REPORT
PRIMARY LOCALIZED CUTANEOUS AMYLOIDOSIS ABDUL-CHANI KIBBI, M.D., NELLY G. RUBEIZ, M.D., SHUKRALLAH T. ZAYNOUN, M.D., AND AMAL K. KURBAN, M.D.»
Abstract Fifty-seven patients with primary localized cutaneous amyloidosis (PLCA) were clinically and histopathologically reviewed. Two-thirds of patients had macular amyloidosis (MA). Intermediate cases having macular lesions with micropapules and/or lichens were identified. A spectrum for the disease is proposed, in which the less itchy classical macular variant occurs at one end and the very pruritic traditional lichen variant at the other. The salient histopathologic findings were similar in the macules, micropapules, and lichens, but were more prominent in the lichens. These consisted of hyperkeratosis, keratinocyte degeneration, satellite cell necrosis, and basal cell destruction. Amyloid deposition in the dermal papillae with transepidermal elimination, dermal melanophages, and superficial perivascular inflammation were also present. These changes represent an interface dermatitis of the vacuolar type, PLCA may be categorized under the group of dermatoses characterized by a lichenoid tissue reaction; inflammation may play a key role in mediating these disorders.
Macular amyloidosis (MA) and lichen amyloidosis (LA) are two closely related forms of primary localized cutaneous amyloidosis (PLCA).' The macular variant is characterized by moderately pruritic macules of dark brown pigmentation arranged in a reticulated or rippled pattern.^ The lesions usually occur in a symmetrical distribution over the upper back and arms. In the lichenoid form, closely-set, discrete, firm and hyperkeratotic papules and plaques are seen on the anterior aspect of the shins and the extensor surfaces of the forearms.^ In this form, intense pruritus is invariably present leading to
From the Department of Dermatology, American University of Beirut Medical Center, Beirut, Lebanon, and the *Department of Dermatology, Boston University Medical Center, Boston, Massachusetts. Presented in part at the American Society of Dermatopathology, San Francisco, California (1989), and published in abstract form in the J Cutan Pathol 1989; 16:312. Address for correspondence: Abdul-Ghani Kibbi, M.D., Department of Dermatology, American University of Beirut Medical Center, 850 Third Avenue, New York, NY 10022.
prominent lichenification. Macular and lichen amyloidosis may frequently coexist giving credence to the concept of biphasic amyloidosis."* Asians, Middle Easterners, and South Americans are particularly predisposed.^"" On histopathologic examination, deposits of amyloid in the papillary body are observed in both forms.'' Marked hyperkeratosis, papillomatosis, and epidermal hyperplasia are noted in tbe lichenoid form.''"'^ In the present study, we have reviewed the clinical and histopathologic findings of 57 cases of PLCA, the largest series of such patients, and compared the findings with those reported from other parts of the world. Materials and Methods Fifty-seven patients with PLCA were examined in the Department of Dermatology at the American University of Beirut Medical Center between 1965 and 1989. All were Caucasians and of Mediterranean origin. The age, sex, country of origin, duration of signs and symptoms, and a detailed clinical description coupled with photographic documentation were included. All cases had formalin-fixed, paraffin-embedded, skin biopsy specimens stained with hematoxylin and eosin and with crystal violet. These were re-examined by light microscopy.
RESULTS
Clinical Features Macular Amyloidosis. There were 43 patients with MA with an age range of 14 to 70 years. The man to woman ratio was 1 to 3 (Table 1). Skin lesions varied in duration from few months to 26 years. Most lesions were located on the upper back. Other sites of involvement included the face, neck, chest, and extremities (Table 2). Almost all the skin lesions were dark-brown macular patches with a variable pattern of pigmentation (Fig. 1). Confluent macular pigmentation was found in 22 of 43 patients. A reticulated or rippled pigmentation was present in 19 patients. In two patients, the pattern of pigmentation was not specified. Eighteen patients had deep brown tiny papules (micropapules or small lichens) within the areas of hyperpigmentation (Fig. 2). Thirty-three patients complained of mild to moderate pruritus at the site of the lesions.
