JWissmille
2004-02-07 01:54:25 UTC
Cutis laxa acquisita: is there any association with Borrelia burgdorferi?
Eur J Dermatol 1999 Oct-Nov;9(7):561-4 (ISSN: 1167-1122)
Ozkan S; Fetil E; Gunes AT; Bozkurt E; Sahin T; Erkizan V; Yuce A
Department of Dermatology, Faculty of Medicine, University of Dokuz Eylul,
35340 Inciralti, Izmir, Turkey.
We report the first case of an acquired form of generalized cutis laxa which
has positive serology and a positive polymerase chain reaction (PCR) result for
lyme borreliosis. A 44-year-old man complained of excessively loose skin for
four years and had no family history of any skin disease. Dermatological
examination showed lax and wrinkled skin all over the body (especially on the
cheeks and the intertriginous areas). Positive serology for lyme borreliosis
and the presence of Borrelia burgdorferi DNA which was demonstrated by nested
PCR in this acquired form of cutis laxa is interesting since it has not been
reported in literature previously.
Indexing Check Tags: Case Report; Female; Human; Male
Language: English
MEDLINE Indexing Date: 199912
Publication Type: Status: Completed
Publication Type: Journal Article
PreMedline Identifier: 0010523738
Unique NLM Identifier: 99455184
Journal Code: IM
______________________________________
Acral localized acquired cutis laxa associated with rheumatoid arthritis
J Am Acad Dermatol 2002 Jan;46(1):128-30 (ISSN: 0190-9622)
Rongioletti F; Cutolo M; Bondavalli P; Rebora A
Department of Endocrinological and Metabolic Disease, Section of Dermatology,
and University of Genoa, Italy.
We report the first case of the acral localization of the acquired form of
cutis laxa associated with severe rheumatoid arthritis. The skin laxity was
preceded by episodes of itching and swelling of the hands and feet.
Histopathology showed that the elastic fibers were lost in the areas of cutis
laxa and decreased in adjacent skin. The pathogenetic relationship with
rheumatoid arthritis or the intake of related drugs is discussed.
Indexing Check Tags: Case Report; Human; Male
Language: English
MEDLINE Indexing Date: 200202
Publication Type: Status: Completed
Publication Type: Journal Article
PreMedline Identifier: 0011756959
Unique NLM Identifier: 21629357
Journal Code: IM
____________________
Mid-dermal elastolysis in an adolescent subsequent to lesions resembling
granuloma annulare.
J Am Acad Dermatol 1997 Nov;37(5 Pt 2):870-2 (ISSN: 0190-9622)
Yen A; Tschen J; Raimer SS
Department of Dermatology, University of Texas Medical Branch, Galveston
77555-0783, USA.
First described by Shelley and Wood in 1977, mid-dermal elastolysis (MDE) is a
rare acquired disorder in which there is a bandlike absence of elastic tissue
limited to the mid-dermis. In their patient, MDE developed in an area
previously involved with recurrent episodes of urticaria. We describe a
15-year-old white girl with well-circumscribed, minimally palpable yellow-white
plaques and wrinkling diagnosed histologically as MDE in areas clinically
diagnosed 5 years previously as granuloma annulare. As in the first described
patient, five years elapsed between clearance of the original skin lesions and
the clinical appearance of MDE. To our knowledge, we report the first
adolescent case of MDE localized to previous sites of lesions clinically
consistent with granuloma annulare and propose that MDE represents an abnormal
end-stage reaction to multiple processes.
Indexing Check Tags: Case Report; Female; Human
Language: English
MEDLINE Indexing Date: 199711
Publication Type: Status: Completed
Publication Type: Journal Article
PreMedline Identifier: 0009366855
Unique NLM Identifier: 98033650
Journal Code: IM
_______________
Anetoderma of Jadassohn-Pellizzari.
J R Soc Med 1995 Oct;88(10):599P-600P (ISSN: 0141-0768)
Roberts NM; Farrell A; Woodrow D; Leibowitch M; Staughton RC
Department of Dermatology, Chelsea and Westminster Hospital, London, England,
UK.
Anetoderma (derived from the Greek anetos, meaning slack) is a term used to
describe localized increased laxity of the skin with herniation or outpouching,
resulting from abnormal dermal elastic tissue. Primary anetoderma is distinctly
rare. We describe a case where we suspect an auto-immune aetiology.
