6
Histopathology of Primary Cutaneous Amyloidoses and Systemic Amyloidosis
Wei-Min Li, MB
From the Department of Dermatology, Veterans General Hospital, Taichung, Taiwan, China
The term primary cutaneous amyloidosis (PCA) usually includes matular (MA), lichenoid (lichen amyloidosus, LA), nodular,‘-” and PUVAinduced amyloidosis.” With the exception of the rare nodular form, they are thought to be caused by a filamentous degeneration” of keratin-type intermediate filaments with subsequent apotosis and conversion of filamentous masses into amyloid material. Histopathologically, amyloid deposits are observed in the papillary and subpapillary dermis. In systemic amyloidosis (SA), amyloid deposition also involves the skin as well as many other organs. Under the light microscope, skin lesions in SA show amyloid material distributed more deeply in the dermis and subcutis. This chapter reports the findings in 514 biopsy specimens taken from patients with PCA (464 LA, and 50 MA) and 17 from patients with SA seen at the dermatologic clinic between 1973 and 1987. In PCA (MA and LA), subepidermal amyloid deposits were detected only in the dermal papillae (495/514) and the subpapillary layers (241514) by crystal violet stain. The most common epidermal findings of PCA were hyperkeratosis, irregular acanthosis with thinning of rete ridges, and expansion of the papillae by amyloid material (Fig. 6-l). Other less common histopathologic findings were pigmentary incontinence and increase of epidermal melanin. The similarity of amyloid distribution made it difficult to differentiate LA from MA, since amyloid deposits were demonstrated only in the upper portion of dermis in both conditions. In systemic amyloidosis, however, amyloid deposits were observed not only in the papillae (8/l?‘) and the subpapillary layers (g/17), but also in the reticular layers (6/17), around appendages (7/17), in the subcutis Cutaneous Amyloidoses 2, 3045, 1990 0 Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010 30
April-June 1990 Volume 8 Number 2
Histopathology
of Primary Cutaneous
Amyloidoses
and Systemic Amyloidosis
31
FIG. 6-l. (upper leff) Typical histopathological picture of lichen amyloidosus showing “engulfment of amyloid”. (H. & E. stain) FIG. 6-2. violet stain. FIG. 6-3. stain.
(upper right) Crystal
(middle left)
Dylon
FIG. 6-4. (middle right) Dylon stain under polarizing microscope, amyloid showing yellowish green color. FIG. 6-5. T stain.
(lowerlef)
FIG. 6-6. (lower white BBU stain.
Thioflavine
right)
Phor-
32
W-M Li
(Z/17), and in and around the blood vessel walls (7/17). Epidermal changes seldom occurred in SA. In the present study, sections of each biopsy specimen were stained with hematoxylin and eosin for routine histopathology. Crystal violet stain’ was routinely employed to detect amyloid deposits. Other special stains including Congo red’+‘* with or without polarized light microscopy, fluorescence with thioflavine T,i.‘Bm”’the cotton dye Dylan,‘” and the Phorwhite BBU’” fluorescence method were also used to confirm the presence of amyloid deposits in some specimens.
Primary Cutaneous Amyloidosis Histopathologic examination of specimens from LA with special stains (Fig. 6-2 to 6-6) revealed that amyloid deposits were detected in the dermal papillae (446 out of 464 cases), the subpapillary layer (24 out of 464), and the upper reticular dermis (2 out of 464) (Table 6-l). Amyloid deposits were also present in the papillary dermis (49 out of 50 cases), but not in the subpapillary layer in MA. In some cases of MA, amyloid deposits were so small in the sections stained with crystal violet that other special stains such as Dylon, Congo red, or fluorescence methods (thioflavine T or Phorwhite BBU) had to be performed for confirmation. In PCA, amyloid deposits varied according to the stage of the lesion. Biopsy of the early papular lesion revealed faintly eosinophilic, amorphous globules grouped in the papillae. In the more advanced lesions, the amyloid deposits were so extensive that the rete ridges became elongated and thinned, expanding the papillae laterally. This histopathologic pattern was seen in 176 out of 464 cases of LA, and 18 out of 50 cases of MA. Occasionally, clefts between the basal layers and the eosinophilic masses were noted. Irregular acanthosis and hyperkeratosis of the overlying epidermis were observed frequently in LA (385/464), and MA (42150); however, they were more pronounced in LA than in MA. Other less common findings included pigmen-
Clinics in Dermatology
tary incontinence (181464 LA, 6150 MA) and increased epidermal melanin (5/464 LA, 6/50 MA). Liquefactive degeneration and intraepidermal amyloid deposition were found only in one case of MA and one case of LA, respectively. We failed to find dyskeratosis in the epidermis in this study.
