Anaemia haemolytic

Many microorganisms minimize the effects of the host s defence system against them by mimicking the antigenic stmcture of the host tissne. The eventual immunological response of the host to infection then leads to the autoimmune destmction of itself. Thus, infections with Mycoplasma pneumoniae can lead to production of antibody against normal Group 0 erythrocytes with concomitant haemolytic anaemia. 

F2. Filosa, S., Calabro, V., Vallone, D., Filosa, S., Calabro, V., Vallone, D Poggi, V., Mason, P., Pagnini, D., Alfinito, F Rotoli, B., Martini, G., Luzzatto, L., and Battistuzzi, G Molecular basis of chronic non-spherocytic haemolytic anaemia A new G6PD variant (393 Arg - His) with abnormal KmG6P and marked in vivo instability. Br. J. Haematol. 80, 111 -116 (1992). 

F4. Filosa, S., Cai, W., Galanello, R., Cao, A., De Mattia, D Schettini, F., and Martini, G., A novel single-base mutation in the glucose 6-phosphate dehydrogenase gene is associated with chronic non-spherocytic haemolytic anaemia. Hum. Genet. 94,560-562 (1994),... 

R8, Rouger, H., Valentin, C Craescu, C. T., Galactdros, F., and Cohen-Solal, M., Five unknown mutations in the LR pyruvate kinase gene associated with severe hereditary nonspherocytic haemolytic anaemia in France. Br. J. Haematol. 92,825-830 (1996). 

T18. Toren, A., Brok-Simoni, F Ben-Bassat, I., Holtman, F., Mandel, M., Neumann, Y., Ramot, B., Rechavi, G and Kende, G., Congenital haemolytic anaemia associated with adenylate kinase deficiency. Br. J. Haematol. 87,376-380 (1994). 

T26. Turner, G., Fletcher, J., Elber, J., Yanagawa, Y Dav6, V., and Yoshida, A., Molecular defect of a phosphoglycerate kinase variant associated with haemolytic anaemia and neurological disorders in a large kindred. Br. J. Haematol. 91,60-65 (1995). 

Fluxes of iron from the plasma towards BM and other tissues can be quantified by ferrokinetic studies, using 59Fe and sophisticated computer models (Ricketts et ah, 1975 Ricketts and Cavill, 1978 Barosi et ah, 1978 Stefanelli et ah, 1980). Plasma iron turnover (PIT), erythroid iron turnover (EIT), non-erythroid iron turnover (NEIT), marrow iron turnover (MIT), and tissue iron turnover (TIT) could be calculated in many disorders of iron metabolism and in all kinds of anaemias. Iron is rapidly cleared from the plasma in iron deficiency and in haemolytic anaemias. If more iron is needed for erythropoiesis, more transferrin receptors (TfR) are expressed on erythroblasts, resulting in an increased flux of iron from intestinal mucosal cells towards the plasma. In haemolytic anaemias MPS, and subsequently hepatocytes, are overloaded. In hereditary haemochromatosis too much iron is absorbed by an intrinsic defect of gut mucosal cells. As this iron is not needed for erythropoiesis,... 

Worlledge, S.M., Carstairs, K.C., and Dacie, J.V., Autoimmune haemolytic anaemia associated with alpha-methyldopa therapy, Lancet 288, 135, 1966. 

Salama, A. et al., Diclofenac-induced immune haemolytic anaemia Simultaneous occurrence of red blood cell autoantibodies and drug-dependent antibodies, Br. J. Haematol., 95, 640, 1996. 

Kramer, M.R., Levene, C., and Hershko, C., Severe reversible autoimmune haemolytic anaemia and thrombocytopenia associated with diclofenac therapy. Scand. J. Haematol., 36, 118, 1986. 

The jaundice could be due to liver damage. Hepatocytes contain AST, ALT and LD red cells also contain AST and LD but do not contain significant amounts of ALT. These data suggest increased red cell destruction rather than liver cell damage and the patient was diagnosed with haemolytic anaemia. 

D. C. McMillan, T. P. Bradshaw, J. A. Hinson, D. J. Jollow, Role of Metabobtes in Prop-anil-Induced Haemolytic Anaemia , Toxicol. Appl. Pharmacol. 1991,110, 70-78. 

Lastly, nomifensine was an interesting antidepressant that also had noradrenaline, dopamine and, due to its 4-hydroxy metabolite, serotonin reuptake properties. It was withdrawn some years ago because of the occurrence of haemolytic anaemia in a small number of patients. It was a particularly effective drug in the treatment of depression in patients with epilepsy as, unlike many antidepressants available at that time, it did not affect the seizure threshold. 

Hallowell M. 1959. Acute haemolytic anaemia following the ingestion of paradichlorobenzene. Arch Dis Child 34 74-75. 

Fig. 8.14 Structure of nomifensine, an antidepressant associated with acute immune haemolytic anaemia.

