadha JS, Leviav A: Hemolysis, renal failure, and local necrosis following scorpion sting. JAMA 241:1038, 1979.

Barretto OCO, Cardoso JL, De Cillo D: Viscerocutaneous form of loxoscelism and erythrocyte glucose-6-phosphate deficiency. Rev Inst Med trop Sao Paulo 27:264, 1985.

Wasserman GS, Siegel C: Loxoscelism (brown recluse spider bites): A review of the literature. Clin Toxicol 14:353, 1979.

Wright SW, Wrenn KD, Murray L, Seger D: Clinical presentation and outcome of brown recluse spider bite. Ann Emerg Med 30:28, 1997.

Reid HA: Cobra-bites. BMJ 2:540, 1964.

Gillissen A, Theakston RD, Barth J, et al: Neurotoxicity, haemostatic disturbances and haemolytic anaemia after a bite by a Tunisian saw-scaled or carpet viper (Echis ‘pyramidum’-complex): failure of antivenom treatment. Toxicon 32:937, 1994.

Ham TH, Shen SC, Fleming EM, Castle WB: Studies on the destruction of red blood cells. IV. Blood 3:373, 1948.

Wagner HN, Jr., Razzak MA, Gaertner RA, Caine WP, Jr., Feagin OT: Removal of erythrocytes from the circulation. Arch Intern Med 110:90, 1962.

Shen SC, Ham TH, Fleming EM: Studies on the destruction of red blood cells. III. Mechanism and complications of hemoglobinuria in patients with thermal burns: Spherocytosis and increased osmotic fragility of red blood cells. N Engl J Med 229:701, 1943.

Topley E, Bull JP, Maycock WDA, Mourant AE, Parkin D: The relation of the isoagglutinins in pooled plasma to the haemolytic anaemia of burns. J Clin Pathol 16:79, 1963.

Stohlman F, Jr., Brecher G, Schneiderman M, Cronkite EP: The hemolytic effect of ionizing radiations and its relationship to the hemorrhagic phase of radiation injury. Blood 12:1061, 1957.

Jin YS, Anderson G, Mintz PD: Effects of gamma irradiation on red cells from donors with sickle cell trait. Transfusion 37:804, 1997.
Copyright © 2001 McGraw-Hill
Ernest Beutler, Marshall A. Lichtman, Barry S. Coller, Thomas J. Kipps, and Uri Seligsohn
Williams Hematology




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