Systemic Amyloidosis Histopathologic examination of the skin specimens with special stains revealed amyloid deposits in the dermal papillae (8/17), the subpapillary layer (8/17), the reticular layer (6/17), the subcutis (2/17), and around the appendages (7/17). The distribution of amyloid substance also varied with the kind of lesions biopsied. Biopsy of the purpuric flat lesions revealed faintly eosinophilic masses in the dermal papillae and subpapillary layers; however, examination of the nodular and plaque lesions showed amyloid deposits in the deeper reticular dermis, around appendages, and in the subcutis. Amyloid infiltration in and around blood vessel walls, pilosebaceous units, arrector pili muscles, and between the fat cells was demonstrated by various special stains. Other epidermal changes shown in PCA were seldom seen in SA, except in two cases where hyperkeratosis of the epidermis was noted.
Conclusion Although PCA is clinically classified into the lichenoid and the macular type, the present study showed that amyloid deposits could only be seen in the upper portion of the dermis in both conditions. Histopathologic examination revealed similar faintly amorphous eosinophilic masses in the dermal papillae and/or the subpapillary layers in both types. The amyloid deposit of MA differed from LA only in that in the former condition the amyloid material was less extensive. Some amyloid deposits in MA were so sparse that repeated biopsies and use of various special stains”’ were necessary in order to reach the diagnosis. Nevertheless, we could not
April-June 1990 Volume 8 Number 2
TABLE
Histopathology
6-l.
of Primary
Cutaneous
Amyloidoses
33
and Systemic Amyloidosis
Distribution of Amyloid and Histopathologic Findings in PLCA and SA PLCA LA
MA
Total
SA
464
50
514
17
Distribution Papillae Subpapillary layer Reticular layer Periappendageal Vessel walls Subcutis
446 24 2 0 0 0
49 0 0 0 0 0
495
8
24
8
2
6
Positive Staining Crystal violet Congo red Thioflavine T Phorwhite BBU Pagoda red
446 2 4 6 24
47 1 1 1 9
493
0
1
18
11
29
0
176
18
194
0
385
42
427
0
5
6
11
0
1
0
1
0
0
0
0
0
Cases analyzed
Liquefactive
degeneration
Pigmentaty
incontinence
Thinning of rete ridges and expansion Hyperkeratosis
and acanthosis
Increased epidermal lntraepidermal
of papillae
melanin
amyloid
Dyskeratosis PLCA: Primary localized cutaneous amyloidosis; LA: Lichen amyloidosus;
these two conditions only on the basis of histopathologic examination alone. Furthermore, in other dermatoses such as lichen planus, colloid milium, and lipoid proteinosis, amorphous materials similar to amyloid can be seen in the upper dermis histopathologically. It is therefore of importance that besides the different special stains, immunohistochemical stainings such as anti-serum amyloid-P eomponent’7.‘x should be employed for the differentiation between amyloid or nonamyloid materials. Sometimes it is not possible to confirm a diagnosis of amyloid without carrying out electron microscopy. In the present study, the frequent finding of coalescent, amyloid globules expanding the papillae and displacing the rete ridges laterally was differentiate
0
7
0
7
0
2
17
3
6
5
4
7
4
33
4
1
0
MA: Macular amyloidosis; SA: Systemic amyloidosis.
a helpful clue in the diagnosis of PCA. This histopathologic pattern appearing as “engulfment of amyloid” (Fig. 6-l) was so characteristic that we could diagnose PCA readily by H. & E. stain. Westermark” has previously reported that liquefactive degeneration and pigmentary incontinence are specific findings in PCA. In our series, however, we seldom found liquefactive degeneration of the basal layer in PCA (one case only), and pigmentary incontinence was not a frequent finding (29/514). Thus, we conclude that liquefactive degeneration and pigmentary incontinence are not specific findings in the diagnosis of PCA, while irregular acanthosis and hyperkeratosis of the overlying epidermis (42’7/514) associated with amyloid deposits are important findings in the diagnosis of PCA.
