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Table 28.1 Causes of anaemia of chronic disorders. Chronic inflammatory diseases Infectious (e.g. pulmonary abscess, tuberculosis, osteomyelitis, pneumonia, bacterial endocarditis) Non-infectious (e.g. rheumatoid arthritis, systemic lupus erythematosus and other connective tissue diseases, sarcoid, Crohn’s disease, cirrhosis) Malignant disease (e.g. carcinoma, lymphoma, sarcoma, myeloma) Table 28.2 Haematological abnormalities in malignant disease. Haematological abnormality Pancytopenia Marrow hypoplasia Myelodysplasia Leucoerythroblastic Megaloblastic Tumour or treatment associated Chemotherapy, radiotherapy Chemotherapy, radiotherapy Metastases in marrow Folate deficiency B12 deficiency (carcinoma of stomach) Red cells Anaemia of chronic disorders Iron deficiency anaemia Pure red cell aplasia Immune haemolytic anaemia Microangiopathic haemolytic anaemia Polycythaemia Most forms Especially gastrointestinal, uterine Thymoma Lymphoma, ovary, other tumours Mucin-secreting carcinoma Kidney, liver, cerebellum, uterus White cells Neutrophil leucocytosis Leukaemoid reaction Eosinophilia Monocytosis Most forms Disseminated tumours, those with necrosis Hodgkin lymphoma, others Various tumours Platelets and coagulation Thrombocytosis Disseminated intravascular coagulation Activation of fibrinolysis Acquired inhibitors of coagulation Paraprotein interfering with platelet function Tumour cell procoagulants – tissue factor and cancer procoagulant (activates factor X) Untitled-5.indd 59 Gastrointestinal tumours with bleeding, others Mucin-secreting carcinoma, prostate Prostate Most forms Lymphomas, myeloma Especially ovarian, pancreas, brain, colon 2/8/2011 11:53:54 AM Table 28.3 Haematological abnormalities in renal failure. Anaemia Reduced erythropoietin production Aluminium excess in dialysis patients Anaemia of chronic disorders Iron deficiency blood loss (e.g. dialysis, venesection, defective platelet function) Folate deficiency chronic haemodialysis without replacement therapy Abnormal platelet function Thrombocytopenia Immune complex-mediated (e.g. systemic lupus erythematosus, polyarteritis nodosa) Some cases of acute nephritis and following allograft Haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura Thrombosis Some cases of the nephrotic syndrome Polycythaemia In renal allograft recipients Rarely in renal cell carcinoma, cysts, arterial disease Table 28.4 Haematological abnormalities in liver disease. Liver failure ± obstructive jaundice ± portal hypertension Refractory anaemia– usually mildly macrocytic, often with target cells; may be associated with: Blood loss and iron deficiency Alcohol (± ring sideroblastic change) Folate deficiency Haemolysis (e.g. Zieve’s syndrome, Wilson’s disease, immune hypersplenism from portal hypertension) Bleeding tendency Deficiency of vitamin K-dependent factors; also of factor V and fibrinogen Thrombocytopenia hypersplenism, immune platelet function defects Functional abnormalities of fibrinogen Increased fibrinolysis Portal hypertension – haemorrhage from varices Viral hepatitis Aplastic anaemia Tumours Polycythaemia Neutrophil leucocytosis and leukaemoid reactions Untitled-5.indd 60 2/8/2011 11:53:54 AM Table 28.5 Blood abnormalities associated with infections. Haematological abnormality Anaemia Anaemia of chronic disorders Aplastic anaemia Transient red cell aplasia Marrow fibrosis Immune haemolytic anaemia Direct red cell damage or microangiopathic Hypersplenism White cell changes Neutrophil leucocytosis Leukaemoid reactions Eosinophilia Monocytosis Neutropenia Lymphocytosis Lymphopenia Thrombocytopenia Megakaryocytic depression, immune complexmediated and direct interaction with platelets Prothrombotic state Infection associated Chronic infections especially tuberculosis Viral hepatitis Human parvovirus Tuberculosis Infectious mononucleosis, Mycoplasma pneumoniae Bacterial septicaemia (associated DIC), Clostridium perfringens, malaria, bartonellosis Viruses – haemolytic uraemic syndrome and TTP Chronic malaria, tropical splenomegaly syndrome, leishmaniasis, schistosomiasis Acute bacterial infections Severe bacterial infections particularly in infants Tuberculosis Parasitic diseases (e.g. hookworm, filariasis, schistosomiasis, trichinosis) Recovery from acute infections Chronic bacterial infections: tuberculosis, brucellosis, bacterial endocarditis, typhoid Viral infections – HIV, hepatitis, influenza Fulminant bacterial infections (e.g. typhoid, miliary tuberculosis) Infectious mononucleosis, toxoplasmosis, cytomegalovirus, rubella, viral hepatitis, pertussis, tuberculosis, brucellosis HIV infection Legionella pneumophila Acute viral infections particularly in children (e.g. measles, varicella, rubella, malaria, severe bacterial infection) All with prolonged inflammation DIC, disseminated intravascular coagulation; HIV, human immunodeficiency virus; TTP, thrombotic thrombocytopenic purpura. Untitled-5.indd 61 2/8/2011 11:53:55 AM Table 28.6 Advantages and disadvantages of the tests used to monitor the acute phase response. Advantages CRP* Specific test of acute phase protein Disadvantages More than one protein required to measure acute (CRP) and chronic inflammation Costly when assayed in small numbers Fast response (6 hours) to change in disease activity High sensitivity – owing Sophisticated to large incremental equipment and change antisera required Can be measured on stored serum Small sample volumes Automated analysis ESR and plasma viscosity Useful in chronic Not sensitive to acute disease changes (<24 hours) ESR inexpensive, Not specific for acute easy, no electrical phase response power required Plasma viscosity – Slow to change with alteration in disease result obtained activity and quickly (15 min) insensitive to small changes in activity Plasma viscosity not Fresh samples (<2 affected by anaemia hours) required for ESR ESR, erythrocyte sedimentation rate. * C-reactive protein (CRP) is normally present in low concentrations (<5 mg/L). Levels are not influenced by anaemia, pregnancy or heart failure. During severe acute infection the plasma concentration may rise 100-fold. Untitled-5.indd 62 2/8/2011 11:53:55 AM