Acrodermatitis chronica atrophicans

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Acrodermatitis chronica atrophicans

Post by Yvonne » Thu 27 Dec 2007 19:45

Acrodermatitis chronica atrophicans (ACA) is the third or late stage of European Lyme borreliosis (LB). This unusual, progressive, fibrosing skin process is due to the effect of continuing active infection with Borrelia afzelii. Buchwald first delineated it in 1883; Herxheimer and Hartmann described it in 1902 as a tissue paper–like cutaneous atrophy. It is evident on the extremities, particularly on the extensor surfaces, beginning with an inflammatory stage with bluish red discoloration and cutaneous swelling and concluding several months or years later with an atrophic phase. Sclerotic skin plaques may also develop. Physicians should use serologic and histologic examination to confirm this diagnosis.

Pathophysiology: B afzelii is the predominant, but may not be the exclusive, etiologic agent of ACA. Another genospecies of the Borrelia burgdorferi sensu lato complex, Borrelia garinii, has also been detected.

ACA is the only form of LB in which no spontaneous remission occurs. Its pathophysiology is not yet fully understood. ACA appears to be associated with long-term persistence of Borrelia organisms in the skin; several nonspecific reactions together with a specific immune response may contribute to its manifestations.

The persistence of the spirochetes despite a marked cutaneous T-cell infiltration and high serum antibody titers may be connected with resistance of the pathogen to the complement system; the ability to escape to immunologically protected sites (eg, endothelial cells, fibroblasts); and the ability to change antigens, which may lead to an inappropriate immune response. Lack of protective antibodies, with a narrow antibody spectrum and a weak cellular response with down-regulation of major histocompatibility system class II molecules on Langerhans cells, has been observed in patients with LB.

A restricted pattern of cytokine expression in ACA, including the lack of interferon-gamma, may contribute to its chronicity. Cross-reactive antibody responses could take part in autoimmune damage, but whether autoimmune reactions play any role in the pathogenesis of the disease is unclear. The pathogenic mechanism of atrophic skin changes has also not been clarified. Perhaps periarticular regions are favorite sites because of reduced acral skin temperatures or reduced oxygen pressure.


In the US: The occurrence of ACA is connected with the ecology of LB, which varies in different geographical regions of the world.
Despite a high incidence of LB in the United States (varying from 95 cases per 100,000 population in Connecticut to 1250 cases per 100,000 population in Nantucket County, Massachusetts [1996 data]), ACA is not seen in the United States, except in a few European immigrants.

Internationally: The occurrence of ACA is connected with the ecology of LB, which varies in different geographical regions of the world.
Ixodes scapularis, Ixodes pacificus, and 4 other tick species distributed in North America transmit B burgdorferi sensu stricto, causing EM and LB arthritis.

Tick vectors of B afzelii, the main etiologic agent of ACA (and erythema migrans [EM]), are Ixodes ricinus, Ixodes hexagonus, and Ixodes persulcatus distributed in western and central Europe and in far eastern Europe and Asia. Almost all of these hard tick species may also transmit B garinii, a causative agent of EM and neurologic symptoms of LB.

In Europe, LB with all its dermatologic manifestations occurs in almost all countries, predominantly in the central part of the continent. The annual incidence per 100,000 population varies from 16 cases in France to 120 cases in northeastern Poland and Slovenia and to 130 cases in Austria (1995 data).

The frequency of ACA is about 1-10% of all European patients with LB, varying according to the region of the population sampled. Among the group of patients with skin manifestations of LB observed in Vienna, the ratio of the number of EM cases to ACA cases and to Borrelia lymphocytoma (BL) cases was 30:3:1. This ratio is 170:5:1 in the authors' as-yet-unpublished studies (provided in the group of patients with LB in northeastern Poland).

Because the clinical diagnosis of ACA is much more difficult than that of EM or BL, the condition is often underdiagnosed, and, in fact, the ratio of EM cases to ACA cases may be higher. The total number of cases could increase with increasing frequency of untreated European LB. ACA is probably the most common late and chronic manifestation of the borreliosis in European patients with Lyme disease.

A Bulgarian survey found that borrelial lymphocytoma and ACA were rare (0.3%) (Christova, 2004

Mortality/Morbidity: The course of ACA is long-standing, lasting from a few to several years, and it leads to extensive flaccid atrophy of the skin and, in some patients, to the limitation of upper and lower limb joint mobility.