34
Clinics in Dermatology
W-M Li
Concerning the difference in amyloid deposits between PCA and SA, it should be pointed out that the distribution of amyloid in the latter condition is much deeper in location than the former. In PCA, the amyloid deposits are usually confined to the upper portion of the dermis including the dermal papillae and subpapillary layer, whereas in SA, the amyloid can also be found in deeper areas of the reticular dermis, around the appendages, in blood vessel walls, and in the subcutis. Epidermal changes, frequently encountered in PCA, are rarely seen in SA. Based on the above observation, we propose that if deeper amyloid deposits are found on histopathologic examination of cutaneous amyloidosis, the possibility of systemic amyloidosis should be considered and further investigations including rectal biopsy, tongue biopsy, bone marrow aspiration, pathologic examination of nerve tissue, etc. should be performed. In secondary systemic amyloidosis, amyloid deposits may also be found in the dermis as well as subcutis.” It cannot be differentiated from primary SA under the light microscope; however, using the potassium permanganate test” we can differentiate primary SA (amyloid L type) from secondary SA (amyloid A type) since amyloid A loses its affinity to Congo red stain and its typical polarizing characteristics after exposure to potassium permanganate, whereas amyloid L still possesses a potassiumpermanganate-resistant nature. Crystal violet stain was routinely employed in the detection of amyloid deposits in our series. Presence of metachromasia is regarded as a positive result. We find that this special stain is not a completely reliable test because not all of our cases were positively stained (4461464); false negative results are occasionally noted. Meanwhile, false positive results may be found in colloid milium and lipoid proteinosis.“’ False positive staining with thioflavine T may occur with stromal hyaline deposits, collagen fibers, and colloid bodies in lichen planus. Therefore, we should realize that all these special stains are either inadequate or lack specificity for detecting amyloid deposits. It has been suggested that specific antisera directed against amyloid fibril’” and ultrastructural examination may be necessary.
References 1. Brownstein MH, Helwig EB. The cutaneous amyloidoses I. Localized forms. Arch Dermatol. 1970;102:8-19. 2. Black MM. Primary localized amyloidosis of the skin: Clinical variants, histochemistry and ultrastructure. In: Wegelius 0, Pasternak A, eds. Amyloidosis. London: Academic Press, 1976;479-513. 3. Wong CK. Lichen amyloidosus. A relatively common skin disorder in Taiwan. Arch Dermatol. 1974;110:438-440. 4. Hashimoto K, Kumakiri M. Colloid-amyloid bodies in PUVA-treated human psoriatic patients. J Invest Dermatol. 1979;72:70-80. 5. Kumakiri M, Hashimoto K. Histogenesis of primary localized cutaneous amyloidosis: Sequential change of epidermal keratinocytes to amyloid via filamentous degeneration. J Invest Dermatol. 1979;73:150-162. 6. Glenner GG. Amvloid denosits and amvloidosis. The Bfibrilloses. N Engl J Med: 1980;302:12&3-1292. 7 Benditt EP, Erikson N, Hermodson MA, et al. The major proteins of human and monkey amyloid substances: Common properties including unusual N-terminal amino sequences. FEBS L&t. 1971;19:169-173. 8 Westermark P. Amyloidosis of the skin: a comparison between localized and systemic amyloidosis. Acta Derm Venereol (Stockh). 1979;59:341-345. 9 Puchtler H, Sweat F, Levine M. On the binding of Congo red by amyloid. J Histochem Cytochem. 1962;10:355-364. 10. Puchtler H. Sweat F. Congo red as a stain for fluorescence microscopy of amyloid. J Histochem Cytochem. 1965; 13:643-644. 11. Hashimoto K, Gross BG, Lever WF. Lichen amyloidosus. Histochemical and electron microscopic studies. J Invest Dermatol. 1965;45:204-219. 