International Journal of Dermatology Vol. 31, No. 2, February 1992
Form
Men
Women
Table 1. Total"
Macular
10
33
43
Lichen
7
8
15
Clinical Data on 57 Patients with PLCA Confluent Macular Pruritus Pigmentation 33 (77%) 22(51%) 3 (20%)
11 (73%)
Rippled Pigmentation 19 (44%)
Lichens
1 (7%)
15 (100%)
18 (42%) (small lichens)
One patient had both MA and LA and was included under both variants bence tbe total number of patients became 58.
Table 2. Form
Face
Neck
Macular Lichen
2
4
Distribution of Lesions in Chest Arms 12 6 1 1
57 Patients
w i t h PLCA
Baclz
Abdomen
Thighs
43
1
1
1
Legs 4 14
dermis showed hyperkeratosis, hypergranulosis, slight degree of hyperplasia, and basal cell vacuolar degeneration. In addition, keratinocytes in various stages of degeneration (including colloid bodies) were found throughout the thickness of the epidermis. Satellite cell necrosis (necrotic epidermal cells closely associated with
Lichen Amyloidosis. This group comprised 15 patients. Their ages ranged from 29 to 69 years. There were 7 men and 8 women (Table 1). The duration of their lesions varied from few months to 16 years. Lesions were located over the shins in all patients except one, where the lesions were over the back, chest, and arms (Table 2). Eleven patients had severe pruritus; the rest were free of symptoms. In all patients, the lesions consisted of closely-set and confluent hyperkeratotic lichens and/or plaques (Fig. 3). In three patients, the lichens were present within areas of brown macular hyperpigmentation over the shins; and in a fourth case, namely the patient who had lesions over the back, chest, and arms, a similar clinical presentation was noted. Histopathologic Features The histopathologic changes were similar in all cases of PLCA though there were differences in degree, being more prominent in LA. The changes affected the epidermis, dermo-epidermal junction, and papillary dermis in a focal manner (Fig. 4). In the involved focal areas, the epi-
Figure 2. Macular hyperpigmented patches with superimposed micropapules (—>) are illustrated in this patient with MA.
Figure 1. Rippled dark-brown hyperpigmented macular patches are noted over the back in a patient with MA.
Figure 3. Discrete and confluent hyperkeratotic lichens are present over the shins in a patient with LA. 96
Cutaneous Amyioidosis Kibbi et al.
lymphocytes) were also seen in a significant number of biopsy specimens. Epidermal melanization seemed to be less than in the adjacent "normal" areas. In LA, the hyperkeratosis was more compact and/or basket woven, and epidermal hyperplasia more pronounced than in MA (Fig. 5). The epidermal changes were accompanied by elongate rete ridges, some of which assumed a clawshaped configuration around dermal papillae. The dermal papillae contained discrete and confluent, homogeneous eosinophilic masses that stained positively with crystal violet. Such masses were larger in LA than in MA. Amyloid deposits were also seen at the dermo-epidermal junction. Striking pigmentary incontinence in association with a mild to moderate superficial perivascular lymptho-histiocytic cell infiltrate were observed.