Chronic, difficult-to-treat ulcerations of atrophic skin may develop after minor trauma. Malignant degeneration has rarely been observed; one should not consider ACA to be a precancerous disorder.
The general status of patients with ACA remains good, though they may experience neurologic and/or rheumatologic signs and symptoms.
Race: ACA is not limited to any one nationality or race. It is much more frequent in whites than in other races, probably because of a far higher exposure to ticks transmitting B afzelii.

Sex: More than two thirds of patients with ACA are women. Among the authors' 19 patients, only 5 were men (Flisiak, 1999).

Age: The disease can occur in any age group, but it is most frequent in adults, usually in their 40s or 50s.

The youngest of the authors' patients was 26 years; the oldest was 73 years (Flisiak, 1999).
The mean age of the female group was 54.3 ± 12.8 years; the mean age of the male group was 46.2 ± 6.5 years.
ACA is rare in adolescents; however, it has been observed in children. A case in a 15-year-old girl was reported by Zalaudek et al in 2005.

History: Because of its late onset, patients with ACA rarely remember a tick bite. Instead, they recall having been in the woods or grassy areas a few months or years previously, especially in a geographically endemic region. A history of EM is recalled by about 20% of patients. ACA can develop directly from EM or after 6-36 months, often involving the same region of the body. Sometimes, the disease may be preceded by a latent phase (lasting up to several years) or by other manifestations of LB; the latter can also develop simultaneously.

The patient notices localized cutaneous swelling on the distal extremity or on only one of the digits and sometimes discovers that one foot is larger than the other when buying shoes. ACA is most often unilateral, although bilateral ACA is also common.
Progressive allodynia, the exaggerated reaction to pain, is a characteristic symptom and, thus, may be a clue to the diagnosis of ACA.
Patients commonly complain of spontaneous acral pain and paresthesia or dysesthesia or cognitive dysfunction.
ACA starts with an inflammatory phase, characterized by few to several soft, erythematous, slowly enlarging cutaneous swellings or flat infiltrations of various sizes or with diffuse bluish red discoloration and edema of the skin.
ACA usually appears on the distal part of at least one extremity, predominantly on the extensor surfaces on the bony prominences.
Common sites are the foot, the lower leg or the hand, the forearm, and the olecranon area; however, they uncommonly appear proximally on the upper arm and the shoulder or the thigh and the buttock.
Sometimes, the erythema is slight and swelling may dominate, or the signs are very subtle and may be overlooked
by the patient or the physician.

Lymphadenopathy may be noticed

Only one part of an extremity may be affected for many months or years. With time, the skin lesions may extend on one extremity or appear on additional ones and also involve other parts of the body.

Fibrotic nodules (often multiple, localized linearly in the vicinity of joints) are typical. They can precede ACA or develop simultaneously. The most common sites of these nodules are the elbows and the knees.

ACA does not heal spontaneously; gradual conversion into its atrophic phase may occur during many years of infection.
The skin becomes thin, atrophic, wrinkled, dry, and translucent.

The hair is lost; the number of sebaceous and sweat glands are decreased.

Even minor trauma may produce large, slow-to-heal ulcerations of the affected skin.
About 5-10% of patients with ACA develop sclerodermalike plaques. Anetodermalike skin lesions can be seen
concomitant with ACA.

ACA is accompanied often by peripheral neuropathy, musculoskeletal pains, and joint damage underneath the cutaneous plaques. Involvement of the small joints of the hands and the feet by the fibrotic reaction is often seen

Physical: The clinical recognition of ACA may be difficult, even in typical cases. A detailed history, including epidemiologic data, is helpful. Physicians should confirm the clinical diagnosis by histopathologic examination and serologic test results.