12. Hobbs JR, Morgan AD. Fluorescence microscopy with thioflavine-T in the diagnosis of amyloid. J Pathol Bacteriol. 1963;86:437-442. 13. Hey1 T. Amyloid staining with thioflavine T in dermatopathology. Trans St Johns Hosp Dermatol Sot. 1966; 52:84-87. 14. Yanagihara M, Mehregan AH, Mehregan DR. Staining of amyloid with cotton dyes. Arch Dermatol. 1984;120:11841185. 15. Waldrop FS, Puchtler H, Valentine LS. Fluorescence microscopy of amyloid using mixed illumination. Arch Pathol. 1973;95:31-41. 16. Black MM. The nature, pathogenesis and staining properties of amyloid. Br J Dermatol. 1972;87%30-283. 17. Breathnach SM, Bhogal B, Dyck RF, et al. Immunohistochemical demonstration of amyloid P component in skin of normal subjects and patients with cutaneous amyloidosis. Br J Dermatol. 1981;105:115-124. 18. Fujihara S, Balow JE, Costa JC, et al. Identification and classification of amyloid in formalinfixed, paraffin-embedded tissue sections by the unlabelled immunoperoxidase methods. Lab Invest. 1980;43:358-365.
April-June 1990 Volume 8 Number 2
Histopathology
of Primely
Cutaneous
Amyloidoses
Systemic
forms of this disease. Lab In-
21. Breathnach SM. Amyloid and amyloidosis. Dermatol. 1988;18:1-16.
Address for correspondence: Dr. W. M. Li, Department eral Hospital, Taichung, Taiwan, China.
of Dermatology,
35
Amyloidosis
to assist in differentiating vest. 1977;36:274-281.
19. Westermark P. Occurrence of amyloid deposits in the skin in secondary systemic amyloidosis. APMIS. 1972;80:718720. 20. Wright JR, Calkins E, Humphrey RL. Potassium permanganate reaction in amyloidosis: A histologic method
and
.J Am Acad
Taichung Veterans
Gen-
Histopathology of Primary Cutaneous Amyloidoses and Systemic Amyloidosis
Wei-Min Li, MB
From the Department of Dermatology, Veterans General Hospital, Taichung, Taiwan, China
The term primary cutaneous amyloidosis (PCA) usually includes matular (MA), lichenoid (lichen amyloidosus, LA), nodular,‘-” and PUVAinduced amyloidosis.” With the exception of the rare nodular form, they are thought to be caused by a filamentous degeneration” of keratin-type intermediate filaments with subsequent apotosis and conversion of filamentous masses into amyloid material. Histopathologically, amyloid deposits are observed in the papillary and subpapillary dermis. In systemic amyloidosis (SA), amyloid deposition also involves the skin as well as many other organs. Under the light microscope, skin lesions in SA show amyloid material distributed more deeply in the dermis and subcutis. This chapter reports the findings in 514 biopsy specimens taken from patients with PCA (464 LA, and 50 MA) and 17 from patients with SA seen at the dermatologic clinic between 1973 and 1987. In PCA (MA and LA), subepidermal amyloid deposits were detected only in the dermal papillae (495/514) and the subpapillary layers (241514) by crystal violet stain. The most common epidermal findings of PCA were hyperkeratosis, irregular acanthosis with thinning of rete ridges, and expansion of the papillae by amyloid material (Fig. 6-l). Other less common histopathologic findings were pigmentary incontinence and increase of epidermal melanin. The similarity of amyloid distribution made it difficult to differentiate LA from MA, since amyloid deposits were demonstrated only in the upper portion of dermis in both conditions. In systemic amyloidosis, however, amyloid deposits were observed not only in the papillae (8/l?‘) and the subpapillary layers (g/17), but also in the reticular layers (6/17), around appendages (7/17), in the subcutis Cutaneous Amyloidoses 2, 3045, 1990 0 Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010 30
April-June 1990 Volume 8 Number 2
Histopathology
of Primary Cutaneous
Amyloidoses
and Systemic Amyloidosis
31
FIG. 6-l. (upper leff) Typical histopathological picture of lichen amyloidosus showing “engulfment of amyloid”. (H. & E. stain) FIG. 6-2. violet stain. FIG. 6-3. stain.