This series of 57 patients with PLCA is probably the largest reported to date, and the highlighting of the salient features may help in elucidating this disorder. The macular variant of PLCA was more common than the lichen variant and accounted for two-thirds of the total number of cases. This is in contrast to the reports in the literature, where LA is said to be more common than MA.8>i2." This difference may be due to the heightened clinical suspicion for MA and subsequent microscopic confirmation, thus eliminating the misdiagnoses of neurodermatitis and postinflammation hyperpigmentation.'^ Women outnumbered men in the MA group of this series. A preponderance of women has been found in a number of studies,2'5.«'"' but not in all.'^ This may be due to the
fact that women seek medical attention earlier than men for such a cosmetically disturbing condition.** Conversely, LA has equally affected both sexes in our series. It is likely that patients of either sex with LA seek medical attention because of its intensely pruritic and cosmetically embarrassing nature. A reticulated or rippled pattern of pigmentation has been emphasized as a characteristic and diagnostic feature of MA,'-' but in only about half of our patients has this been present; the remaining patients had confluent macular pigmentation. In both groups, tiny papules were observed within the pigmented areas. These were much smaller than those noted in the classical lichen variety. Our findings are similar to those of Black and Wilson Jones," who in a study of 21 cases of MA, found only nine cases with reticulated or rippled pigmentation and six cases with micropapules superimposed on the pigmentation. The microscopic changes in the epidermis and the upper dermis of the tiny papules in our series were at variance from the LA group, in that hyperkeratosis, papillomatosis, epidermal hyperplasia, and the size of the amyloid globules were not as prominent. In four of the 15 patients with LA, the papular lesions arose on a background of macular hyperpigmentation. Such patients, as well as those patients with micropapules in the macular variant, may represent an intermediate stage in the clinical presentation of PLCA. A spectrum for the disease is thus suggested ranging from MA with reticulated or confluent hyperpigmentation at one end, to LA with classical lichens at the opposite end. The term biphasic amyloidosis may be an oversimplification and does not account for the intermediate cases. The localization of LA to the shins in a significant num-
Figure 4. In a biopsy specimen of MA, two adjacent dermal papillae contain amyloid deposits. In the center, basal cell destruction and a tiny subepidermal split are noted (^). H &c E stain (original magnification x 100).
Figure 5. Prominent hyperkeratosis, hypergranulosis, irregular rete ridges, and epidermal hyperplasia characterize this lesion of LA. The dermal papillae display clumps of amyloid deposits. H & E stain (original magnification x 40).
DISCUSSION
97
International Journal of Dermatology Vol. 31, No. 2, February 1992
2.
ber of patients with this dermatosis and the associated intense pruritus are intriguing and remain unexplained. It is noteworthy, however, that other conditions such as lichen planus also have a tendency to lichenify when they occur on the shins.'' "Whether LA is lichenified cutaneous macular amyloidosis on the shins or is a site-specific variant of PLCA awaits further investigation. The histologic features of PLCA include varying degrees of hyperkeratosis, hypergranulosis, satellite cell necrosis, basal cell degeneration, and superficial perivascular lymphohistiocytic inflammatory cell infiltrate, as well as pigment-laden macrophages. These findings suggest an interface dermatitis of the vacuolar type and that PLCA is a lichenoid tissue reaction. It is noteworthy to mention that a lichenoid tissue reaction is a cutaneous reaction pattern in which the hallmark event is epidermal basal cell vacuolar alteration that in turn leads to a cascade of histopathologic changes in the epidermis and in the dermis.'^ These changes include almost all the features that were noted in our cases of PLCA. A band-like infiltrate in the papillary dermis is not a constant feature of this reaction pattern. Thus disorders such as erythema dyschromicum perstans and lichen pigmentosus are dermatoses with a lichenoid tissue reaction and in which perivascular rather than band-like inflammation in the papillary dermis is observed. The role of the inflammatory cells need to be defined in the hope that this might help in understanding the pathogenesis of this disorder.
3. 4.
5.
1.
6.
Harahap M, Hutapea NO. Lichen amyloidosis in Indonesia. Int J Dermatol 1970; 9:114-118.
7.
Leong YO, Tay CH, Foo J, et al. Lichen amyloidosus in Singapore. Int J Dermatol 1971; 10:151-155.
8.
Kurban AK, Malak JA, Afifi AK, et al. Primary localized macular cutaneous amyloidosis: Histochemistry and electron microscopy. BrJ Dermatol 1971; 85:52-60. Wong C-K. Lichen amyloidosus: A relatively common skin disorder in Taiwan. Arch Dermatol 1974; 110: 438^40. Piamphongsant T. Primary cutaneous amyloidosis. J Med Assoc Thai 1976; 59:435^39. Hahermann MC, Montenegro MR. Primary cutaneous amyloidosis. Dermatoiogica 1980; 160:240-248. Brownstein MH, Helwig EB. The cutaneous amyloidoses: I. Localized forms. Arch Dermatol 1970; 102:8-19. Black MM, Wilson Jones E. Macular amyloidosis: A study of 21 cases with special reference to the role of the epidermis in its histogenesis. Br J Dermatol 1971; 84:199-209. Shanon J, Sagher F. Interscapular cutaneous amyloidosis. Arch Dermatol 1970; 102:195-198. Kerdel-Vegas F. Cutaneous amyloidosis. Br J Dermatol 1967; 79:717-718.
