Acute haemolysis

Body iron content is the principal factor in the regulation of iron absorption (Marx,1979a,b). However, other physiological variables, such as erythropoietic rate (Bothwell, 1968), hypoxia (Raja et ah, 1988) and inflammation (Weber et ah, 1988) also influence iron absorption. In normal individuals, if the rate of erythropoiesis is stimulated by blood loss, dyserythropoiesis or acute haemolysis, iron absorption is increased. Conversely, if erythropoiesis is inhibited by hypertransfusion, starvation or descent from high altitude to sea level, then iron absorption decreases. The adaptive response of iron absorption to increased erythropoiesis, stimulated... 

Rees DC, Kelsey H, Richards JD. Acute haemolysis induced by high dose ascorbic acid in glucose-6-phosphate dehydrogenase deficiency. BMJ 1993 306(6881) 841-2. 

Watson A. Reversible acute haemolysis associated with indinavir. AIDS 2000 14(4) 465-6. 

McCaffrey RP, Farid Z, Kent DC. Acute haemolysis with Ambilhar treatment in glucose-6-phosphate dehydrogenase deficiency. Trans R Soc Trop Med Hyg 1972 66(5) 795-7. 

Massive acute haemolysis in neonates with glucose-6-phosphate dehydrogenase deficiency. 

Rare congenital enzyme deficiencies which have effects that are of particular interest to the dental profession include hypophosphatasia, acatalasia and the Lesch-Nyhan syndrome. Furthermore, some drug idiosyncracies are known to result from inherited defects in an enzyme which, in normal subjects, is concerned with the metabolism of the drug. For example, certain subjects who are deficient in serum cholinesterase show an abnormally prolonged respiratory paralysis after administration of suxamethonium given to produce muscular relaxation. Other subjects develop an acute haemolysis when given the antimalarial drug primaquine or certain sulphonamides. 

In Hb Torino, the 43 a (GDI) phenylalanine is replaced by valine. Heinz bodies and increased methaemoglobin levels ( > 4%) are found in fresh blood. The application of a sulphonamide is followed by acute haemolysis and formation of Heinz bodies which represent precipitated haemoglobin. 

Soluble inorganic arsenic is acutely toxic, and ingestion of large doses leads to gastrointestinal symptoms, disturbances of cardiovascular and nervous system functions, and eventually death. In survivors, bone marrow depression, haemolysis, hepatomegaly, melanosis, polyneuropathy, and encephalopathy may be observed. 

Sharma BK, Singhal PC, Chugh KS. 1978. Intravascular haemolysis and acute renal failure following potassium dichromate poisoning. Postgrad Med J 54 414-415. 

The symptoms of acute and chronic poisoning by arsenic have been described by Rentoul and Smith [10], Davidson and Henry [11] and Fowler [12]. Acute symptoms include gastrointestinal damage, convulsions and haemorrhage at autopsy, fatty degeneration of the liver and kidneys is frequently noted. Acute inhalation of arsine is followed by extensive haemolysis, haemoglobinuria and death from renal failure. 

Drugs that carry a possible risk of haemolysis in some G6PD deficient subjects inclulde aspirin (when dose exceeds 1 g/d), menadione, probenecid, quini-dine chloroquine and quinine (both are acceptable in acute malaria). 

Suspicion Detection of acute or chronic liver disease of unclear aetiology (in particular fatty liver) and/or haemolysis, and/or neurological or psychological peculiarities in children above the age of 6, in juveniles and in... 

Forbes CD, Craig JA, Mitchell R, McNicol GP. Acute intravascular haemolysis associated with cephalexin therapy. Postgrad Med J 1972 48(557) 186-8. 

Kumana CR, Chan GT, Yu YL, Lauder IJ, Chan TK, Kou M. Investigation of intravascular haemolysis during treatment of acute stroke with intravenous glycerol. Br J Clin Pharmacol 1990 29(3) 347-53. 

Hagnevik K, Gordon E, Lins LE, et al. Glycerol-induced haemolysis with haemoglobinuria and acute renal failure. Lancet 1974 i 75-77. 

Acute intravascular haemolysis in glucose-6-phosphate dehydrogenase deficient patients following ingestion of herbal broth containing Acalypha indica. 

Lambden SP, Akeru J, Barrett NA. Acute intravascular haemolysis associated with intravenous administration of meropenem in a sixty four year old man. Can J Clin Pharmacol 2010 17(1) e64-6. 

A combination of haematin (oxidized haem, containing iron in the ferric state) and albumin. It is found in the blood when there is intravascular haemolysis and in cases of acute haemorrhagic pancreatitis. It can be identified in blood by its spectral characteristics or by Schumm s test, in which an albumin haemo-chromogen, which has a distinctive absorption spectrum, is formed. 

A 57-year-old healthy man on treatment for pulmonary TB presented with haemolysis and severe acute renal failure. His kidney biopsy showed acute tubulointersitital nephritis with no evidence of granulomas. RMP was discontinued, and he was treated with fluid repletion, iv furosemide and dialysis therapy. Patient significantly improved and discharged subsequently. 

Viral infection The authors report a case in which a child became infected with Epstein-Barr virus developed immune thrombocytopenic purpura, and treatment with anti-D Ig caused intravascular haemolysis as well as acute kidney injury [118 ]. Although some degree of extravascular haemolysis is expected, this case is tmusual because of tile severity and intravascular nature. The authors speculate that the use of intravenous anti-D triggered an xmusual virus-induced immune response that resulted in the pattern of haemolysis seen, which has been reported previously. 

Another report describes the balloon-occluded retrograde transvenous obliteration, which is traditionally based on liquid sclerotherapy. However, overdose and systemic spillage of liquid sclerosant can cause severe complications, such as haemolysis that can lead to haemoglobinuria, allergy, acute respiratory distress S5mdrome and other disorders. 

Anaemia Acute oxidative haemolysis may occur in glucose-6-phosphate dehydrogenase deficiency and rarely in individuals with a genetically determined abnormality of phenacetin metabolism (136, 189 ). Chronic haemolytic anaemia induced by phenacetin may result in splenomegaly (190 ). 

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