(upper right) Crystal
(middle left)
Dylon
FIG. 6-4. (middle right) Dylon stain under polarizing microscope, amyloid showing yellowish green color. FIG. 6-5. T stain.
(lowerlef)
FIG. 6-6. (lower white BBU stain.
Thioflavine
right)
Phor-
32
W-M Li
(Z/17), and in and around the blood vessel walls (7/17). Epidermal changes seldom occurred in SA. In the present study, sections of each biopsy specimen were stained with hematoxylin and eosin for routine histopathology. Crystal violet stain’ was routinely employed to detect amyloid deposits. Other special stains including Congo red’+‘* with or without polarized light microscopy, fluorescence with thioflavine T,i.‘Bm”’the cotton dye Dylan,‘” and the Phorwhite BBU’” fluorescence method were also used to confirm the presence of amyloid deposits in some specimens.
Primary Cutaneous Amyloidosis Histopathologic examination of specimens from LA with special stains (Fig. 6-2 to 6-6) revealed that amyloid deposits were detected in the dermal papillae (446 out of 464 cases), the subpapillary layer (24 out of 464), and the upper reticular dermis (2 out of 464) (Table 6-l). Amyloid deposits were also present in the papillary dermis (49 out of 50 cases), but not in the subpapillary layer in MA. In some cases of MA, amyloid deposits were so small in the sections stained with crystal violet that other special stains such as Dylon, Congo red, or fluorescence methods (thioflavine T or Phorwhite BBU) had to be performed for confirmation. In PCA, amyloid deposits varied according to the stage of the lesion. Biopsy of the early papular lesion revealed faintly eosinophilic, amorphous globules grouped in the papillae. In the more advanced lesions, the amyloid deposits were so extensive that the rete ridges became elongated and thinned, expanding the papillae laterally. This histopathologic pattern was seen in 176 out of 464 cases of LA, and 18 out of 50 cases of MA. Occasionally, clefts between the basal layers and the eosinophilic masses were noted. Irregular acanthosis and hyperkeratosis of the overlying epidermis were observed frequently in LA (385/464), and MA (42150); however, they were more pronounced in LA than in MA. Other less common findings included pigmen-
Clinics in Dermatology
tary incontinence (181464 LA, 6150 MA) and increased epidermal melanin (5/464 LA, 6/50 MA). Liquefactive degeneration and intraepidermal amyloid deposition were found only in one case of MA and one case of LA, respectively. We failed to find dyskeratosis in the epidermis in this study.
Systemic Amyloidosis Histopathologic examination of the skin specimens with special stains revealed amyloid deposits in the dermal papillae (8/17), the subpapillary layer (8/17), the reticular layer (6/17), the subcutis (2/17), and around the appendages (7/17). The distribution of amyloid substance also varied with the kind of lesions biopsied. Biopsy of the purpuric flat lesions revealed faintly eosinophilic masses in the dermal papillae and subpapillary layers; however, examination of the nodular and plaque lesions showed amyloid deposits in the deeper reticular dermis, around appendages, and in the subcutis. Amyloid infiltration in and around blood vessel walls, pilosebaceous units, arrector pili muscles, and between the fat cells was demonstrated by various special stains. Other epidermal changes shown in PCA were seldom seen in SA, except in two cases where hyperkeratosis of the epidermis was noted.
Conclusion Although PCA is clinically classified into the lichenoid and the macular type, the present study showed that amyloid deposits could only be seen in the upper portion of the dermis in both conditions. Histopathologic examination revealed similar faintly amorphous eosinophilic masses in the dermal papillae and/or the subpapillary layers in both types. The amyloid deposit of MA differed from LA only in that in the former condition the amyloid material was less extensive. Some amyloid deposits in MA were so sparse that repeated biopsies and use of various special stains”’ were necessary in order to reach the diagnosis. Nevertheless, we could not
April-June 1990 Volume 8 Number 2
TABLE
Histopathology
6-l.