9. 10. 11. 12. 13.
14. 15.
REFERENCES
16.
Breathnach SM. The cutaneous amyloidoses: Pathogenesis and therapy. Arch Dermatol 1985; 121:470-475.
Brownstein MH, Hashimoto K. Macular amyloidosis. Arch Dermatol 1972; 106:50-57. Wong C-K. Cutaneous amyloidoses. Int J Dermatol 1987; 26:273-277. Brownstein MH, Hashimoto K, Greenwald G. Biphasic amyloidosis: Link between macular and lichenoid forms. BrJ Dermatol 1973; 88:25-29. Cortes A. Primary cutaneous amyloidosis. Dermatoiogica 1969; 139:109-114.
Pinkus H. Lichenoid tissue reactions. Arch Dermatol 1973; 107:840-846. . -
Condyloma Accuminata Anogenital warts are one manifestation of human papillomavirus (HPV) infection of the anogenital tract. Such HPV infections have an adjusted annual incidence of about 8% in an unselected Scandinavian female population and anogenital warts are the commonest viral sexually transmissible disease in England. The patient's immune response probably determines whether infection will become manifested clinically and how well the resulting condylomas respond to treatment. HPV DNA replicates in the suprabasal cells of the epidermis, but the considerably more antigenic complete viral particles are produced only in differentiating keratinocytes, which are distant from cutaneous immunological defences. HPV infections may also be associated with local immunoparesis. Whatever treatment is used, efficacy probably depends on (a) removal of tissue containing viral particles and (b) disruption and release of previously sequestered viral antigens and their exposure to the immune system. From Editorial. 1993 and all that. Lancet 1991; 338: 1113-1114. 98
PRIMARY LOCALIZED CUTANEOUS AMYLOIDOSIS ABDUL-CHANI KIBBI, M.D., NELLY G. RUBEIZ, M.D., SHUKRALLAH T. ZAYNOUN, M.D., AND AMAL K. KURBAN, M.D.»
Abstract Fifty-seven patients with primary localized cutaneous amyloidosis (PLCA) were clinically and histopathologically reviewed. Two-thirds of patients had macular amyloidosis (MA). Intermediate cases having macular lesions with micropapules and/or lichens were identified. A spectrum for the disease is proposed, in which the less itchy classical macular variant occurs at one end and the very pruritic traditional lichen variant at the other. The salient histopathologic findings were similar in the macules, micropapules, and lichens, but were more prominent in the lichens. These consisted of hyperkeratosis, keratinocyte degeneration, satellite cell necrosis, and basal cell destruction. Amyloid deposition in the dermal papillae with transepidermal elimination, dermal melanophages, and superficial perivascular inflammation were also present. These changes represent an interface dermatitis of the vacuolar type, PLCA may be categorized under the group of dermatoses characterized by a lichenoid tissue reaction; inflammation may play a key role in mediating these disorders.
Macular amyloidosis (MA) and lichen amyloidosis (LA) are two closely related forms of primary localized cutaneous amyloidosis (PLCA).' The macular variant is characterized by moderately pruritic macules of dark brown pigmentation arranged in a reticulated or rippled pattern.^ The lesions usually occur in a symmetrical distribution over the upper back and arms. In the lichenoid form, closely-set, discrete, firm and hyperkeratotic papules and plaques are seen on the anterior aspect of the shins and the extensor surfaces of the forearms.^ In this form, intense pruritus is invariably present leading to
From the Department of Dermatology, American University of Beirut Medical Center, Beirut, Lebanon, and the *Department of Dermatology, Boston University Medical Center, Boston, Massachusetts. Presented in part at the American Society of Dermatopathology, San Francisco, California (1989), and published in abstract form in the J Cutan Pathol 1989; 16:312. Address for correspondence: Abdul-Ghani Kibbi, M.D., Department of Dermatology, American University of Beirut Medical Center, 850 Third Avenue, New York, NY 10022.
