Page 401 - Essential Haematology
P. 401
Chapter 28 Haematological changes in systemic disease / 387
(a heavily glycosylated derivative) or monthly (a Liver d isease
pegolated derivative). Complications of therapy
The haematological abnormalities in liver disease
have been initial transient flu - like symptoms,
are listed in Table 28.4 . Chronic liver disease is
hypertension, clotting of the dialysis lines and,
associated with anaemia that is mildly macrocytic
rarely, fits. A poor response to erythropoietin sug-
and often accompanied by target cells, mainly as a
gests iron or folate deficiency, infection, aluminium
result of increased cholesterol in the membrane
toxicity or hyperparathyroidism. Intravenous iron is
(Fig. 28.5 a). Contributing factors to the anaemia
often needed to correct iron deficiency shown by
may include blood loss (e.g. bleeding varices) with
serum ferritin, percentage saturation of total iron -
iron deficiency, dietary folate deficiency and direct
binding capacity or percentage hypochromic red
suppression of haemopoiesis by alcohol.
cells in the blood.
Haemolytic anaemia may occur in patients with
alcohol intoxication (Zieve s syndrome) (Fig. 28.5 b)
’
and in Wilson s disease (caused by copper oxidation
’
Platelet and c oagulation a bnormalities of red cell membranes); autoimmune haemolytic
anaemia is found in some patients with chronic
A bleeding tendency with purpura, gastrointestinal
immune hepatitis. Haemolysis may also occur in
or uterine bleeding occurs in 30 – 50% of patients
end - stage liver disease because of abnormal red cell
with chronic renal failure and is marked in patients
membranes resulting from lipid changes. Viral hep-
with acute renal failure. The bleeding is out of pro-
portion to the degree of thrombocytopenia and has
been associated with abnormal platelet or vascular
function, which can be reversed by dialysis. Table 28.4 Haematological abnormalities in
Correction of the anaemia with erythropoietin also liver disease.
improves the bleeding tendency. Immune complex -
Liver failure ± obstructive jaundice ± portal
mediated thrombocytopenia occurs in some patients
hypertension
with acute nephritis, SLE and polyarteritis nodosa
Refractory anaemia – usually mildly macrocytic,
and also following renal allografts. Renal allografts
often with target cells; may be associated with:
may also lead to polycythaemia in 10 – 15% of
Blood loss and iron defi ciency
patients.
Alcohol ( ± ring sideroblastic change)
The haemolytic uraemic syndrome and throm- Folate defi ciency
botic thrombocytopenic purpura are discussed on Haemolysis (e.g. Zieve ’ s syndrome, Wilson ’ s
p. 337 . Patients with the nephrotic syndrome have disease, immune hypersplenism from portal
an increased risk of venous thrombosis. hypertension)
Bleeding tendency
Defi ciency of vitamin K - dependent factors; also
Congestive h eart f ailure of factor V and fi brinogen
Thrombocytopenia hypersplenism, immune
Anaemia is common in congestive heart failure due platelet function defects
to a variety of causes. These include haemodilution, Functional abnormalities of fi brinogen
chronic kidney disease, release of cytokines increas- Increased fi brinolysis
ing hepcidin synthesis and so reducing iron absorp- Portal hypertension – haemorrhage from varices
tion and recycling of iron from macrophages, and
Viral hepatitis
reducing erythropoetin secretion and erythropoie-
Aplastic anaemia
tin responsiveness of erythroblasts. Iron defi ciency
may develop. Treatment with oral or intravenous Tumours
iron may reduce anaemia, fatigue and increase Polycythaemia
cardiac function, exercise capacity and quality of Neutrophil leucocytosis and leukaemoid
reactions
life.