The early, inflammatory phase of ACA is marked by soft, painless, poorly demarcated, bluish reddish plaques tending to coalescence or by diffuse erythema and edema localized on the distal extremities that spread proximally.
In the authors' experience, not only the distal extremities but also the proximal parts, the trunk, and the face may be involved in the early stage (see Image 1).
Skin changes are often associated with regional or generalized lymphadenopathy.
The later, atrophic phase of ACA is more characteristic clinically. The affected skin has a dark red or brownish red discoloration; focal hyperpigmentation; telangiectasias; and a thin, wrinkled, cigarette paper–like, translucent appearance.
Because of the loss of subcutaneous fat, the skin vessels become prominent.
Atrophy of the epidermis and lack of hairs, sebaceous glands, and often sweat glands make the skin poorly protected and vulnerable.
Large ulcerations can be observed, and malignant lesions may also occur.
The atrophic poikilodermic changes are often bilateral and most noticeable over the knees, the elbows, and the dorsal surfaces of the hands and the feet. They may also involve the trunk (particularly the chest) and the face.
Sclerodermalike changes may appear in patients with ACA in both the inflammatory phase and the atrophic phase.
These changes are usually limited to the legs and the feet, but they occasionally occur on the trunk.
The lesions, similar to morphea and lichen sclerosus and atrophicus, may appear in regions where no ACA is present.
Single or multiple fibrotic nodules or bands may be seen on the extensor surfaces of the elbows and the knees or adjacent to other joints. They are generally firm; bluish-red, yellowish, or skin-colored; and 0.5 to 2-3 cm in diameter.

ACA has been described in association with localized amyloidosis, eczema, psoriasis, lupus erythematosus, leprosy, and Hodgkin disease. These associations may be coincidental. One of the authors' patients with histologically and serologically confirmed ACA was a 68-year-old woman first seen with prominent livedo racemosa on the leg where typical ACA inflammatory phase patches developed (Flisiak, 1999). Others also observed the same phenomenon, so perhaps this may be more than a chance linkage.

Detailed clinical and neurophysiologic examinations in patients with ACA-associated polyneuropathy often show a sensory polyneuropathy.
Neuropathy symptoms, most often pain and/or paresthesia, are evident in one half of patients with ACA.
One of the authors' patients had paresis of the brachial plexus (Flisiak, 1999).
Marked abnormality of the vibratory threshold is a common finding.
Patients with localized or asymmetric neuropathy seem to have changes more often found in the extremities with, rather than without, visible ACA lesions.
Abnormalities in cerebrospinal fluid seldom have been found in patients with ACA.
ACA can produce deformities of the fingers and the toes if it is not treated promptly. Persistent reducible deformities of the fingers may be consistent with Jaccoud arthropathy.
Causes: Lack of adequate or appropriate treatment of early LB facilitates ACA development.

Further Inpatient Care:

Patients with ACA without concurrent extracutaneous disease do not require hospitalization.
Consider a possible concurrent infection.
Co-infections include babesiosis, ehrlichiosis, and tick-borne encephalitis.
About 10% of patients with Lyme disease in southern New England are co-infected with babesiosis, and about the same percentage in parts of the midwestern United States have human granulocytic ehrlichiosis.
Babesiosis can cause a persistent infection and coexist with ACA, unlike ehrlichiosis, which is usually a short-lived infection

Further Outpatient Care:

Assure patients in the early phase of ACA that the resolution of symptoms may occur gradually during several weeks or months after treatment.
Inform patients treated in the atrophic phase that the disease progression can be stopped, but the symptoms may be only partially reversible.
Follow-up care should be performed initially every 3-6 months and later once a year.
Physical examination for signs and symptoms of cutaneous and extracutaneous manifestations of LB is important.
Quantitative serologic tests show a lack of changes in IgG antibody titer or show it declining only to a certain extent in most patients with ACA after antibiotic therapy.

Despite the persistence of IgG antibody response in late LB (serologic scar) similar to that observed in syphilis cases, the authors do serologic follow-up testing according to the recommendation for late syphilis. A sudden increase in antibody titer can point to the activation of infection and precede a clinical recurrence of the disease
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Re: Acrodermatitis chronica atrophicans

Post by Yvonne » Sun 20 Jun 2010 16:01

Cutis. 2010 May;85(5):247-52.

Acrodermatitis chronica atrophicans: a case report and review of the literature.

Smetanick MT, Zellis SL, Ermolovich T.

Department of Dermatology, Philadelphia College of Osteopathic Medicine/Frankford Hospital, Pennsylvania, USA.

Acrodermatitis chronica atrophicans (ACA) is a rare tertiary manifestation of Lyme borreliosis, manifesting as inflammatory and atrophic lesions on acral skin. Although ACA rarely has been reported in the United States, it may be seen in approximately 10% of European cases of Lyme borreliosis, most commonly associated with the genospecies Borrelia afzelii. We report a presumptive case of ACA involving an American woman from Pennsylvania with convincing clinical, histopathologic, and serologic findings. We also provide an overview of the history, epidemiology, pathogenesis, clinical and histopathologic presentation, and treatment of ACA.

