Histopathobgu 1992, 21,143-147
Localized amyloidosis of the lower genitourinary tract: a clinicopathological and immunohistochemical study of nine cases S.M.KHAN, P.J.BIRCH, P.S.BASS*, J.H. WILLIAMS* & J.M.THEAKER* Departments of Histopathology, St. Mary’s General Hospital, Portsmouth and *Southampton General Hospital, Southampton, UK Date of submission 2 5 November 199 1 Accepted for publication 21 February 1992
KHAN S.M., BIRCH P . J . , BASS P.S., WILLIAMS J . H . & THEAKER J.M.
(1992) Histopathology 21, 143-147
Localized amyloidosis of the lower genitourinary tract: a clinicopathological and immunohistochemical study of nine cases A series of nine cases of localized amyloidosis of the lower genitourinary tract are reported. The patients comprised six males and three females with an age range of 50-79 years at initial presentation. Clinically and on cystoscopy, the lesions were often diagnosed as neoplasms. Histologically, seven cases had typical features of localized amyloid deposits, while two cases had an unusual appearance with a florid histiocytic and giant cell reaction. Using an immunoperoxidase staining method the deposits were non-reactive with antibodies to serum amyloid A protein, prealbumin and Bz microglobulii, while equivocal immunoreactivity was seen with anti-light chain antibodies.
Keywords: localized amyloidosis, bladder, ureter, urethra, immunohistochemistry
Introduction Amyloidosis of the lower genitourinary tract is an uncommon disease. The majority of patients have localized deposits in the bladder, ureter or urethra. This is an important entity as, both clinically and on cystoscopy, the lesions frequently mimic neoplasms. The aetiology is unknown and few studies have attempted to classify the amyloid t y ~ e l - ~ . In view of its rarity, a series of nine cases of localized lower genitourinary tract amyloidosis were studied in order to further document the clinicopathological features and to attempt to clarify the amyloid derivation using a panel of immunohistochemical stains.
Materials and methods Nine cases of localized amyloidosis of the lower genitourinary tract were retrieved from the files of Southampton General Hospital, St. Mary’s General Hospital, Ports-
mouth and Salisbury General Infirmary, between 1964 and 1990. Clinical data were obtained from case notes, where available, and surgical request forms. Routinely formalin-fixed, paraffin-embedded tissue blocks were obtained for all cases. Sections 5 /,an thick were cut and stained with haematoxylin and eosin, haematoxylii van Gieson and Sirius red. Immunohistological studies were carried out using a panel of commercially available antibodies (Dakopatts) and a standard Streptavidi-biotin complex (StreptAJ3C) immunoperoxidase staining method4 (Table 1). Positive controls consisted of known cases of amyloidosis of amyloid A type, a carcinoid tumour (pre-albumin control), prostatic corpora amylacea and light-chain restricted B-cell lymphomas. Negative controls were obtained by omission of the primary antibody.
Results CLINICAL FINDINGS
Address for correspondence: Dr S.M.Khan. Department of Histopathology,St. Mary’s General Hospital, Milton Road, Fratton. Portsmouth PO3 6AG. UK.
These are summarized in Table 2 . In three cases, notes were unavailable and therefore the presence or absence 143