Indexing Check Tags: Case Report; Human; Male
Language: English
MEDLINE Indexing Date: 199602
Publication Type: Status: Completed
Publication Type: Journal Article
PreMedline Identifier: 0008537953
Unique NLM Identifier: 96138252
Journal Code: IM
________
Anetoderma arising in cutaneous B-cell lymphoproliferative disease.
Am J Dermatopathol 2001 Apr;23(2):124-32 (ISSN: 0193-1091)
Kasper RC; Wood GS; Nihal M; Le Boit PE
Department of Pathology, University of California, San Francisco 94115, USA.
Anetoderma is circumscribed atrophy of the skin due to a localized deficiency
in elastic tissue. It can follow inflammatory skin diseases of several types,
and occasionally is present in the skin around neoplasms. There are a few
reports of anetoderma in the lesional skin of cutaneous lymphoma. We report on
two patients who presented with multiple lesions of anetoderma and who later
proved to have low-grade cutaneous B-cell lymphomas. One patient (Patient 1) is
a 39-year-old man and the other patient is a 26-year-old woman who is a renal
transplant recipient (Patient 2). Some biopsy specimens from the anetodermic
skin of Patient 1 appeared to show an urticarial reaction, although plasma
cells were present. A large nodule showed lymphoid follicles surrounded by
plasmacytoid lymphocytes, with loss of elastic tissue in the adjacent dermis.
The plasmacytoid cells stained overwhelmingly for lambda light chain, and
staining of the urticarial lesions from this patient also showed a marked
majority of lambda positive cells. Immunoglobulin heavy chain gene (IgH)
rearrangements showed a dominant clonal pattern in the nodular lesion. We
classified the disease in Patient 1 as marginal zone lymphoma and the disease
in Patient 2 as a post-transplant lymphoproliferative disorder. Because of the
intimate association of anetoderma and cutaneous B-cell lymphoproliferative
disorders in these two patients, it seems possible that anetoderma could result
from either a local effect of the neoplastic cells or associated inflammatory
cells, especially neutrophils as in Case 1. The infiltrates of Case 1 had many
interstitial neutrophils and only a few clonal plasmacytoid lymphocytes,
indicating that this presentation of B-cell lymphoma can be a diagnostic
pitfall. Given these two cases and similar ones in the literature, biopsy of
lesional skin in anetoderma should be performed to ensure that lymphomatous
infiltrates are not present. Even if plasma cells are sparse, studies to detect
clonality are appropriate. Cutaneous B-cell lymphoma can be added to the list
of associations of elastolysis and cutaneous lymphoma, which includes
granulomatous slack skin (T-cell lymphoma) and cutis laxa (myeloma).
Indexing Check Tags: Case Report; Female; Human; Male
Language: English
MEDLINE Indexing Date: 200106
Publication Type: Status: Completed
Publication Type: Journal Article
PreMedline Identifier: 0011285407
Unique NLM Identifier: 21181420
Journal Code: IM
_________________________________
"........ Some cases of
anetoderma might be caused by Borrelia and patients with
anetoderma should be examined for borreliosis ...."
J Am Acad Dermatol. 2003 May;48(5 Suppl):S86-8. Related
Articles, Links
Anetoderma: another facet of Lyme disease?
Bauer J, Leitz G, Palmedo G, Hugel H.
Department of Dermatology, Eberhard Karls University, Tubingen,
Germany. ***@J.Bauer.de
Lyme disease has been suspected to be one cause of secondary
anetoderma. We present a 25-year-old male patient with multiple
lesions of anetoderma with a diameter of up to 2 cm that
developed within the last 4 weeks without subjective symptoms.
The histopathologic pattern was similar to the inflammatory stage
of acrodermatitis chronica atrophicans. Polymerase chain reaction
analysis out of the paraffin-embedded tissue, confirmed by
sequencing of the obtained nucleotide product, revealed a part of
the 23 S ribosomal RNA gene of Borrelia burgdorferi sensu lato.