PMID: 20540415
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Re: Acrodermatitis chronica atrophicans

Post by Dr Googlittle » Tue 22 Jun 2010 7:56

The media files (figure 10 & 11) in the eMedline article about ACA ( are notheworthy, since Some people get diagnoses like Acne Rosasea instead of Borrelia. Facial ACA in inflammatory phase may cause quite painful blisters.

However, facial ACA may have alternate presentations like in the paper "Skin-coloured facial oedema as an initial manifestation of acrodermatitis chronica atrophicans"
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Re: Acrodermatitis chronica atrophicans

Post by Yvonne » Tue 22 Jun 2010 8:53

J Invest Dermatol. 1998 Mar;110(3):211-4. Links

Identification of three species of Borrelia burgdorferi sensu lato (B. burgdorferi sensu stricto, B. garinii, and B. afzelii) among isolates from acrodermatitis chronica atrophicans lesions.

Picken RN, Strle F, Picken MM, Ruzic-Sabljic E, Maraspin V, Lotric-Furlan S, Cimperman J.
Research Service, Hines Veterans' Administration Hospital, Maywood, Illinois, USA.

In Europe, at least three species of Borrelia are known to be causative agents of Lyme borreliosis: B. burgdorferi sensu stricto, B. garinii, and B. afzelii. Observable differences in the molecular characteristics of the three species have led to speculation that they may also differ in their pathogenic potential and/or tissue tropisms. Several studies have found an association between the chronic skin manifestation of Lyme borreliosis, acrodermatitis chronica atrophicans, and infection by B. afzelii. We sought to find further evidence for such a correlation by studying the genetic profiles of 22 strains of B. burgdorferi sensu lato derived from 21 patients who presented to the University Medical Center, Ljubljana, Slovenia between 1992 and 1995. Strains were isolated in culture from skin biopsies of acrodermatitis chronica atrophicans lesions; in the case of one patient two separate acrodermatitis chronica atrophicans lesions were cultured. All 21 patients had clinically typical lesions with "classic" histopathology and high IgG antibody titers to B. burgdorferi sensu lato. Strains were characterized and typed by 16S ribosomal RNA-specific polymerase chain reaction and determination of their large restriction fragment patterns using pulsed-field gel electrophoresis of MluI-digested genomic DNA. Of the 22 isolates studied, 17 possessed the highly conserved MLa1 pattern characteristic of B. afzelii. The remaining five isolates possessed large restriction fragment patterns that were typical of B. garinii (MLg2, four isolates from three patients) and B. burgdorferi sensu stricto (MLb2, one isolate). The results of 16S ribosomal RNA-specific polymerase chain reaction were concordant with these species designations. These data show that B. afzelii is the predominant, but not the exclusive, etiologic agent of acrodermatitis chronica atrophicans.

PMID: 9506437
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Re: Acrodermatitis chronica atrophicans

Post by Yvonne » Tue 22 Jun 2010 8:55 ... tNr=224164

Metastatic Squamous Cell Carcinoma of the Ankle in Long-Standing Untreated Acrodermatitis Chronica Atrophicans
Case Report

Metastatic Squamous Cell Carcinoma of the Ankle in Long-Standing Untreated Acrodermatitis Chronica Atrophicans

M. Leverkus, A.M. Finner, A. Pokrywka, I. Franke, H. Gollnick

Department of Dermatology and Venereology, Otto von Guericke University, Magdeburg, Germany

Address of Corresponding Author

Dermatology 2008;217:215-218 (DOI: 10.1159/000142946)


Acrodermatitis chronica atrophicans (ACA) represents the persistent late stage of borreliosis in which Borrelia species may survive for decades. Occasionally, B-cell lymphoma may develop in these patients, and additional neoplastic complications such as basal cell carcinoma or squamous cell carcinoma (SCC) have been reported once each over the past 60 years. Here we describe, to the best of our knowledge, the first case of metastatic SCC in a European patient with long-standing ACA caused by Borrelia burgdorferi sensu stricto. Our case highlights a potential pathophysiological connection of untreated Borrelia infection with the initiation or progression of SCC and should alert dermatologists to this rare complication
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Re: Acrodermatitis chronica atrophicans

Post by Yvonne » Tue 22 Jun 2010 8:56

Two Unusual Cases of Diffuse Acrodermatitis Chronica Atrophicans Seronegative for Lyme Borreliosis
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Re: Acrodermatitis chronica atrophicans

Post by Yvonne » Tue 22 Jun 2010 8:57

Rev Rhum Engl Ed. 1998 Oct;65(10):567-70. Links

Rheumatic manifestations related to acrodermatitis chronica atrophicans. A review of four cases.