144 S.M.Khan et aJ.
Table 1. Antibodies used in present study and results obtained ~~
Antibody specificity
Dilution
Result
P-component (monoclonal) Serum amyloid A protein
1/3000
Positive
(monoclonal) Pre-albumin (monoclonal)
1/2000 1/20 000 & 1/40000 1/8000
Negative Negative
pz microglobulin (polyclonal) Kappa light chain (polyclonal) Lambda light chain (polyclonal)
1/2000
lj6000
Negative Equivocal Equivocal
of systemic amyloidosis could not be adequately assessed. The remaining six patients had no evidence of generalized amyloidosis on clinical examination or laboratory investigation, which included rectal biopsy (two cases), serum or urine electrophoresis only (two cases) and autopsy (one case). In addition there was no history of disease associated with systemic amyloidosis in these six cases. The bladder biopsy was accompanied by a trans-urethral resection of the prostate in case 7 and partial excision was performed in case 4. LIGHT MICROSCOPY
Typical features of localized amyloidosis5were present in seven cases. These showed extracellular aggregates of homogeneous eosinophilic material, predominantly in the lamina propria and inner half of the muscle wall, where this was included in the specimen (Figure 1).The deposits gave a red reaction with sirius red and showed apple-green birefnhgence with cross-polarized light. Minor deposits were present in vessel walls and there was a focal foreign body giant cell reaction. Microcalcfication was occasionally seen (cases 3 & 8). Two cases (4 & 7)had an unusual appearance and showed a florid histiocytic and foreign body giant cell reaction to scanty granular deposits of amyloid (Figure 2). Vessel involvement was inconspicuousin these two cases. In all cases there was a focal lymphoplasmacytic infiltrate admixed with a variable number of eosinophtls; no consistent spatial relationship to the amyloid deposits was apparent. In patients who had repeat biopsies, the light microscopic features were similar in all specimens. There was no evidence of amyloid deposition in the prostatic specimens of patients who had had previous transurethral prostatic resections. IMMUNOHISTOCHBMISTRY
All deposits gave similar reactions. These are sum-
marized in Table 1. Anti-P component gave a reaction comparable with sirius red (Figure 3). The plasma cell infiltrate was polyclonal with no predominance of kappa or lambda light chain expression in any of the cases.
Discussion The cases described here showed typical clinical and gross features of localized amyloidosis of the lower genitourinary tract, with lesions often resembling neoplasm#. Although systemic disease could not be confidently excluded in at least three cases, the characteristic microscopic appearance of systemic amyloidosis, with heavy vascular deposition and minimal muscle involvewas not seen. A foreign body giant cell reaction to amyloid has been noted to be rare at this site5. However, in two cases a florid giant cell reaction was seen. The correct diagnosis may be missed if the pathologist is unaware of this pattern of disease and if appropriate stains are not performed. It is noteworthy that both of these patients had a past history of transurethral prostatic resection. Most patients with localized genitourinary tract amyloidosis have no preceding genitourinary disease. However, a previous history of gonococcal7 or nongonococcal* urethritis and urinary tract instrumentationg has been documented. Two patients in this study had past histories of urinary tract infection and two had had previous instrumentation. Four patients had repeat biopsies for persistent abnormalities on cystoscopy or for recurrent symptoms, with a time interval of up to 21 years. Whether the initial biopsies were performed for diagnosis or excision of the lesion was not specified, the recurrence rate appears higher than that cited in other series6. It has been advocated that all suspicious lesions be biopsied and that recurrences be reassessed thoroughly, as amyloid deposits are often clinically indistinguishable from neoplasms and a malignancy may co-exist with amyloidosis' or develop subsequently6. In this study, antibodies against several different amyloid proteins were used in an attempt to classify the amyloid type. Protein AL. found in primary systemic amyloidosis, is composed of immunoglobulin light chains and/or light-chain fragments. Protein AA,found in secondary or reactive systemic amyloidosis is antigenically related to the acute phase reactant, serum amyloid A protein1" and is deposited as a consequence of inflammation or neoplastic disease". Plasmaderived pre-albumin is the precursor of amyloid in senile cardiac amyloidosis while amyloid derived from @Z microglobulin (BzM) is seen in chronic haemodialysis patients12.Bz microglobulin is also deposited locally in the lower
TURP 9 years ago: repeated genitouxkary dilatationscrotal leak abscess Nil
Urethra
Bladder
Bladder
66/M
50fF
70fM
77/F
67fM
2
3
4
5
6
7
Nil Nil
Bladder
Bladder Bladder
79fM
65fM
53/F
8
9
Presenting complaint
surgical diagnosis
Red patches R. upper quadrant Trabeculated bladder: nodular trigone
Nodular area: L. ureteric orifice
Irregularly stenosed urethra
? Ca prostate
? Neoplasm ? Inflammation
? Neoplasm
? Neoplasm
3 Scar
NA Neoplasm Submucosal elevations ? Bilharzia Bullous cystitis Papilliferous growth L. ureteric orifice
CYStoSCoPY
NA NA 7 Neoplasm Painless haematuria; bilateral Red areas inferolateral ? Neoplasm loin pain surface ? cystitis
Acute retention
Haematuria; abdominal pain
Painless haematuria
Poor stream: scrotal lump
NA Painless haematuria Recurrent cystitis
NA =not available: TURP =transurethral resection of prostate.