prominent lichenification. Macular and lichen amyloidosis may frequently coexist giving credence to the concept of biphasic amyloidosis."* Asians, Middle Easterners, and South Americans are particularly predisposed.^"" On histopathologic examination, deposits of amyloid in the papillary body are observed in both forms.'' Marked hyperkeratosis, papillomatosis, and epidermal hyperplasia are noted in tbe lichenoid form.''"'^ In the present study, we have reviewed the clinical and histopathologic findings of 57 cases of PLCA, the largest series of such patients, and compared the findings with those reported from other parts of the world. Materials and Methods Fifty-seven patients with PLCA were examined in the Department of Dermatology at the American University of Beirut Medical Center between 1965 and 1989. All were Caucasians and of Mediterranean origin. The age, sex, country of origin, duration of signs and symptoms, and a detailed clinical description coupled with photographic documentation were included. All cases had formalin-fixed, paraffin-embedded, skin biopsy specimens stained with hematoxylin and eosin and with crystal violet. These were re-examined by light microscopy.
RESULTS
Clinical Features Macular Amyloidosis. There were 43 patients with MA with an age range of 14 to 70 years. The man to woman ratio was 1 to 3 (Table 1). Skin lesions varied in duration from few months to 26 years. Most lesions were located on the upper back. Other sites of involvement included the face, neck, chest, and extremities (Table 2). Almost all the skin lesions were dark-brown macular patches with a variable pattern of pigmentation (Fig. 1). Confluent macular pigmentation was found in 22 of 43 patients. A reticulated or rippled pigmentation was present in 19 patients. In two patients, the pattern of pigmentation was not specified. Eighteen patients had deep brown tiny papules (micropapules or small lichens) within the areas of hyperpigmentation (Fig. 2). Thirty-three patients complained of mild to moderate pruritus at the site of the lesions.
International Journal of Dermatology Vol. 31, No. 2, February 1992
Form
Men
Women
Table 1. Total"
Macular
10
33
43
Lichen
7
8
15
Clinical Data on 57 Patients with PLCA Confluent Macular Pruritus Pigmentation 33 (77%) 22(51%) 3 (20%)
11 (73%)
Rippled Pigmentation 19 (44%)
Lichens
1 (7%)
15 (100%)
18 (42%) (small lichens)
One patient had both MA and LA and was included under both variants bence tbe total number of patients became 58.
Table 2. Form
Face
Neck
Macular Lichen
2
4
Distribution of Lesions in Chest Arms 12 6 1 1
57 Patients
w i t h PLCA
Baclz
Abdomen
Thighs
43
1
1
1
Legs 4 14
dermis showed hyperkeratosis, hypergranulosis, slight degree of hyperplasia, and basal cell vacuolar degeneration. In addition, keratinocytes in various stages of degeneration (including colloid bodies) were found throughout the thickness of the epidermis. Satellite cell necrosis (necrotic epidermal cells closely associated with
Lichen Amyloidosis. This group comprised 15 patients. Their ages ranged from 29 to 69 years. There were 7 men and 8 women (Table 1). The duration of their lesions varied from few months to 16 years. Lesions were located over the shins in all patients except one, where the lesions were over the back, chest, and arms (Table 2). Eleven patients had severe pruritus; the rest were free of symptoms. In all patients, the lesions consisted of closely-set and confluent hyperkeratotic lichens and/or plaques (Fig. 3). In three patients, the lichens were present within areas of brown macular hyperpigmentation over the shins; and in a fourth case, namely the patient who had lesions over the back, chest, and arms, a similar clinical presentation was noted. Histopathologic Features The histopathologic changes were similar in all cases of PLCA though there were differences in degree, being more prominent in LA. The changes affected the epidermis, dermo-epidermal junction, and papillary dermis in a focal manner (Fig. 4). In the involved focal areas, the epi-
Figure 2. Macular hyperpigmented patches with superimposed micropapules (—>) are illustrated in this patient with MA.