of Primary
Cutaneous
Amyloidoses
33
and Systemic Amyloidosis
Distribution of Amyloid and Histopathologic Findings in PLCA and SA PLCA LA
MA
Total
SA
464
50
514
17
Distribution Papillae Subpapillary layer Reticular layer Periappendageal Vessel walls Subcutis
446 24 2 0 0 0
49 0 0 0 0 0
495
8
24
8
2
6
Positive Staining Crystal violet Congo red Thioflavine T Phorwhite BBU Pagoda red
446 2 4 6 24
47 1 1 1 9
493
0
1
18
11
29
0
176
18
194
0
385
42
427
0
5
6
11
0
1
0
1
0
0
0
0
0
Cases analyzed
Liquefactive
degeneration
Pigmentaty
incontinence
Thinning of rete ridges and expansion Hyperkeratosis
and acanthosis
Increased epidermal lntraepidermal
of papillae
melanin
amyloid
Dyskeratosis PLCA: Primary localized cutaneous amyloidosis; LA: Lichen amyloidosus;
these two conditions only on the basis of histopathologic examination alone. Furthermore, in other dermatoses such as lichen planus, colloid milium, and lipoid proteinosis, amorphous materials similar to amyloid can be seen in the upper dermis histopathologically. It is therefore of importance that besides the different special stains, immunohistochemical stainings such as anti-serum amyloid-P eomponent’7.‘x should be employed for the differentiation between amyloid or nonamyloid materials. Sometimes it is not possible to confirm a diagnosis of amyloid without carrying out electron microscopy. In the present study, the frequent finding of coalescent, amyloid globules expanding the papillae and displacing the rete ridges laterally was differentiate
0
7
0
7
0
2
17
3
6
5
4
7
4
33
4
1
0
MA: Macular amyloidosis; SA: Systemic amyloidosis.
a helpful clue in the diagnosis of PCA. This histopathologic pattern appearing as “engulfment of amyloid” (Fig. 6-l) was so characteristic that we could diagnose PCA readily by H. & E. stain. Westermark” has previously reported that liquefactive degeneration and pigmentary incontinence are specific findings in PCA. In our series, however, we seldom found liquefactive degeneration of the basal layer in PCA (one case only), and pigmentary incontinence was not a frequent finding (29/514). Thus, we conclude that liquefactive degeneration and pigmentary incontinence are not specific findings in the diagnosis of PCA, while irregular acanthosis and hyperkeratosis of the overlying epidermis (42’7/514) associated with amyloid deposits are important findings in the diagnosis of PCA.
34
Clinics in Dermatology
W-M Li
Concerning the difference in amyloid deposits between PCA and SA, it should be pointed out that the distribution of amyloid in the latter condition is much deeper in location than the former. In PCA, the amyloid deposits are usually confined to the upper portion of the dermis including the dermal papillae and subpapillary layer, whereas in SA, the amyloid can also be found in deeper areas of the reticular dermis, around the appendages, in blood vessel walls, and in the subcutis. Epidermal changes, frequently encountered in PCA, are rarely seen in SA. Based on the above observation, we propose that if deeper amyloid deposits are found on histopathologic examination of cutaneous amyloidosis, the possibility of systemic amyloidosis should be considered and further investigations including rectal biopsy, tongue biopsy, bone marrow aspiration, pathologic examination of nerve tissue, etc. should be performed. In secondary systemic amyloidosis, amyloid deposits may also be found in the dermis as well as subcutis.” It cannot be differentiated from primary SA under the light microscope; however, using the potassium permanganate test” we can differentiate primary SA (amyloid L type) from secondary SA (amyloid A type) since amyloid A loses its affinity to Congo red stain and its typical polarizing characteristics after exposure to potassium permanganate, whereas amyloid L still possesses a potassiumpermanganate-resistant nature. Crystal violet stain was routinely employed in the detection of amyloid deposits in our series. Presence of metachromasia is regarded as a positive result. We find that this special stain is not a completely reliable test because not all of our cases were positively stained (4461464); false negative results are occasionally noted. Meanwhile, false positive results may be found in colloid milium and lipoid proteinosis.“’ False positive staining with thioflavine T may occur with stromal hyaline deposits, collagen fibers, and colloid bodies in lichen planus. Therefore, we should realize that all these special stains are either inadequate or lack specificity for detecting amyloid deposits. It has been suggested that specific antisera directed against amyloid fibril’” and ultrastructural examination may be necessary.
