Ultrastructural and histochemical investigations of spindle-shaped corpuscles in phagocytic cells of lymph nodes

Roggendorf, Wolfgang; Groß, U.

doi:10.1016/s0005-8165(77)80082-6

Cited by 2 publications

(1 citation statement)

References 25 publications

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“…The bodies masquerade under a number of aliases, including yellow bodies (Tudway 1979), yellow-brown bodies (Doyle et al 1973, Tudway 1979), curious bodies (Carter et al 1969, spindle bodies (Hamazaki 1938, Menne 1952, Hall & Eusebi 1978 , ceroid bodies (Symmers 1978), spindle-shaped corpuscles (Roggendorf & Gross 1977), pleomorphic chromogenic bodies (Moscovic 1978), Hamazaki corpuscles (Moscovic 1978) and Hamazaki-Wesenberg bodies (Boutet 1975, Moscovic 1978, Symmers 1978, Tudway 1979. Their histochemical features are consistent with those of lipofuscin, ceroid, or both.…”

Section: Discussionmentioning

confidence: 99%

Chromolipid‐induced portal lymphadenopathy in primary biliary cirrhosis

Benbow

Mcmahon

1987

Histopathology

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Yellow or brown granules of chromolipid, often called Hamazaki-Wesenberg bodies, have previously been described in the sinuses of lymph nodes. They have been seen in normal nodes and nodes showing non-specific reactive changes; particular interest has been shown in a suggested association with sarcoidosis. We describe two patients, both with primary biliary cirrhosis, in whom the accumulation of large numbers of such bodies in the sinuses of lymph nodes of the porta hepatis led to a prominent lymphadenopathy.

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Section: Discussionmentioning

confidence: 99%

Chromolipid‐induced portal lymphadenopathy in primary biliary cirrhosis

Benbow

Mcmahon

1987

Histopathology

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Portal lymphadenopathy associated with lipofuscin in chronic cholestatic liver disease.

Hübscher

Harrison²

1989

J Clin Pathol

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To determine whether portal lymphadenopathy in primary biliary cirrhosis is caused by deposition of lipofuscin pigment in sinus histiocytes and to compare primary biliary cirrhosis with other liver diseases a retrospective study on a consecutive series of 169 livers obtained at transplantation was carried out. There were grouped into eight diagnostic categories: primary biliary cirrhosis (n = 51), primary sclerosing cholangitis (n = 10), extrahepatic biliary atresia (n = 6), chronic rejection (n = 9), cirrhosis (other causes) (n = 38), primary liver neoplasia (n = 21), acute liver disease (n = 20), and retransplantation (other) (n = 14). Lymph nodes were present in 66 specimens. Fifty of these contained granules of lipofuscin pigment. The highest incidence of lymph node enlargement and the largest amounts of pigment were present in cases of primary biliary cirrhosis. A similar pattern oflymph node enlargement was also commonly observed in other chronic cholestatic conditions (primary sclerosing cholangitis, biliary atresia, chronic rejection). Much less pigment was seen in nodes draining livers with non-cholestatic cirrhosis or primary tumours. Nodes were not found in acute liver disease. It is concluded that portal lymphadenopathy associated with lipofuscin is a common finding in various chronic cholestatic liver diseases. The pathogenesis of this lesion is uncertain. Most cases are asymptomatic with enlarged nodes which may be detected only at laperotomy or necropsy and may be wrongly attributed to neoplastic disease. Diagnostically, the finding of large amounts of lipofuscin in enlarged portal lymph nodes is a good indicator of underlying chronic cholestatic liver disease. Enlarged, pigmented portal lymph nodes are often seen in end-stage primary biliary cirrhosis. The pigment, initially thought to be bile,' has recently been shown to have the staining characteristics oflipofuscin in two cases reported by Benbow and McMahon.2 To investigate this phenomenon further and to compare primary biliary cirrhosis with other liver diseases we carried out a retrospective histological and histochemical study on lymph nodes attached to livers obtained at liver transplantation.

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Ultrastructural and histochemical investigations of spindle-shaped corpuscles in phagocytic cells of lymph nodes

Cited by 2 publications

References 25 publications

Chromolipid‐induced portal lymphadenopathy in primary biliary cirrhosis

Chromolipid‐induced portal lymphadenopathy in primary biliary cirrhosis

Portal lymphadenopathy associated with lipofuscin in chronic cholestatic liver disease.

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