Figure 1. Rippled dark-brown hyperpigmented macular patches are noted over the back in a patient with MA.
Figure 3. Discrete and confluent hyperkeratotic lichens are present over the shins in a patient with LA. 96
Cutaneous Amyioidosis Kibbi et al.
lymphocytes) were also seen in a significant number of biopsy specimens. Epidermal melanization seemed to be less than in the adjacent "normal" areas. In LA, the hyperkeratosis was more compact and/or basket woven, and epidermal hyperplasia more pronounced than in MA (Fig. 5). The epidermal changes were accompanied by elongate rete ridges, some of which assumed a clawshaped configuration around dermal papillae. The dermal papillae contained discrete and confluent, homogeneous eosinophilic masses that stained positively with crystal violet. Such masses were larger in LA than in MA. Amyloid deposits were also seen at the dermo-epidermal junction. Striking pigmentary incontinence in association with a mild to moderate superficial perivascular lymptho-histiocytic cell infiltrate were observed.
This series of 57 patients with PLCA is probably the largest reported to date, and the highlighting of the salient features may help in elucidating this disorder. The macular variant of PLCA was more common than the lichen variant and accounted for two-thirds of the total number of cases. This is in contrast to the reports in the literature, where LA is said to be more common than MA.8>i2." This difference may be due to the heightened clinical suspicion for MA and subsequent microscopic confirmation, thus eliminating the misdiagnoses of neurodermatitis and postinflammation hyperpigmentation.'^ Women outnumbered men in the MA group of this series. A preponderance of women has been found in a number of studies,2'5.«'"' but not in all.'^ This may be due to the
fact that women seek medical attention earlier than men for such a cosmetically disturbing condition.** Conversely, LA has equally affected both sexes in our series. It is likely that patients of either sex with LA seek medical attention because of its intensely pruritic and cosmetically embarrassing nature. A reticulated or rippled pattern of pigmentation has been emphasized as a characteristic and diagnostic feature of MA,'-' but in only about half of our patients has this been present; the remaining patients had confluent macular pigmentation. In both groups, tiny papules were observed within the pigmented areas. These were much smaller than those noted in the classical lichen variety. Our findings are similar to those of Black and Wilson Jones," who in a study of 21 cases of MA, found only nine cases with reticulated or rippled pigmentation and six cases with micropapules superimposed on the pigmentation. The microscopic changes in the epidermis and the upper dermis of the tiny papules in our series were at variance from the LA group, in that hyperkeratosis, papillomatosis, epidermal hyperplasia, and the size of the amyloid globules were not as prominent. In four of the 15 patients with LA, the papular lesions arose on a background of macular hyperpigmentation. Such patients, as well as those patients with micropapules in the macular variant, may represent an intermediate stage in the clinical presentation of PLCA. A spectrum for the disease is thus suggested ranging from MA with reticulated or confluent hyperpigmentation at one end, to LA with classical lichens at the opposite end. The term biphasic amyloidosis may be an oversimplification and does not account for the intermediate cases. The localization of LA to the shins in a significant num-
Figure 4. In a biopsy specimen of MA, two adjacent dermal papillae contain amyloid deposits. In the center, basal cell destruction and a tiny subepidermal split are noted (^). H &c E stain (original magnification x 100).
Figure 5. Prominent hyperkeratosis, hypergranulosis, irregular rete ridges, and epidermal hyperplasia characterize this lesion of LA. The dermal papillae display clumps of amyloid deposits. H & E stain (original magnification x 40).