Enzyme-linked immunosorbent assay showed an increased serum IgG
titer against B burgdorferi corroborated by Western blot
analysis. After a treatment with oral doxycycline (100 mg twice a
day) for 30 days the anti-B burgdorferi titer decreased
significantly and no new lesions appeared. Some cases of
anetoderma might be caused by Borrelia and patients with
anetoderma should be examined for borreliosis including serology
and polymerase chain reaction of lesional skin. In cases of
Borrelia-induced anetoderma, early antibiotic treatment could
prevent further progression of the disfiguring skin lesions and
the underlying disease.
____________________________________
: Parazitologiia 1999 May-Jun;33(3):267-9 Related Articles, Books
[No title available].
[Article in Russian]
[Medline record in process]
The borreliosis etiology was verified in 60% cases of the morphea, 100% cases
of the atrophoderma of Pasini-Pierini and 100% cases of anetoderma by means of
IFA with Ip-21 antigen (B. afzelii) and silver staining after Levadity.
Borreliae were located near the capilars, muscular and areolar tissue fibers of
the derm and near the granulated cells of epidermis.
PMID: 10771775, UI: 20234270
______________
Intern Med 1991 Mar 15;114(6):490-8
Diagnosis of Lyme disease based on dermatologic manifestations.
Malane MS, Grant-Kels JM, Feder HM Jr, Luger SW
University of Connecticut, Farmington.
Lyme disease, or Lyme borreliosis, is an infection caused by the spirochete
Borrelia burgdorferi, which is most commonly transmitted to humans by a tick
bite. Characterized by early and late phases, Lyme disease is a multisystem
illness involving the skin, heart, joints, and nervous system. Diagnosis is
based predominantly on clinical manifestations, the most specific being
dermatologic. Thus, recognizing the dermatologic manifestations of Lyme disease
is important for diagnosis and institution of appropriate, effective therapy.
Approximately 75% of patients with Lyme disease present with the pathognomonic
skin lesion erythema migrans, an expanding erythematous lesion. During early
infection, secondary erythema migrans lesions or Borrelia lymphocytoma may
occur. Borrelia lymphocytoma commonly presents as an erythematous nodule on the
ear lobe or nipple. During late infection, acrodermatitis chronica atrophicans,
an erythematous, atrophic plaque unique to Lyme disease may appear; it has been
described in about 10% of patients with Lyme disease in Europe. Fibrotic
nodules associated with acrodermatitis chronica atrophicans as well as other
sclerotic and atrophic lesions, such as morphea, lichen sclerosus et
atrophicus, anetoderma, and atrophoderma of Pasini and Pierini, have been seen
late in the course of Lyme disease. In a few cases, other sclerodermatous
lesions, such as eosinophilic fasciitis and progressive facial hemiatrophy,
have been linked to B. burgdorferi infection. We review the cutaneous lesions
associated with Lyme disease.
Publication Types:
Review
Review, tutorial
PMID: 1994797, UI: 91136056
_______________
source: "Acrodermatitis Chronica
Atrophicans: Historical and Clinical Overview,"
by Rudolph J.
Scrimenti, Associate Clinical Professor of
Dermatology, Medical College of Wisconsin, Milwaukee.
LABORATORY FINDINGS. Increased erythrocyte sedimentation rates are
noted regularly. The organism
can be cultured slowly on modified Barbour-Stoenner-Kelly medium from
skin lesions, even decade-old
lesions at temperatures of 32 to 33 C. Focal areas of plasma cells
may be present in the deeper dermis.
With progression, epidermal thinning, degeneration of elastic fibers
and collagen occurs. Eventually
after many years, advanced atrophy of the dermis, including all
appendages, follows the inflammation.
Later, the inflammation disappears, and a pronounced thinning of the
entire dermis and subcutis
develops. A rich mixture of plasma cells, if present may be the only
feature ifferentiating sclerotic and
atrophic ACA from idiopathic scleroderma (morphea) and lichen
sclerosus, except for the presence of
the spirochete. Immunohistologic staining shows a predominance of
CD4 lymphocytes. Most, but not
all, studies show no association between the development of ACA and
HLA class II alleles. (Newly
identiied species may not culture and other tests may be negative -D.
B.).
DIFFERENTIAL DIAGNOSIS. The distinctive plasmacytic infiltrate
(if present), unique clinical features
and serologic findings differentiate ACA from arterial and venous
insufficiency, acrocyanosis, livedo
reticularis, vasculitis, contact dermatitis and collagen diseases.