Gerster JC, Peter O.
Rheumatology and Rehabilitation Center, CHUV, Lausanne, Switzerland.

BACKGROUND: Acrodermatitis chronica atrophicans is a delayed manifestation of Lyme disease caused by a Borrelia burgdorferi subspecies, B. afzelii. Although rheumatic manifestations are rare, they can result in deformities of the fingers and toes if they are not treated promptly. METHODS: We report four cases of acrodermatitis chronica atrophicans seen over a 15-year period. RESULTS: Two patients had a noninflammatory unilateral knee effusion and one had swelling of the dorsum of one hand. Antimicrobial therapy was followed by a full recovery in the three patients who received an early diagnosis. The remaining patient, a 63-year-old woman, had swelling and dysesthesia in the fingers of both hands. She developed finger deformities over a period of two years. Although the swelling resolved under antimicrobial therapy, she had persistent reducible deformities of the fingers consistent with Jaccoud's arthropathy. CONCLUSION: The diagnosis of acrodermatitis chronica atrophicans rests on a history of a tick bite, a suggestive skin biopsy histology and a positive Western blot for B. afzelii. A positive response to antimicrobial therapy is also required. Acrodermatitis chronica atrophicans, a common condition in central and northern Europe, can cause joint manifestations and persistent finger deformities in the absence of early treatment.

PMID: 9809360
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Re: Acrodermatitis chronica atrophicans

Post by Yvonne » Tue 22 Jun 2010 8:58

J Med. 1999;30(3-4):267-78. Links

Clinical features and specific immunological response to Borrelia afzelii in patients with acrodermatitis chronica atrophicans.

Flisiak I, Schwartz RA, Chodynicka B.
Department of Dermatology and Venereology, Medical Academy of Bialystok, Sw. Rocha 3 15-879 Bialystok, Poland.

Acrodermatitis chronica atrophicans (ACA) occurs mostly in Europe. Borrelia afzelii is considered to be responsible for this manifestation of Lyme borreliosis. The aim of the study was to observe the clinical features of the ACA and evaluate the specific immunological response to Borrelia afzelii. Nine patients from an endemic Lyme borreliosis region in northeastern Poland were studied. The serum samples were tested routinely with IFA and EIA and, following testing, with immunoblots using Borrelia afzelii antigens. ACA was located mainly on the skin of the arms, forearms, thighs and chest. The only extracutaneal manifestation of Lyme borreliosis was paresis of the brachial plexus observed in one patient. Analysis of the immunoblot-banding pattern revealed positive reactions in all patients against flagellar antigen (41 kDa). Interpretation of the immunoblots revealed positive IgG results in all cases and IgM in five of them. Concluding, ACA develops not only on the extremities, but also on the trunk. The immunoblot technique using Borrelia afzelii antigens is of value in the diagnosis of ACA.

PMID: 17312680
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Re: Acrodermatitis chronica atrophicans

Post by Yvonne » Tue 22 Jun 2010 9:00

ACA in the Netherlands
Ned Tijdschr Geneeskd. 1991 Jul 27;135(30):1358-63. Links

Chronic atrophic acrodermatitis; a deceptive form of Lyme borreliosis

[Article in Dutch]

Tazelaar DJ, Velders AJ, de Koning J, Hoogkamp-Korstanje JA.
Algemeen Ziekenhuis de Tjongerschans, afd. Dermatologie, Heerenveen.