DISCUSSION
97
International Journal of Dermatology Vol. 31, No. 2, February 1992
2.
ber of patients with this dermatosis and the associated intense pruritus are intriguing and remain unexplained. It is noteworthy, however, that other conditions such as lichen planus also have a tendency to lichenify when they occur on the shins.'' "Whether LA is lichenified cutaneous macular amyloidosis on the shins or is a site-specific variant of PLCA awaits further investigation. The histologic features of PLCA include varying degrees of hyperkeratosis, hypergranulosis, satellite cell necrosis, basal cell degeneration, and superficial perivascular lymphohistiocytic inflammatory cell infiltrate, as well as pigment-laden macrophages. These findings suggest an interface dermatitis of the vacuolar type and that PLCA is a lichenoid tissue reaction. It is noteworthy to mention that a lichenoid tissue reaction is a cutaneous reaction pattern in which the hallmark event is epidermal basal cell vacuolar alteration that in turn leads to a cascade of histopathologic changes in the epidermis and in the dermis.'^ These changes include almost all the features that were noted in our cases of PLCA. A band-like infiltrate in the papillary dermis is not a constant feature of this reaction pattern. Thus disorders such as erythema dyschromicum perstans and lichen pigmentosus are dermatoses with a lichenoid tissue reaction and in which perivascular rather than band-like inflammation in the papillary dermis is observed. The role of the inflammatory cells need to be defined in the hope that this might help in understanding the pathogenesis of this disorder.
3. 4.
5.
1.
6.
Harahap M, Hutapea NO. Lichen amyloidosis in Indonesia. Int J Dermatol 1970; 9:114-118.
7.
Leong YO, Tay CH, Foo J, et al. Lichen amyloidosus in Singapore. Int J Dermatol 1971; 10:151-155.
8.
Kurban AK, Malak JA, Afifi AK, et al. Primary localized macular cutaneous amyloidosis: Histochemistry and electron microscopy. BrJ Dermatol 1971; 85:52-60. Wong C-K. Lichen amyloidosus: A relatively common skin disorder in Taiwan. Arch Dermatol 1974; 110: 438^40. Piamphongsant T. Primary cutaneous amyloidosis. J Med Assoc Thai 1976; 59:435^39. Hahermann MC, Montenegro MR. Primary cutaneous amyloidosis. Dermatoiogica 1980; 160:240-248. Brownstein MH, Helwig EB. The cutaneous amyloidoses: I. Localized forms. Arch Dermatol 1970; 102:8-19. Black MM, Wilson Jones E. Macular amyloidosis: A study of 21 cases with special reference to the role of the epidermis in its histogenesis. Br J Dermatol 1971; 84:199-209. Shanon J, Sagher F. Interscapular cutaneous amyloidosis. Arch Dermatol 1970; 102:195-198. Kerdel-Vegas F. Cutaneous amyloidosis. Br J Dermatol 1967; 79:717-718.
9. 10. 11. 12. 13.
14. 15.
REFERENCES
16.
Breathnach SM. The cutaneous amyloidoses: Pathogenesis and therapy. Arch Dermatol 1985; 121:470-475.
Brownstein MH, Hashimoto K. Macular amyloidosis. Arch Dermatol 1972; 106:50-57. Wong C-K. Cutaneous amyloidoses. Int J Dermatol 1987; 26:273-277. Brownstein MH, Hashimoto K, Greenwald G. Biphasic amyloidosis: Link between macular and lichenoid forms. BrJ Dermatol 1973; 88:25-29. Cortes A. Primary cutaneous amyloidosis. Dermatoiogica 1969; 139:109-114.
Pinkus H. Lichenoid tissue reactions. Arch Dermatol 1973; 107:840-846. . -
Condyloma Accuminata Anogenital warts are one manifestation of human papillomavirus (HPV) infection of the anogenital tract. Such HPV infections have an adjusted annual incidence of about 8% in an unselected Scandinavian female population and anogenital warts are the commonest viral sexually transmissible disease in England. The patient's immune response probably determines whether infection will become manifested clinically and how well the resulting condylomas respond to treatment. HPV DNA replicates in the suprabasal cells of the epidermis, but the considerably more antigenic complete viral particles are produced only in differentiating keratinocytes, which are distant from cutaneous immunological defences. HPV infections may also be associated with local immunoparesis. Whatever treatment is used, efficacy probably depends on (a) removal of tissue containing viral particles and (b) disruption and release of previously sequestered viral antigens and their exposure to the immune system. From Editorial. 1993 and all that. Lancet 1991; 338: 1113-1114. 98