Fibrotic nodules histologically are
distinguished from gouty tophi, calcinosis cutis, rheumatoid nodules
and xanthomas.
Eur J Dermatol 1999 Oct-Nov;9(7):561-4 (ISSN: 1167-1122)
Ozkan S; Fetil E; Gunes AT; Bozkurt E; Sahin T; Erkizan V; Yuce A
Department of Dermatology, Faculty of Medicine, University of Dokuz Eylul,
35340 Inciralti, Izmir, Turkey.
We report the first case of an acquired form of generalized cutis laxa which
has positive serology and a positive polymerase chain reaction (PCR) result for
lyme borreliosis. A 44-year-old man complained of excessively loose skin for
four years and had no family history of any skin disease. Dermatological
examination showed lax and wrinkled skin all over the body (especially on the
cheeks and the intertriginous areas). Positive serology for lyme borreliosis
and the presence of Borrelia burgdorferi DNA which was demonstrated by nested
PCR in this acquired form of cutis laxa is interesting since it has not been
reported in literature previously.
Indexing Check Tags: Case Report; Female; Human; Male
Language: English
MEDLINE Indexing Date: 199912
Publication Type: Status: Completed
Publication Type: Journal Article
PreMedline Identifier: 0010523738
Unique NLM Identifier: 99455184
Journal Code: IM
______________________________________
Acral localized acquired cutis laxa associated with rheumatoid arthritis
J Am Acad Dermatol 2002 Jan;46(1):128-30 (ISSN: 0190-9622)
Rongioletti F; Cutolo M; Bondavalli P; Rebora A
Department of Endocrinological and Metabolic Disease, Section of Dermatology,
and University of Genoa, Italy.
We report the first case of the acral localization of the acquired form of
cutis laxa associated with severe rheumatoid arthritis. The skin laxity was
preceded by episodes of itching and swelling of the hands and feet.
Histopathology showed that the elastic fibers were lost in the areas of cutis
laxa and decreased in adjacent skin. The pathogenetic relationship with
rheumatoid arthritis or the intake of related drugs is discussed.
Indexing Check Tags: Case Report; Human; Male
Language: English
MEDLINE Indexing Date: 200202
Publication Type: Status: Completed
Publication Type: Journal Article
PreMedline Identifier: 0011756959
Unique NLM Identifier: 21629357
Journal Code: IM
____________________
Mid-dermal elastolysis in an adolescent subsequent to lesions resembling
granuloma annulare.
J Am Acad Dermatol 1997 Nov;37(5 Pt 2):870-2 (ISSN: 0190-9622)
Yen A; Tschen J; Raimer SS
Department of Dermatology, University of Texas Medical Branch, Galveston
77555-0783, USA.
First described by Shelley and Wood in 1977, mid-dermal elastolysis (MDE) is a
rare acquired disorder in which there is a bandlike absence of elastic tissue
limited to the mid-dermis. In their patient, MDE developed in an area
previously involved with recurrent episodes of urticaria. We describe a
15-year-old white girl with well-circumscribed, minimally palpable yellow-white
plaques and wrinkling diagnosed histologically as MDE in areas clinically
diagnosed 5 years previously as granuloma annulare. As in the first described
patient, five years elapsed between clearance of the original skin lesions and
the clinical appearance of MDE. To our knowledge, we report the first
adolescent case of MDE localized to previous sites of lesions clinically
consistent with granuloma annulare and propose that MDE represents an abnormal
end-stage reaction to multiple processes.
Indexing Check Tags: Case Report; Female; Human
Language: English
MEDLINE Indexing Date: 199711
Publication Type: Status: Completed
Publication Type: Journal Article
PreMedline Identifier: 0009366855
Unique NLM Identifier: 98033650
Journal Code: IM
_______________
Anetoderma of Jadassohn-Pellizzari.
J R Soc Med 1995 Oct;88(10):599P-600P (ISSN: 0141-0768)
Roberts NM; Farrell A; Woodrow D; Leibowitch M; Staughton RC
Department of Dermatology, Chelsea and Westminster Hospital, London, England,
UK.
Anetoderma (derived from the Greek anetos, meaning slack) is a term used to
describe localized increased laxity of the skin with herniation or outpouching,
resulting from abnormal dermal elastic tissue. Primary anetoderma is distinctly
rare. We describe a case where we suspect an auto-immune aetiology.
