The classification of amyloid deposits in clinicopathological practice

被引:95
作者
Rocken, C
Schwotzer, EB
Linke, RP
Saeger, W
机构
[1] MARIEN HOSP, DEPT PATHOL, D-22087 HAMBURG, GERMANY
[2] MAX PLANCK INST BIOCHEM, D-82152 MARTINSRIED, GERMANY
[3] HALTON GEN HOSP, RUNCORN, CHESHIRE, ENGLAND
关键词
amyloid; biopsy; immunohistochemistry;
D O I
10.1111/j.1365-2559.1996.tb01416.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
A series of 104 biopsy cases with histopathological proof of amyloid, submitted to our department of pathology over the last 19 years, were re-examined, The survey investigated the medical indication for surgery, the origin and quality of the biopsy and the clinical information as documented on the request form for histopathological examination and in hospital records. Amyloid deposits were classified using antisera directed against five major amyloid fibril proteins, i.e. AA, ATTR, A lambda, A kappa and A beta 2M and optimal conditions were sought for the reliable and early characterization of amyloid disease in clinicopathological practice, This survey revealed that 98% of the biopsy cases already suffered from a disease which was either a cause or a result of amyloidosis. In only 2% of the biopsy cases was amyloidosis detected without any clinical indication, Immunohistochemical classification of the amyloid deposits and comparison with hospital records demonstrated diagnostic pitfalls such as immunostaining of amyloid by two or more antibodies recognizing different fibril proteins, and disagreement between immunohistochemical typing of amyloid and the initial clinical diagnosis. Based on these observations we assume that the characterization of amyloid disease and its biological significance is impossible in clinicopathological practice without clinical information or without immunohistochemical classification of the fibril protein in biopsy specimens, Different aspects of histopathological detection of AA- and AL-amyloidosis are discussed.
引用
收藏
页码:325 / 335
页数:11
相关论文
共 62 条
[1]  
BARETTON G, 1990, PATHOLOGE, V11, P71
[2]  
BLUM A, 1962, LANCET, V7, P721
[3]   THE LONG-TERM PROGNOSIS OF AA AND AL RENAL AMYLOIDOSIS AND THE PATHOGENESIS OF CHRONIC-RENAL-FAILURE IN RENAL AMYLOIDOSIS [J].
BOHLE, A ;
WEHRMANN, M ;
EISSELE, R ;
VONGISE, H ;
MACKENSENHAEN, S ;
MULLER, C ;
MULLER, GA .
PATHOLOGY RESEARCH AND PRACTICE, 1993, 189 (03) :316-331
[4]   CHARACTERIZATION OF DIFFERENT AMYLOIDS WITH IMMUNOLOGICAL TECHNIQUES [J].
CHASTONAY, P ;
HURLIMANN, J .
PATHOLOGY RESEARCH AND PRACTICE, 1986, 181 (06) :657-663
[5]   MIXED SYSTEMIC AMYLOIDOSIS IN A PATIENT RECEIVING LONG-TERM HEMODIALYSIS [J].
FERNANDEZALONSO, J ;
RIOSCAMACHO, C ;
VALENZUELACASTANO, A ;
HERNANZMEDIANO, W .
JOURNAL OF CLINICAL PATHOLOGY, 1994, 47 (06) :560-561
[6]   CARDIAC AMYLOID DEPOSITS IN ENDOMYOCARDIAL BIOPSIES - LIGHT MICROSCOPIC, ULTRASTRUCTURAL, AND IMMUNOHISTOCHEMICAL STUDIES [J].
FRENZEL, H ;
SCHWARTZKOPFF, B ;
KUHN, H ;
LOSSE, B ;
THORMANN, J ;
HORT, W ;
LINKE, RP .
AMERICAN JOURNAL OF CLINICAL PATHOLOGY, 1986, 85 (06) :674-680
[7]  
FUJIHARA S, 1980, LAB INVEST, V43, P358
[8]  
FUJIHARA S, 1982, ACTA PATHOL JAPON, V32, P771
[9]  
GAFNI J, 1960, AM J MED SCI, V240
[10]  
GALLO G, 1994, AM J PATHOL, V145, P526