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Chronic haemolysis

Iron absorption may also be increased secondary to chronic haemolysis as in patients with thalassaemia intermedia. In this group of patients, the anaemia is not usually sufficiently severe to necessitate regular blood transfusions as in thalassaemia major, but iron accumulates over many years from increased absorption via the gut. However, unlike haemochromatosis, venesection is not a therapeutic option, and iron chelation is the only effective way to remove the excess iron. [Pg.193]

Main pathophysiological mechanisms of iron loading that may result in an infectious risk 1.1 Increased gastrointestinal absorption of iron I.2a Parenteral administration of iron I.2b Increased release of iron in the blood stream (haemolysis) 1.3 Increased inhalation of iron II Chronic inflammation III Diabetic ketoacidosis increased... [Pg.307]

Gopinath, C. and J.M. Howell. 1975. Experimental chronic copper toxicity in sheep. Changes that follow the cessation of dosing at the onset of haemolysis. Res. Veterin. Sci. 19 35 43. [Pg.221]

This outline is not exhaustive. For example there is an increasing awareness of the role played by infection with the human immunodeficiency virus while infiltration of the marrow with fibrous tissue or tumour cells will decrease production. In much the same way massive splenomegaly, so common in tropical Africa, sequesters significant volumes of red cells while malarial infection results in their accelerated breakdown. In some cases defects are multifactorial as in chronic lymphocytic leukaemia where infiltration decreases production, splenomegaly traps large amounts of blood while immune mechanisms lead to shortened survival or haemolysis. [Pg.730]

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. [Pg.385]

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... [Pg.614]

Vitamin E plays an important role in cell metabolism as an antioxidant for the elimination of reactive oxygen intermediates. Subsequent to intestinal resorption, vitamin E is transported in chylomicrons into the liver, from where it reaches other organs together with VLDL. Vitamin E deficiency is observed in chronic liver diseases caused by alcohol, Wilson s disease, haemochromatosis and abetalipoproteinaemia. In vitamin E deficiency, neurologic disturbances (areflexia, dysbasia, ocular palsy, reduced perception of vibration) occur haemolysis can likewise be induced or become more pronounced due to epoxide formation of unsaturated fatty acids within the erythrocyte membranes. [Pg.730]

Warm autoimmune haemolytic anaemia may be either idiopathic or secondary to chronic lymphocytic leukaemia, lymphomas, systemic lupus erythematosus, or other autoimmune disorders or infections. Warm autoantibodies are responsible for 48-70% of autoimmune haemolytic anaemia cases and may occur at any age due to the secondary causes, however, the incidence increases starting around 40 years of age. There is an approximate 2 1 female predilection, possibly due to the association with other autoimmune diseases. Warm autoimmune haemolytic anaemia presents as a haemolytic anaemia of varying severity. The symptoms are those of anaemia (i.e. weakness, dizziness, fatigue, pallor, oedema, and dyspnoea on exertion) and haemolysis (i.e. jaundice, dark urine, and splenomegaly). The laboratory evaluation shows a reduced... [Pg.57]

The concentration of potassium in erythrocytes is 25-fold greater than in plasma. The analysis of hem-olyzed samples therefore does not yield clinically meaningful results. Generally, any process that allows potassium to leave erythrocytes or thrombocytes, such as blood storage with or without visible hemolysis (in a refrigerator, no haemolysis), will falsify the potassium concentration. Even clotting of blood will increase potassium concentration hence, its concentration is 0.4 mmol 1 higher in serum (Table 1) than in plasma. Thrombocytosis or chronic myelosis may cause pseudohyperkalemia as well as in vivo haemolysis. For these reasons, heparinized plasma is preferable to serum, as it decreases potassium release from cells. [Pg.717]

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 ). [Pg.73]


See other pages where Chronic haemolysis is mentioned: [Pg.614]    [Pg.814]    [Pg.814]    [Pg.814]    [Pg.817]    [Pg.349]    [Pg.614]    [Pg.814]    [Pg.814]    [Pg.814]    [Pg.817]    [Pg.349]    [Pg.313]    [Pg.90]    [Pg.218]    [Pg.613]    [Pg.820]    [Pg.58]    [Pg.125]    [Pg.320]    [Pg.612]    [Pg.167]    [Pg.406]   
See also in sourсe #XX -- [ Pg.193 ]




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