Indexing Check Tags: Case Report; Human; Male
Language: English
MEDLINE Indexing Date: 199602
Publication Type: Status: Completed
Publication Type: Journal Article
PreMedline Identifier: 0008537953
Unique NLM Identifier: 96138252
Journal Code: IM
________
Anetoderma arising in cutaneous B-cell lymphoproliferative disease.
Am J Dermatopathol 2001 Apr;23(2):124-32 (ISSN: 0193-1091)
Kasper RC; Wood GS; Nihal M; Le Boit PE
Department of Pathology, University of California, San Francisco 94115, USA.
Anetoderma is circumscribed atrophy of the skin due to a localized deficiency
in elastic tissue. It can follow inflammatory skin diseases of several types,
and occasionally is present in the skin around neoplasms. There are a few
reports of anetoderma in the lesional skin of cutaneous lymphoma. We report on
two patients who presented with multiple lesions of anetoderma and who later
proved to have low-grade cutaneous B-cell lymphomas. One patient (Patient 1) is
a 39-year-old man and the other patient is a 26-year-old woman who is a renal
transplant recipient (Patient 2). Some biopsy specimens from the anetodermic
skin of Patient 1 appeared to show an urticarial reaction, although plasma
cells were present. A large nodule showed lymphoid follicles surrounded by
plasmacytoid lymphocytes, with loss of elastic tissue in the adjacent dermis.
The plasmacytoid cells stained overwhelmingly for lambda light chain, and
staining of the urticarial lesions from this patient also showed a marked
majority of lambda positive cells. Immunoglobulin heavy chain gene (IgH)
rearrangements showed a dominant clonal pattern in the nodular lesion. We
classified the disease in Patient 1 as marginal zone lymphoma and the disease
in Patient 2 as a post-transplant lymphoproliferative disorder. Because of the
intimate association of anetoderma and cutaneous B-cell lymphoproliferative
disorders in these two patients, it seems possible that anetoderma could result
from either a local effect of the neoplastic cells or associated inflammatory
cells, especially neutrophils as in Case 1. The infiltrates of Case 1 had many
interstitial neutrophils and only a few clonal plasmacytoid lymphocytes,
indicating that this presentation of B-cell lymphoma can be a diagnostic
pitfall. Given these two cases and similar ones in the literature, biopsy of
lesional skin in anetoderma should be performed to ensure that lymphomatous
infiltrates are not present. Even if plasma cells are sparse, studies to detect
clonality are appropriate. Cutaneous B-cell lymphoma can be added to the list
of associations of elastolysis and cutaneous lymphoma, which includes
granulomatous slack skin (T-cell lymphoma) and cutis laxa (myeloma).
Indexing Check Tags: Case Report; Female; Human; Male
Language: English
MEDLINE Indexing Date: 200106
Publication Type: Status: Completed
Publication Type: Journal Article
PreMedline Identifier: 0011285407
Unique NLM Identifier: 21181420
Journal Code: IM
_________________________________
"........ Some cases of
anetoderma might be caused by Borrelia and patients with
anetoderma should be examined for borreliosis ...."
J Am Acad Dermatol. 2003 May;48(5 Suppl):S86-8. Related
Articles, Links
Anetoderma: another facet of Lyme disease?
Bauer J, Leitz G, Palmedo G, Hugel H.
Department of Dermatology, Eberhard Karls University, Tubingen,
Germany. ***@J.Bauer.de
Lyme disease has been suspected to be one cause of secondary
anetoderma. We present a 25-year-old male patient with multiple
lesions of anetoderma with a diameter of up to 2 cm that
developed within the last 4 weeks without subjective symptoms.
The histopathologic pattern was similar to the inflammatory stage
of acrodermatitis chronica atrophicans. Polymerase chain reaction
analysis out of the paraffin-embedded tissue, confirmed by
sequencing of the obtained nucleotide product, revealed a part of
the 23 S ribosomal RNA gene of Borrelia burgdorferi sensu lato.
Enzyme-linked immunosorbent assay showed an increased serum IgG
titer against B burgdorferi corroborated by Western blot
analysis. After a treatment with oral doxycycline (100 mg twice a
day) for 30 days the anti-B burgdorferi titer decreased
significantly and no new lesions appeared. Some cases of
anetoderma might be caused by Borrelia and patients with
anetoderma should be examined for borreliosis including serology
and polymerase chain reaction of lesional skin. In cases of
Borrelia-induced anetoderma, early antibiotic treatment could
prevent further progression of the disfiguring skin lesions and
the underlying disease.