References 1. Brownstein MH, Helwig EB. The cutaneous amyloidoses I. Localized forms. Arch Dermatol. 1970;102:8-19. 2. Black MM. Primary localized amyloidosis of the skin: Clinical variants, histochemistry and ultrastructure. In: Wegelius 0, Pasternak A, eds. Amyloidosis. London: Academic Press, 1976;479-513. 3. Wong CK. Lichen amyloidosus. A relatively common skin disorder in Taiwan. Arch Dermatol. 1974;110:438-440. 4. Hashimoto K, Kumakiri M. Colloid-amyloid bodies in PUVA-treated human psoriatic patients. J Invest Dermatol. 1979;72:70-80. 5. Kumakiri M, Hashimoto K. Histogenesis of primary localized cutaneous amyloidosis: Sequential change of epidermal keratinocytes to amyloid via filamentous degeneration. J Invest Dermatol. 1979;73:150-162. 6. Glenner GG. Amvloid denosits and amvloidosis. The Bfibrilloses. N Engl J Med: 1980;302:12&3-1292. 7 Benditt EP, Erikson N, Hermodson MA, et al. The major proteins of human and monkey amyloid substances: Common properties including unusual N-terminal amino sequences. FEBS L&t. 1971;19:169-173. 8 Westermark P. Amyloidosis of the skin: a comparison between localized and systemic amyloidosis. Acta Derm Venereol (Stockh). 1979;59:341-345. 9 Puchtler H, Sweat F, Levine M. On the binding of Congo red by amyloid. J Histochem Cytochem. 1962;10:355-364. 10. Puchtler H. Sweat F. Congo red as a stain for fluorescence microscopy of amyloid. J Histochem Cytochem. 1965; 13:643-644. 11. Hashimoto K, Gross BG, Lever WF. Lichen amyloidosus. Histochemical and electron microscopic studies. J Invest Dermatol. 1965;45:204-219. 12. Hobbs JR, Morgan AD. Fluorescence microscopy with thioflavine-T in the diagnosis of amyloid. J Pathol Bacteriol. 1963;86:437-442. 13. Hey1 T. Amyloid staining with thioflavine T in dermatopathology. Trans St Johns Hosp Dermatol Sot. 1966; 52:84-87. 14. Yanagihara M, Mehregan AH, Mehregan DR. Staining of amyloid with cotton dyes. Arch Dermatol. 1984;120:11841185. 15. Waldrop FS, Puchtler H, Valentine LS. Fluorescence microscopy of amyloid using mixed illumination. Arch Pathol. 1973;95:31-41. 16. Black MM. The nature, pathogenesis and staining properties of amyloid. Br J Dermatol. 1972;87%30-283. 17. Breathnach SM, Bhogal B, Dyck RF, et al. Immunohistochemical demonstration of amyloid P component in skin of normal subjects and patients with cutaneous amyloidosis. Br J Dermatol. 1981;105:115-124. 18. Fujihara S, Balow JE, Costa JC, et al. Identification and classification of amyloid in formalinfixed, paraffin-embedded tissue sections by the unlabelled immunoperoxidase methods. Lab Invest. 1980;43:358-365.
April-June 1990 Volume 8 Number 2
Histopathology
of Primely
Cutaneous
Amyloidoses
Systemic
forms of this disease. Lab In-
21. Breathnach SM. Amyloid and amyloidosis. Dermatol. 1988;18:1-16.
Address for correspondence: Dr. W. M. Li, Department eral Hospital, Taichung, Taiwan, China.
of Dermatology,
35
Amyloidosis
to assist in differentiating vest. 1977;36:274-281.
19. Westermark P. Occurrence of amyloid deposits in the skin in secondary systemic amyloidosis. APMIS. 1972;80:718720. 20. Wright JR, Calkins E, Humphrey RL. Potassium permanganate reaction in amyloidosis: A histologic method
and
.J Am Acad
Taichung Veterans
Gen-