Acrodermatitis chronica atrophicans (ACA) was diagnosed in 15 patients from the southern and eastern part of Friesland (the Netherlands). Twelve patients had one leg affected; three had more than one extremity involved. Frequent complaints were fatigue, paraesthesia, swelling and blue discoloration. The symptoms persisted for many years in most cases. The inflammatory stage was observed most frequently (13/15): violet-blue erythema, oedema, firm swelling and nodules. Atrophy (4/15) was observed once in the form of a scleroderma-like lesion. Neuropathy was found in five patients. Histological investigation showed infiltration with lymphocytes and plasma cells (13/15) and atrophy (2/15). Spirochaetes were demonstrated in biopsies of 13 patients. Specific antibodies against Borrelia burgdorferi were found in all patients. ACA appears to be not infrequent and must be distinguished from other inflammatory and vascular diseases, such as chronic venous insufficiency.

PMID: 1865945
Neth J Med. 1999 Jan;54(1):5-9. Links

Joint and bone involvement in Dutch patients with Lyme borreliosis presenting with acrodermatitis chronica atrophicans.

Houtman PM, Tazelaar DJ.
Department of Rheumatology, Tjongerschans Hospital Heerenveen, The Netherlands.

We report on the radiological abnormalities of bones and joints in Dutch patients suffering from Lyme borreliosis presenting with acrodermatitis chronica atrophicans (A.C.A.). In a highly endemic area of the Netherlands rheumatic complaints were mentioned by 26 out of 60 patients suffering from a late stage of Lyme disease. Radiological findings in our group of patients were subluxation of the toe joint and periostitis of the bones of the lower limb.

PMID: 10048289
J Cutan Pathol. 1995 Feb;22(1):23-32. Links

Acrodermatitis chronica atrophicans: a light and electron microscopic study.

de Koning J, Tazelaar DJ, Hoogkamp-Korstanje JA, Elema JD.
Department of Pathology, Public Health Laboratory, Leeuwarden, The Netherlands.

Degeneration of the elastica and collagen fibres in skin biopsies from patients with acrodermatitis chronica atrophicans was studied with light and electron microscopy. Elastic fibres were involved in the infiltrative stage while the elastin plexus was still present. In the atrophic phase, only fragments of elastic and oxytalan fibres were seen and the elaunin plexus was absent. Some collagen fibres were surrounded by osmiophilic material. In all biopsies, myelin sheaths were collapsed without axon structures. Spirochetes could be demonstrated in 69% of the biopsies and were most numerous in infiltrative and nodular lesions. The loss of elasticity of the skin in the atrophic phase may be caused by the destruction of both elastic and elastin fibres.

PMID: 7751475

Erythematous pigmentation of the arm for more than ten years

M.J. Agterof1*, E.J. ter Borg2
Departments of 1Internal Medicine and 2Rheumatology, St Antonius Hospital, Nieuwegein,
the Netherlands, *corresponding author: tel.: +31 (0)30-609 91 11, fax: +31 (0)3- 605 63 57,

A 43-year-old female visited the outpatient department
because of an erythematous pigmentation of the left arm
for more than ten years. The fading started on the forearm
and extended to the upper arm. She developed cutaneous
swelling and nodules on the elbow. She did not complain of
any joint pain. Physical examination revealed a red-purple
pigmentation on a thin atrophic skin ( figure 1) and four
firm nodules on the left elbow ( figure 2).


A biopsy of the skin showed a small epidermis and a
lymphohistiocytic infiltration of the dermis. Biopsy of
a nodule showed collagenous connective tissue with
histiocytic elements. Laboratory investigations showed a
positive test for Borrelia burgdorferi (IgG).
On the basis of the clinical, histopathological and
serological findings, the diagnosis acrodermatitis chronica
atrophicans (ACA) with juxta-articular fibrotic nodules was
established. ACA is a late stage of Lyme borreliosis. It is
usually distributed on the lower legs and feet. In 10 to 20%
of patients with ACA, localised increase of dermal collagen
leads to juxta-articular fibrotic nodules.1,2 As in most cases,
our patient did not remember a tick bite or erythema
chronicum migrans at the site of the ACA.
Treatment is important to prevent progression and the
development of extracutaneous complications such as
neuropathy, tendinitis and arthritis.3 Our patient was
treated with doxycycline 100 mg twice daily for one month.
Seven months later the noduli had disappeared ( figure 3)
and there was a clear decrease in the pigmentation
( figure 4).
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Re: Acrodermatitis chronica atrophicans

Post by Yvonne » Tue 22 Jun 2010 9:06

Acrodermatitis chronica atrophicans : Histopathologic Findings and clinical correlations in 111 cases : ... 07-213.pdf
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