Malarial Antibodies in Idiopathic Splenomegaly in Uganda

Gebbie, Donald A. M.; Hamilton, P. J. S.; Hutt, M. S. R.; Marsden, Philip D.; Voller, A.; Wilks, N. E.

doi:10.1016/s0140-6736(64)90396-4

Cited by 41 publications

(22 citation statements)

References 3 publications

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“…Stools were examined by the formol-ether-concentration technique (Ridley and Hawgood, 1956) for ova, cysts, and parasites. Rectal snips were examined for schistosome ova.Sera from 40 patients were examined by a fluorescent antibody technique (Voller, 1964) for the presence of malarial antibodies. Control sera from patients without splenomegaly were also examined.…”

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An Investigation of Tropical Splenomegaly at Mulago Hospital, Kampala, Uganda

Marsden¹,

Hutt²,

Wilks³

et al. 1965

BMJ

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Idiopathic, cryptogenic, or tropical splenomegaly, as it is variously termed, is often encountered at the Mulago Hospital in Kampala. Trowell (1950) reported several cases in which no good reason could be found for gross splenomegaly, and discussed the current theories of aetiology. Leather (1961) made the important observation that many cases had a mild portal hypertension in the absence of any evidence of cirrhosis on liver biopsy. Of the 41 cases he investigated 29 showed sinusoidal infiltrates by lymphocytes, histiocytes, and plasma cells, an appearance that had been noted elsewhere in the tropics by Fawdry (1955) from Aden, and by Chaudhuri et al. (1956) from India.The present report describes a series of cases of marked splenomegaly admitted to the New Mulago Hospital, Kampala, in which combined clinical, haematological, parasitological, and pathological investigations were carried out to assess the cause and effect of the large spleens. Materials and MethodsOver a period of eight months 64 patients with marked splenomegaly were investigated in the New Mulago Hospital, Kampala.Routine haematological investigations were prepared by standard techniques (Dacie, 1956). In five patients the red-cell survival and splenic uptake were estimated, using 5Cr-tagged red cells (Mollison and Veall, 1955), and the sites of red-cell destruction were assessed by the method of Hughes Jones and Szur (1957 BudtzOlsen, 1952;Atkinson and Sherlock, 1954). Splenic puncture specimens were examined for malaria parasites and leishmaniae. Initially, random peripheral thick blood was examined for malaria parasites and trypanosomes, but in the latter part of the study a minimum of 10 consecutive daily blood films were examined for malaria parasites by two observers.Stools were examined by the formol-ether-concentration technique (Ridley and Hawgood, 1956) for ova, cysts, and parasites. Rectal snips were examined for schistosome ova.Sera from 40 patients were examined by a fluorescent antibody technique (Voller, 1964) for the presence of malarial antibodies. Control sera from patients without splenomegaly were also examined. The antigen used was Plasmodium bastianellii.

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An Investigation of Tropical Splenomegaly at Mulago Hospital, Kampala, Uganda

Marsden¹,

Hutt²,

Wilks³

et al. 1965

BMJ

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“…Such cases often have a very high fluorescent malarial antibody titre (Gebbie et al, 1964), absence of malarial pigment in liver biopsy specimens, excessive Kupffer cell hyperplasia, and a high incidence of P. malariae parasitaemia (Marsden et al, 1965). The term " tropical splenomegaly syndrome " has recently been suggested for these cases of gross splenomegaly seen in the tropics in which no definitive cause can be established (Brit.…”

Section: Methodsmentioning

confidence: 99%

“…These cases have been called " idiopathic tropical splenomegaly" of childhood, and may be compared with the same syndrome in adults. Recent investigation of idiopathic tropical splenomegaly in Ugandan adults suggests that the majority of such cases are due to malarial infection, though whether this is an altered host response or an infection by a specific type of malaria is still uncertain (Gebbie et al, 1964;Marsden et al, 1965). The problem of gross splenomegaly in childhood in Uganda has not hitherto been investigated.…”

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Childhood splenomegaly in Uganda, and its relation to malaria.

Vanier¹,

Hutt²,

Cook³

1968

BMJ

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Gastric Surgery-Ashurst BiNL 649 wich " technique. In no case were circulating P.C.A. detected postoperatively that had not been found in the preoperative specimen. The incidence of P.C.A. was below the normal range for the age and sex of the patients, but 2 of 22 (9%) patients with gastric cancer showed circulating P.C.A. The failure to demonstrate circulating parietal-cell antibodies in serial specimens of serum taken from patients who had undergone gastric surgery does not support the hypothesis that autoimmunization, is the result of damage to the gastric mucosa.

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“…A number of investigators have ascribed the condition to an abnormal immunological response to malaria (Gebbie et al, 1964;Marsden et al, 1967;Pryor, 1967). A diligent search for malarial parasites among patients with tropical splenomegaly syndrome in Uganda revealed Plasmodium malaiae in 45%, as compared with a 4% yield among controls (Marsden et al, 1965).…”

Section: Introductionmentioning

confidence: 99%

“…An association with P. malariae, however was not shown in similar cases in New Guinea (Marsden et al, 1967). Patients with tropical splenomegaly syndrome have raised antimalaria antibody titres and live in malarious areas of Uganda (Gebbie et al, 1964;Marsden et al, 1965;Hamilton et al, 1965). Dramatic reduction in spleen size following long-term antimalarial prophylaxis has been reported (Watson-Williams et al, 1967;Watson-Williams and Allan, 1968).…”

Section: Introductionmentioning

confidence: 99%