A series of 137 patients with amoebic liver abscess has been studied. Recognition of clearly defined but diverse clinical syndromes was found to be necessary not only in diagnosis but also in planned surgical management. The majority of patients had the classic syndrome of fever, right abdominal or chest pain, hepatomegaly, hepatic tenderness and radiological abnormalities. Other syndromes of presentation included the silent abscess, acute amoebic colitis, the acute abdomen, the intraabdominal lump, the external sinus, pyrexia of obscure origin, obstructive jaundice and renal, pleuro-pulmonary and cardiac symptoms. The syndromes due to an abscess in different parts of the right lobe and in the left lobe of the liver are to some extent distinct. In spite of the varied modes of presentation of amoebic liver abscess, the key to diagnosis is an understanding of the chronological sequence of the disease and its progression from one syndrome to another. Diagnostic methods of value and the mortality are discussed.

A case is presented of a 55‐year old woman with longstanding rheumatoid arthritis who presented with a lump in her right breast and a markedly enlarged right axillary lymph node. Carcinoma of the breast with lymphadenopathy was diagnosed clinically, but excisional biopsy revealed an amyloid tumour of the breast and amyloid lymphadenopathy. Aniyloid tutnour of the breast is an infrequently reported lesion and the association of axillary lymphadenopathy has not been reported before. The literature is reviewed and the need for a tissue diagnosis prior to embarkation on specific therapy is emphasized.

There appears to be no constant relationship between the modes of clinical presentation and the varying pathological processes in patients with amoebic liver abscesses who present with or develop the abdominal man~festations suggestive of peritonitis. In a proportion of the patients (37 per cent) there is no evidence of a leakage from or rupture of the abscess. In spite of the abdominal manifestations there is no pus, either localized or generalized, in the peritoneal cavity. These patients constitute the group with the syndrome of 'pre-rupture'. The cases with 'pre-rupture' invariably have superjicial abscesses situated in the right lobe of the liver, together with fibrinous adhesions between the visceral and parietal peritoneum over the abscess site. It appears that the hepatic lesion responsible for the syndrome is at a stage just prior to leakage or frank rupture of the abscess. The pathogenesis of the syndrome is discussed and valuable physical signs in the diagnosis of the syndrome are described. By recognizing the existence of this syndrome a laparotomy could be avoided, as closed aspiration of the liver abscess and amoebicidal therapy are the only measures necessary in the management of these patients.