Mumps orchitis: prostatitis epididymitis TURP 5 years ago
+
NA NA Nil
Bladder Bladder L.ureter
73fM
1
Previous genitourinary history
Site
Age/sex
Case
Table 2. Clinical details of patients studied
NA 3 years-recurrences at 1 & 2 years
Ca prostate
Persistent amyloidosis at 6 & 7 years; died at 9 yearsCa stomach 7/12 Alive & well
+
NA NA 22 years-local recurrence at 2 1years bladder stones 13/12 Alive & well
PO~~OW-UP
B ci
E
2
g
6
m
146
S.M.Khan et al.
Figure 1. Typtcal appearance of localized amyloidosis.Bladder biopsy. Case 6. H & E.
Flgure 2. Florid histimytic and giant cell reactfon to scanty amyloid deposits. Urethral biopsy. Case 4. H & E.
genitourinary tract in prostatic corpora amylacea13and was considered an important protein to search for at this site. Immunohistochemistry was found to be useful in the gross characterization of the amyloid deposits as nonAA, non-pre-albumin, non-fl2M type. Polyclonal antilight chain antibodies gave equivocal results and the plasma cell infiltrate was found to be polyclonal. Other workers have also shown localized lower genitourinary
Figure 3. Positive staining of amyloid deposits with anti-P component. Ureteric biopsy. Case 3. StreptABC immunoperoxidase.
tract amyloid to be of non-AA type, using the potassium permanganate pretreatment r e a c t i ~ n ~ -However, ’~. few workers have used commercially available immunoperoxidase stains to study the nature of the deposits and these have been reported in single case studies. Johnston & Ewen’ found negative reactions with antibodies to serum AA protein, pre-albumin, p2M and light chains. Loke et al.’ also found deposits to be non-reactive with anti-light chain antibodies and noted the plasma cell infiltrate to be polyclonal, as did Brown and coworker~~~. Pujihara & Glenner3, using antibodies raised against amyloid light chains which are not commercially available, found nine of 11cases of lower genitourinary tract amyloidosis to have amyloid lambda antigenic fibril determinants. In three cases more than three-quarters of the infiltrating plasma cells were anti-amyloid-lambda positive but unreactive with congo red. A pathogenlc mechanism was postulated, with chronic inflammation leading to a monoclonal proliferationof plasma cells and the secretion of an aberrant type of ‘amyloidogenic’light chain, which is deposited locally as amyloid fibrils. We were unable to demonstrate differentialstaining of amyloid deposits with polyclonal anti-light chain antibodies. However,this is not necessarily inconsistent with a light chain origin and may be due to the presence of antigenic determinants not recognized by the antibodies used”, or non-speci6ic trapping of immunoglobulins16.
Lower genitourinary tract amyloidosis
Acknowledgements We would like to thank consultants in the Wessex Region and Wing Commander E.P.Turk (RAF Halton), who have histologicd and 'Iinica1 material, and given their permission to report these cases.
References 1. Johnston PW. Ewen SWB. Localized amyloidosis and transitional cell carcinoma of the same ureter. Histopathology 1990; 17; 5 79582. 2. Loke S-L, Ma L, Yiu T-F. Wong K-K.Localized amyloidosis of the ureter. Pathology 1987; 19: 91-94. 3. Fujihara S, Glenner GG. Primary l o c a l i d amyloidosis of the genitourinarytract. Imrnunohistochemicalstudy on eleven cases. Lab. Invest. 1981: 44; 55-60. 4. Mepham BL, Britten KJM.Immunostaining methods for frozen and para& sections. In Jones DB, Wright DH eds. Lymphoprol$zrative Diseases. lmrnunology and Medicine Series. Lancaster, United Kingdom: Kluwer Academic Publishers. 1 9 9 0 187-211. 5. Kinzel RC. Harrison EG Jr, Utz DC.Primary localized amyloidosisof the bladder. ]. Urol. 1961; 85, 785-795.