____________________________________
: Parazitologiia 1999 May-Jun;33(3):267-9 Related Articles, Books
[No title available].
[Article in Russian]
[Medline record in process]
The borreliosis etiology was verified in 60% cases of the morphea, 100% cases
of the atrophoderma of Pasini-Pierini and 100% cases of anetoderma by means of
IFA with Ip-21 antigen (B. afzelii) and silver staining after Levadity.
Borreliae were located near the capilars, muscular and areolar tissue fibers of
the derm and near the granulated cells of epidermis.
PMID: 10771775, UI: 20234270
______________
Intern Med 1991 Mar 15;114(6):490-8
Diagnosis of Lyme disease based on dermatologic manifestations.
Malane MS, Grant-Kels JM, Feder HM Jr, Luger SW
University of Connecticut, Farmington.
Lyme disease, or Lyme borreliosis, is an infection caused by the spirochete
Borrelia burgdorferi, which is most commonly transmitted to humans by a tick
bite. Characterized by early and late phases, Lyme disease is a multisystem
illness involving the skin, heart, joints, and nervous system. Diagnosis is
based predominantly on clinical manifestations, the most specific being
dermatologic. Thus, recognizing the dermatologic manifestations of Lyme disease
is important for diagnosis and institution of appropriate, effective therapy.
Approximately 75% of patients with Lyme disease present with the pathognomonic
skin lesion erythema migrans, an expanding erythematous lesion. During early
infection, secondary erythema migrans lesions or Borrelia lymphocytoma may
occur. Borrelia lymphocytoma commonly presents as an erythematous nodule on the
ear lobe or nipple. During late infection, acrodermatitis chronica atrophicans,
an erythematous, atrophic plaque unique to Lyme disease may appear; it has been
described in about 10% of patients with Lyme disease in Europe. Fibrotic
nodules associated with acrodermatitis chronica atrophicans as well as other
sclerotic and atrophic lesions, such as morphea, lichen sclerosus et
atrophicus, anetoderma, and atrophoderma of Pasini and Pierini, have been seen
late in the course of Lyme disease. In a few cases, other sclerodermatous
lesions, such as eosinophilic fasciitis and progressive facial hemiatrophy,
have been linked to B. burgdorferi infection. We review the cutaneous lesions
associated with Lyme disease.
Publication Types:
Review
Review, tutorial
PMID: 1994797, UI: 91136056
_______________
source: "Acrodermatitis Chronica
Atrophicans: Historical and Clinical Overview,"
by Rudolph J.
Scrimenti, Associate Clinical Professor of
Dermatology, Medical College of Wisconsin, Milwaukee.
LABORATORY FINDINGS. Increased erythrocyte sedimentation rates are
noted regularly. The organism
can be cultured slowly on modified Barbour-Stoenner-Kelly medium from
skin lesions, even decade-old
lesions at temperatures of 32 to 33 C. Focal areas of plasma cells
may be present in the deeper dermis.
With progression, epidermal thinning, degeneration of elastic fibers
and collagen occurs. Eventually
after many years, advanced atrophy of the dermis, including all
appendages, follows the inflammation.
Later, the inflammation disappears, and a pronounced thinning of the
entire dermis and subcutis
develops. A rich mixture of plasma cells, if present may be the only
feature ifferentiating sclerotic and
atrophic ACA from idiopathic scleroderma (morphea) and lichen
sclerosus, except for the presence of
the spirochete. Immunohistologic staining shows a predominance of
CD4 lymphocytes. Most, but not
all, studies show no association between the development of ACA and
HLA class II alleles. (Newly
identiied species may not culture and other tests may be negative -D.
B.).
DIFFERENTIAL DIAGNOSIS. The distinctive plasmacytic infiltrate
(if present), unique clinical features
and serologic findings differentiate ACA from arterial and venous
insufficiency, acrocyanosis, livedo
reticularis, vasculitis, contact dermatitis and collagen diseases.
Fibrotic nodules histologically are
distinguished from gouty tophi, calcinosis cutis, rheumatoid nodules
and xanthomas.