Rifampicin Shock, haemolytic anaemia, renal failure... 

The Yellow Card Scheme was soon beginning to pay dividends. In early 1966, the YeUow Card Scheme had identified methyldopa as a cause of haemolytic anaemia and an appropriate advice was issued. Another success was the detection of a faulty batch of a particular product, which the manufacturer immediately withdrew, underlining the value of an efficient procedure for tracing a batch. During June 1967, the Committee distributed a leaflet on the use of aerosols in asthma. This was prompted by the death rate amongst asthmatic patients aged 5 to 34 years that had risen some 300% above the level in 1959-60 when such preparations were introduced. By September 1968, the rate had dropped to only 50% above that seen in 1959-60 despite sales having dropped only 20%. 

Adverse effects include drowsiness, diarrhoea, rashes (withdraw treatment), thrombocytopenia, haemolytic anaemia, aplastic anaemia. Convulsions may occur in overdosage. 

Anaemia due to excessive destruction, of blood e.g. sickle cell anaemia and haemolytic anaemia. 

Adverse reactions include visual disturbances (transient, at the beginning of therapy), nausea and epigastric bloating (rare) and diarrhoea. Hypersensitivity including allergic skin reactions, thrombocytopenia, leucopenia, agranulocytosis, haemolytic anaemia, vasculitis, cholestatic jaundice and hepatitis. 

Adverse effects include hypoglycemia, temporary visual impairment, gastrointestinal disturbances. Rarely leucopenia, haemolytic anaemia. Occasionally allergic or pseudoaUergic reactions like itching, urticaria or rashes. In isolated cases allergic vasculitis, photosensitivity or a decrease in serum sodium may occur. 

The uncommon allergic reactions include acute toxic hepatitis, toxic nephrosis and acute haemolytic anaemia. 

Adverse effects are nausea, diarrhoea, haemolytic anaemia in persons with G-6-PD deficiency and peripheral neuritis (on longterm use). 

It is used exclusively for urinary tract infections. The side effects include nausea, vomiting, diarrhoea, anorexia, leukopenia, haemolytic anaemia, jaundice, dizziness and headache. On chronic use can lead to peripheral neuritis and interstitial pulmonary fibrosis. 

However the reported adverse effects include mild gastrointestinal reactions (nausea, vomiting, abdominal cramps and diarrhoea). Symptoms of pseudomembranous colitis may appear either during or after antibiotic treatment. The other side effects are allergic in nature viz. skin rash, itching, bronchospasm, hypotension, erythema multiforme, Steven-Johnson syndrome. Other side effects viz. haemolytic anaemia, hypoprothrombine-mia, seizures and thrombophlebitis have been rarely reported. 

Adverse effects include nausea, vomiting, diarrhoea, abdominal discomfort, dry mouth, taste disturbances headache, dizziness, insomnia myalgia, rash, pruritus, dry skin, hyperpigmentation, nephrolithiasis, dysuria, haematuria, crystalluria, proteinuria elevated liver enzymes and bilirubin, hepatitis neutropenia, haemolytic anaemia and hyperglycaemia etc. 

Adverse effects include nausea, vomiting, weakness, abdominal pain and methaemoglobinaemia. Haemolytic anaemia in patients with G-6-PD deficiency. Passage of dark urine is indication of haemolysis. In larger dose it can cause leucopenia. 

Adverse effects include nausea, vomiting, fatigue, dermatitis, fever, photophobia, haemolytic anaemia, albuminuria and hematuria. 

Adverse effects include skin rash, drug fever, nausea, vomiting, peripheral neuropathy, fatigue, hepatitis and jaundice, haemolytic anaemia, diarrhoea, drowsiness, ataxia, headache, flu like syndrome and stomatitis. 

Adverse effects include increased blood pressure, burning sensation in lips, mouth and throat nausea, vomiting, sweating, pain in chest, throat or hands painful sterile abscess at site of injection haemolytic anaemia in patients with G-6-PD enzyme deficiency hypertension, tachycardia, salivation, lacrimation and conjunctivitis. 

It is indicated in renal transplantation, severe active rheumatoid arthritis unresponsive to other therapy, certain autoimmune diseases, chronic active hepatitis, idiopathic thrombocytopenic purpura and acquired haemolytic anaemia. 

Saffouri B, Cho JH, Felber N. Chlorpropamide-induced haemolytic anaemia. Postgrad Med J 1981 57(663) 44-5. 

Nataas OB, Nesthus I. Immune haemolytic anaemia induced by glibenclamide in selective IgA deficiency. BMJ (Clin Res Ed) 1987 295(6594) 366-7. 

Vinzio S, Andres E, Perrin A-E, Schlienger J-L, Goichot B. Glibenclamide-induced acute haemolytic anaemia revealing a G6PD-deficiency. Diabetes Res Clin Pract 2004 64 181-3. 

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