147
6. Malek RS. Greene LF, Farrow GM. Amyloidosis of the urinary bladder. Br. 1. Urol. 1971: 43: 189-200. 7. Gerami S. Easley GW, Payan H.Primary localized amyloidosis of theurethra and bladder (arnyloidoma).Am. Surg. 1970: 36; 375-__ 377.
8. Constantian HM, W p a n p. Localized amyloidosis ofthe urethra: report of a case. ]. Urol. 1980: 124; 728-729. 9. Carris CK. McLaughlin AP III. Gittes RF. Amyloidosis of the lower genitourinary tract. ]. Urol. 1976; 115: 423-426. 10. Glenner GG. Amyloid deposits and amyloidosis. The B-fibrilloses (First of two parts). N. Engl. ]. Med. 1980: 302; 1283-1292. 11. Glenner GG. Amyloid deposits and amyloidosis. The B-fibrilloses (Second of two parts). N . Engl. ]. Med. 1 9 8 0 302: 1333-1343. 12. Pepys MB. Amyloidosis: some recent developments. Q. ]. Med. 1988: 67: 283-298. 13. Cross PA, Bartley CJ,McClure J. Amyloid in prostatic corpora amylacea. (Abstract)]. Puthol. 1990: 1 6 0 153A. 14. Robinson CR, Fowler JE. Localid amyloidosis of the ureter. ]. Urol. 1 9 8 4 131: 110-111. 15. Brown RD. Mulhollan.JA.Childers JH. Preminger GM. Locallzed amyloidosis of the urethra: diagnostic implications and management.]. Urol. 1988; 1 4 0 1536-1538. 16. h i LM. The pattern of amyloidosis in a Malaysian patient population. Histopathologu 1991: 18: 133-141.
Localized amyloidosis of the lower genitourinary tract: a clinicopathological and immunohistochemical study of nine cases S.M.KHAN, P.J.BIRCH, P.S.BASS*, J.H. WILLIAMS* & J.M.THEAKER* Departments of Histopathology, St. Mary’s General Hospital, Portsmouth and *Southampton General Hospital, Southampton, UK Date of submission 2 5 November 199 1 Accepted for publication 21 February 1992
KHAN S.M., BIRCH P . J . , BASS P.S., WILLIAMS J . H . & THEAKER J.M.
(1992) Histopathology 21, 143-147
Localized amyloidosis of the lower genitourinary tract: a clinicopathological and immunohistochemical study of nine cases A series of nine cases of localized amyloidosis of the lower genitourinary tract are reported. The patients comprised six males and three females with an age range of 50-79 years at initial presentation. Clinically and on cystoscopy, the lesions were often diagnosed as neoplasms. Histologically, seven cases had typical features of localized amyloid deposits, while two cases had an unusual appearance with a florid histiocytic and giant cell reaction. Using an immunoperoxidase staining method the deposits were non-reactive with antibodies to serum amyloid A protein, prealbumin and Bz microglobulii, while equivocal immunoreactivity was seen with anti-light chain antibodies.
Keywords: localized amyloidosis, bladder, ureter, urethra, immunohistochemistry
Introduction Amyloidosis of the lower genitourinary tract is an uncommon disease. The majority of patients have localized deposits in the bladder, ureter or urethra. This is an important entity as, both clinically and on cystoscopy, the lesions frequently mimic neoplasms. The aetiology is unknown and few studies have attempted to classify the amyloid t y ~ e l - ~ . In view of its rarity, a series of nine cases of localized lower genitourinary tract amyloidosis were studied in order to further document the clinicopathological features and to attempt to clarify the amyloid derivation using a panel of immunohistochemical stains.
