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Splenomegaly
Published in K. Gupta, P. Carmichael, A. Zumla, 100 Short Cases for the MRCP, 2020
K. Gupta, P. Carmichael, A. Zumla
Five common causes are: Chronic myeloid leukaemia.Myelofibrosis.Polycythaemia rubra vera.Tropical splenomegaly syndrome (P. malariae).Kala-Azar (visceral leishmaniasis).
Infections
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Some adults in endemic zones may develop massive splenomegaly with secondary Hypersplenism (anaemia and cytopenias) (see Chapter 9). Splenomegaly is essentially a lymphoreticular reactive hyperplasia to chronic infection that is idiosyncratic (there is an inherited tendency). There are high immunoglobulin levels in the blood, but parasite numbers are very few. This condition is also referred to as ‘tropical splenomegaly syndrome’.
The Problems of Undernutrition
Published in R. J. Jarrett, Nutrition and Disease, 1979
In addition to the direct effect on the erythrocytes, repeated malarial infection is also responsible for a chronic anaemia associated with enlarged spleen. In the so-called tropical splenomegaly syndrome, parasitaemia is scanty or absent and the red cell morphology resembles that of iron deficiency. Studies with labelled iron have shown a high plasma turnover of iron. A large number of erythrocytes are trapped in the enlarged spleen and represent a considerable portion of the red cell mass, which may be between 50 and 75 per cent of the total pool. It is likely that sequestration of such a large number of erythrocytes results in active erythropoiesis by the marrow, using up the available stores of iron and folic acid.
The enemy at home: leishmaniasis in the Mediterranean basin, Italy on the focus
Published in Expert Review of Anti-infective Therapy, 2020
Elena Gianchecchi, Emanuele Montomoli
The incubation period of VL infection lasts 3 to 8 months. VL encompasses a broad spectrum of manifestations of infection whose clinical presentations and severity depend on the clinical stage of the disease. More specifically in many cases it may be asymptomatic, or it may manifest in a mild form that recovers spontaneously but it can follow an acute, subacute, or chronic course. VL is the most severe subtype of the disease, caused by the spread of Leishmania parasites from the initial site of cutaneous infection through the reticuloendothelial system to internal organs, mainly the bone marrow, spleen and the liver, leading to the destruction of immune cells at these organs. VL develops with generalized symptoms, including cachexia, cough, diarrhea, fever, hypergammaglobulinemia (primarily IgG from polyclonal B-cell activation), hypoalbuminaemia, pancytopenia (anemia, thrombocytopenia, and leukopenia, with neutropenia, marked eosinopenia, and a relative lymphocytosis and monocytosis) and hepatosplenomegaly (with a predominance of splenomegaly) [132], usually present since early infection phases [125]. On the other hand, at late stages of the disease VL patients present gingival hemorrhage, epistaxis, ascites, distension of the abdomen, and peripheral edema [106]. In children, retardation of growth has been described [133]. Some pathologies can mimic VL and they include tropical splenomegaly syndrome, malaria, typhoid fever, African trypanosomiasis, bacterial endocarditis, schistosomiasis or cirrhosis with portal hypertension, miliary tuberculosis, lymphoma and leukemia [132].