The histological location of amyloid within various organs in 25 cases of systemic AA amyloidosis was studied with a view to determine whether different morphological patterns exist in this category of amyloidosis. Although morphological variations due to progressive severity of disease were observed, there were appreciable variations in the patterns of amyloid deposition in the kidney and spleen that could not be simply explained on those grounds. Eleven (61%) of 18 kidneys examined showed severe glomerular involvement with mild degrees of vascular deposition while the remaining seven showed predominantly vascular involvement. The glomerular pattern appeared to be more ominous, being significantly associated with severe proteinuria or chronic renal failure. In nine (69%) of 13 spleens examined, amyloid was confined to the walls of small and medium-sized arteries while in the remaining four, vascular involvement was less severe and amyloid was deposited mainly along the reticulin of the white pulp. Possible explanations for these different patterns included resorption and redistribution of amyloid within the body during the course of the disease, and variation in tissue deposition as a manifestation of polymorphism of amyloid proteins. The latter appeared more feasible in view of the recent demonstration of SAA polymorphism and AA heterogeneity in man.
INTRODUCTION: There is an awareness of the increased incidence of splenic abscess in Southeast Asia giving rise to unexplained fever. This study looks at the role of computed tomography (CT) in evaluating focal splenic lesions in patients presenting with fever.
METHODS: 37 patients presenting with fever of unknown origin underwent CT and this study retrospectively analyses the findings in these patients. 13 patients also had associated abdominal pain. Patients with conditions at high risk for splenic infection include: diabetes mellitus in ten patients, leukaemia in seven patients, human immunodeficiency virus infection in five patients, intravenous drug abuse in six patients, and steroid therapy in two patients. No risk factors could be identified in seven patients.
RESULTS: Splenic abscess was diagnosed in 28 patients. A range of infecting organisms was isolated but the most frequent were Staphylococcus aureus (eight), tuberculosis (four), Streptococcus (four), fungal (four) and melioidosis (four). No infecting organism could be identified in ten cases though in patients with leukaemia with multiple low attenuation areas, the cause was presumed to be fungal. Six patients were diagnosed to have splenic infarcts though differentiation from splenic abscess could be difficult; these patients were treated for an abscess and all had endocarditis. Three patients were subsequently diagnosed with lymphoma. Percutaneous abscess drainage was performed in five patients and splenectomy was carried out in six patients.
CONCLUSION: CT proved to be very useful as it not only revealed the size and extent of any splenic abnormality but it assisted with guidance for percutaneous drainage, determined the site for biopsy, and provided follow-up after treatment.
Splenic nodules from 38 cynomolgus monkeys (Macaca fascicularis) which were captured in Malaysia and Indonesia were studied histologically. The lesions were characterized by well-circumscribed focal fibrosis, accumulation of eosinophils and histiocytes, hemorrhage or hemosiderosis, and loss of normal splenic architecture. Small arteries in the lesion frequently had intimal thickening and narrowing of the lumen in addition to the presence of microfilariae. Microfilariae were also seen in the extravascular area of the lesion, and were occasionally engulfed by multinucleated giant cells. The splenic lesion was thought to have been initiated by incomplete infarction caused by intimal thickening and microfilarial occupation of the small arteries.