Materials and methods Nine cases of localized amyloidosis of the lower genitourinary tract were retrieved from the files of Southampton General Hospital, St. Mary’s General Hospital, Ports-
mouth and Salisbury General Infirmary, between 1964 and 1990. Clinical data were obtained from case notes, where available, and surgical request forms. Routinely formalin-fixed, paraffin-embedded tissue blocks were obtained for all cases. Sections 5 /,an thick were cut and stained with haematoxylin and eosin, haematoxylii van Gieson and Sirius red. Immunohistological studies were carried out using a panel of commercially available antibodies (Dakopatts) and a standard Streptavidi-biotin complex (StreptAJ3C) immunoperoxidase staining method4 (Table 1). Positive controls consisted of known cases of amyloidosis of amyloid A type, a carcinoid tumour (pre-albumin control), prostatic corpora amylacea and light-chain restricted B-cell lymphomas. Negative controls were obtained by omission of the primary antibody.
Results CLINICAL FINDINGS
Address for correspondence: Dr S.M.Khan. Department of Histopathology,St. Mary’s General Hospital, Milton Road, Fratton. Portsmouth PO3 6AG. UK.
These are summarized in Table 2 . In three cases, notes were unavailable and therefore the presence or absence 143
144 S.M.Khan et aJ.
Table 1. Antibodies used in present study and results obtained ~~
Antibody specificity
Dilution
Result
P-component (monoclonal) Serum amyloid A protein
1/3000
Positive
(monoclonal) Pre-albumin (monoclonal)
1/2000 1/20 000 & 1/40000 1/8000
Negative Negative
pz microglobulin (polyclonal) Kappa light chain (polyclonal) Lambda light chain (polyclonal)
1/2000
lj6000
Negative Equivocal Equivocal
of systemic amyloidosis could not be adequately assessed. The remaining six patients had no evidence of generalized amyloidosis on clinical examination or laboratory investigation, which included rectal biopsy (two cases), serum or urine electrophoresis only (two cases) and autopsy (one case). In addition there was no history of disease associated with systemic amyloidosis in these six cases. The bladder biopsy was accompanied by a trans-urethral resection of the prostate in case 7 and partial excision was performed in case 4. LIGHT MICROSCOPY
Typical features of localized amyloidosis5were present in seven cases. These showed extracellular aggregates of homogeneous eosinophilic material, predominantly in the lamina propria and inner half of the muscle wall, where this was included in the specimen (Figure 1).The deposits gave a red reaction with sirius red and showed apple-green birefnhgence with cross-polarized light. Minor deposits were present in vessel walls and there was a focal foreign body giant cell reaction. Microcalcfication was occasionally seen (cases 3 & 8). Two cases (4 & 7)had an unusual appearance and showed a florid histiocytic and foreign body giant cell reaction to scanty granular deposits of amyloid (Figure 2). Vessel involvement was inconspicuousin these two cases. In all cases there was a focal lymphoplasmacytic infiltrate admixed with a variable number of eosinophtls; no consistent spatial relationship to the amyloid deposits was apparent. In patients who had repeat biopsies, the light microscopic features were similar in all specimens. There was no evidence of amyloid deposition in the prostatic specimens of patients who had had previous transurethral prostatic resections. IMMUNOHISTOCHBMISTRY
All deposits gave similar reactions. These are sum-
marized in Table 1. Anti-P component gave a reaction comparable with sirius red (Figure 3). The plasma cell infiltrate was polyclonal with no predominance of kappa or lambda light chain expression in any of the cases.
Discussion The cases described here showed typical clinical and gross features of localized amyloidosis of the lower genitourinary tract, with lesions often resembling neoplasm#. Although systemic disease could not be confidently excluded in at least three cases, the characteristic microscopic appearance of systemic amyloidosis, with heavy vascular deposition and minimal muscle involvewas not seen. A foreign body giant cell reaction to amyloid has been noted to be rare at this site5. However, in two cases a florid giant cell reaction was seen. The correct diagnosis may be missed if the pathologist is unaware of this pattern of disease and if appropriate stains are not performed. It is noteworthy that both of these patients had a past history of transurethral prostatic resection. Most patients with localized genitourinary tract amyloidosis have no preceding genitourinary disease. However, a previous history of gonococcal7 or nongonococcal* urethritis and urinary tract instrumentationg has been documented. Two patients in this study had past histories of urinary tract infection and two had had previous instrumentation. Four patients had repeat biopsies for persistent abnormalities on cystoscopy or for recurrent symptoms, with a time interval of up to 21 years. Whether the initial biopsies were performed for diagnosis or excision of the lesion was not specified, the recurrence rate appears higher than that cited in other series6. It has been advocated that all suspicious lesions be biopsied and that recurrences be reassessed thoroughly, as amyloid deposits are often clinically indistinguishable from neoplasms and a malignancy may co-exist with amyloidosis' or develop subsequently6. In this study, antibodies against several different amyloid proteins were used in an attempt to classify the amyloid type. Protein AL. found in primary systemic amyloidosis, is composed of immunoglobulin light chains and/or light-chain fragments. Protein AA,found in secondary or reactive systemic amyloidosis is antigenically related to the acute phase reactant, serum amyloid A protein1" and is deposited as a consequence of inflammation or neoplastic disease". Plasmaderived pre-albumin is the precursor of amyloid in senile cardiac amyloidosis while amyloid derived from @Z microglobulin (BzM) is seen in chronic haemodialysis patients12.Bz microglobulin is also deposited locally in the lower
TURP 9 years ago: repeated genitouxkary dilatationscrotal leak abscess Nil
Urethra
Bladder
Bladder
66/M
50fF
70fM
77/F
67fM
2
3
4
5
6
7
Nil Nil
Bladder
Bladder Bladder
79fM
65fM
53/F
8
9
Presenting complaint
surgical diagnosis
Red patches R. upper quadrant Trabeculated bladder: nodular trigone
Nodular area: L. ureteric orifice
Irregularly stenosed urethra
? Ca prostate
? Neoplasm ? Inflammation
? Neoplasm
? Neoplasm
3 Scar
NA Neoplasm Submucosal elevations ? Bilharzia Bullous cystitis Papilliferous growth L. ureteric orifice
CYStoSCoPY
NA NA 7 Neoplasm Painless haematuria; bilateral Red areas inferolateral ? Neoplasm loin pain surface ? cystitis
Acute retention
Haematuria; abdominal pain
Painless haematuria
Poor stream: scrotal lump
NA Painless haematuria Recurrent cystitis
NA =not available: TURP =transurethral resection of prostate.
Mumps orchitis: prostatitis epididymitis TURP 5 years ago
+
NA NA Nil
Bladder Bladder L.ureter
73fM
1
Previous genitourinary history
Site
Age/sex
Case
Table 2. Clinical details of patients studied
NA 3 years-recurrences at 1 & 2 years
Ca prostate
Persistent amyloidosis at 6 & 7 years; died at 9 yearsCa stomach 7/12 Alive & well
+
NA NA 22 years-local recurrence at 2 1years bladder stones 13/12 Alive & well
PO~~OW-UP
B ci
E
2
g
6
m
146
S.M.Khan et al.
Figure 1. Typtcal appearance of localized amyloidosis.Bladder biopsy. Case 6. H & E.
Flgure 2. Florid histimytic and giant cell reactfon to scanty amyloid deposits. Urethral biopsy. Case 4. H & E.
genitourinary tract in prostatic corpora amylacea13and was considered an important protein to search for at this site. Immunohistochemistry was found to be useful in the gross characterization of the amyloid deposits as nonAA, non-pre-albumin, non-fl2M type. Polyclonal antilight chain antibodies gave equivocal results and the plasma cell infiltrate was found to be polyclonal. Other workers have also shown localized lower genitourinary
Figure 3. Positive staining of amyloid deposits with anti-P component. Ureteric biopsy. Case 3. StreptABC immunoperoxidase.
tract amyloid to be of non-AA type, using the potassium permanganate pretreatment r e a c t i ~ n ~ -However, ’~. few workers have used commercially available immunoperoxidase stains to study the nature of the deposits and these have been reported in single case studies. Johnston & Ewen’ found negative reactions with antibodies to serum AA protein, pre-albumin, p2M and light chains. Loke et al.’ also found deposits to be non-reactive with anti-light chain antibodies and noted the plasma cell infiltrate to be polyclonal, as did Brown and coworker~~~. Pujihara & Glenner3, using antibodies raised against amyloid light chains which are not commercially available, found nine of 11cases of lower genitourinary tract amyloidosis to have amyloid lambda antigenic fibril determinants. In three cases more than three-quarters of the infiltrating plasma cells were anti-amyloid-lambda positive but unreactive with congo red. A pathogenlc mechanism was postulated, with chronic inflammation leading to a monoclonal proliferationof plasma cells and the secretion of an aberrant type of ‘amyloidogenic’light chain, which is deposited locally as amyloid fibrils. We were unable to demonstrate differentialstaining of amyloid deposits with polyclonal anti-light chain antibodies. However,this is not necessarily inconsistent with a light chain origin and may be due to the presence of antigenic determinants not recognized by the antibodies used”, or non-speci6ic trapping of immunoglobulins16.
Lower genitourinary tract amyloidosis
Acknowledgements We would like to thank consultants in the Wessex Region and Wing Commander E.P.Turk (RAF Halton), who have histologicd and 'Iinica1 material, and given their permission to report these cases.
References 1. Johnston PW. Ewen SWB. Localized amyloidosis and transitional cell carcinoma of the same ureter. Histopathology 1990; 17; 5 79582. 2. Loke S-L, Ma L, Yiu T-F. Wong K-K.Localized amyloidosis of the ureter. Pathology 1987; 19: 91-94. 3. Fujihara S, Glenner GG. Primary l o c a l i d amyloidosis of the genitourinarytract. Imrnunohistochemicalstudy on eleven cases. Lab. Invest. 1981: 44; 55-60. 4. Mepham BL, Britten KJM.Immunostaining methods for frozen and para& sections. In Jones DB, Wright DH eds. Lymphoprol$zrative Diseases. lmrnunology and Medicine Series. Lancaster, United Kingdom: Kluwer Academic Publishers. 1 9 9 0 187-211. 5. Kinzel RC. Harrison EG Jr, Utz DC.Primary localized amyloidosisof the bladder. ]. Urol. 1961; 85, 785-795.
147
6. Malek RS. Greene LF, Farrow GM. Amyloidosis of the urinary bladder. Br. 1. Urol. 1971: 43: 189-200. 7. Gerami S. Easley GW, Payan H.Primary localized amyloidosis of theurethra and bladder (arnyloidoma).Am. Surg. 1970: 36; 375-__ 377.
8. Constantian HM, W p a n p. Localized amyloidosis ofthe urethra: report of a case. ]. Urol. 1980: 124; 728-729. 9. Carris CK. McLaughlin AP III. Gittes RF. Amyloidosis of the lower genitourinary tract. ]. Urol. 1976; 115: 423-426. 10. Glenner GG. Amyloid deposits and amyloidosis. The B-fibrilloses (First of two parts). N. Engl. ]. Med. 1980: 302; 1283-1292. 11. Glenner GG. Amyloid deposits and amyloidosis. The B-fibrilloses (Second of two parts). N . Engl. ]. Med. 1 9 8 0 302: 1333-1343. 12. Pepys MB. Amyloidosis: some recent developments. Q. ]. Med. 1988: 67: 283-298. 13. Cross PA, Bartley CJ,McClure J. Amyloid in prostatic corpora amylacea. (Abstract)]. Puthol. 1990: 1 6 0 153A. 14. Robinson CR, Fowler JE. Localid amyloidosis of the ureter. ]. Urol. 1 9 8 4 131: 110-111. 15. Brown RD. Mulhollan.JA.Childers JH. Preminger GM. Locallzed amyloidosis of the urethra: diagnostic implications and management.]. Urol. 1988; 1 4 0 1536-1538. 16. h i LM. The pattern of amyloidosis in a Malaysian patient population. Histopathologu 1991: 18: 133-141.
