Acrodermatitis Chronica Atrophicans Medication

  • Author: Bozena Chodynicka, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: May 14, 2012
 

Medication Summary

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications. Various antibiotics are used to treat acrodermatitis chronica atrophicans (ACA).

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Antibiotics

Class Summary

Empiric antimicrobial therapy for ACA must be comprehensive and should cover all pathogens likely to be present in the context of this clinical setting.

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Amoxicillin (Moxatag)

 

Amoxicillin is bactericidal against Borrelia species. It is a semisynthetic penicillin of the aminopenicillin group that demonstrates a wide spectrum of bactericidal activity related to gram-positive and gram-negative bacteria. Its mechanism of action involves inhibition of

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Doxycycline (Vibramycin, Adoxa, Doryx, Monodox)

 

Doxycycline is a tetracycline antibiotic that inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. It is used for its antibacterial and anti-inflammatory effect and may be considered when there is concern about possible coexistent infection.

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Ceftriaxone (Rocephin)

 

Ceftriaxone is bactericidal against Borrelia species. It is a third-generation cephalosporin with broad-spectrum gram-negative activity. Ceftriaxone has lower efficacy against gram-positive organisms and higher efficacy against resistant organisms. It arrests bacterial growth by binding to 1 or more penicillin-binding proteins.

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Cefotaxime (Claforan)

 

Cefotaxime is a third-generation semisynthetic cephalosporin with broad-spectrum bactericidal activity against gram-negative bacteria and Staphylococcus and Streptococcus species. It is resistant to beta-lactamases. Its mechanism of action is related to inhibition of bacteria cell wall synthesis.

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Penicillin G (Pfizerpen)

 

Penicillin G is a beta-lactam antibiotic. Its mechanism of action is related to inhibition of bacterial cell wall synthesis in the growth phase as a result of penicillin and bacterial transpeptidase binding.

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Contributor Information and Disclosures
Author

Bozena Chodynicka, MD  Head, Professor, Department of Dermatology and Venereology, Medical University of Bialystok, Poland

Bozena Chodynicka, MD is a member of the following medical societies: Central Neuropsychiatric Association

Disclosure: Nothing to disclose.

Coauthor(s)

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Iwona Flisiak, MD  Assistant Professor, Department of Dermatology and Venereology,Medical University of Bialystok, Poland

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Peter Fritsch, MD Chair, Department of Dermatology and Venereology, University of Innsbruck, Austria

Peter Fritsch, MD is a member of the following medical societies: American Dermatological Association, International Society of Pediatric Dermatology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Lester F Libow, MD Dermatopathologist, South Texas Dermatopathology Laboratory

Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association

Disclosure: Nothing to disclose.

References

  1. Bhate C, Schwartz RA. Lyme disease: Part I. Advances and perspectives. J Am Acad Dermatol. Apr 2011;64(4):619-36; quiz 637-8. [Medline].

  2. Bhate C, Schwartz RA. Lyme disease: Part II. Management and prevention. J Am Acad Dermatol. Apr 2011;64(4):639-53; quiz 654, 653. [Medline].

  3. Buchwald A. Ein Fall von diffuser idiopathischer Haut-Atrophie. Vrtljschr Derm. 1883;10:553-6.

  4. Herxheimer K, Hartmann K. Ueber Acrodermatitis chronica atrophicans. Arch f Dermatol u Syph (Wien). 1902;61:57-76.

  5. Smetanick MT, Zellis SL, Ermolovich T. Acrodermatitis chronica atrophicans: a case report and review of the literature. Cutis. May 2010;85(5):247-52. [Medline].

  6. Aberer E. Country report - Austria. Report of WHO Workshop on Lyme Borreliosis Diagnosis and Surveillance, Warsaw. Warsaw, Poland: World Health Organization; 1995.

  7. Christova I, Komitova R. Clinical and epidemiological features of Lyme borreliosis in Bulgaria. Wien Klin Wochenschr. Jan 31 2004;116(1-2):42-6. [Medline].

  8. Flisiak I, Schwartz RA, Chodynicka B. Clinical features and specific immunological response to Borrelia afzelii in patients with acrodermatitis chronica atrophicans. J Med. 1999;30(3-4):267-78. [Medline].

  9. Zalaudek I, Leinweber B, Kerl H, Mullegger RR. Acrodermatitis chronica atrophicans in a 15-year-old girl misdiagnosed as venous insufficiency for 6 years. J Am Acad Dermatol. 2005;52:1091-4. [Medline].

  10. Andres C, Ziai M, Bruckbauer H, Ring J, Hofmann H. Acrodermatitis chronica atrophicans in two children. Int J Dermatol. Feb 2010;49(2):180-3. [Medline].

  11. Leverkus M, Finner AM, Pokrywka A, Franke I, Gollnick H. Metastatic squamous cell carcinoma of the ankle in long-standing untreated acrodermatitis chronica atrophicans. Dermatology. 2008;217(3):215-8. [Medline].

  12. Danz B, Kreft B, Radant K, Marsch WCh, Fiedler E. Skin-coloured facial oedema as an initial manifestation of acrodermatitis chronica atrophicans. J Eur Acad Dermatol Venereol. Jun 2008;22(6):751-3. [Medline].

  13. Mullegger RR, Glatz M. Skin manifestations of lyme borreliosis: diagnosis and management. Am J Clin Dermatol. 2008;9(6):355-68. [Medline].

  14. Maraspin V, Ogrinc K, Ružic-Sabljic E, Lotric-Furlan S, Strle F. Isolation of Borrelia burgdorferi sensu lato from blood of adult patients with borrelial lymphocytoma, Lyme neuroborreliosis, Lyme arthritis and acrodermatitis chronica atrophicans. Infection. Feb 2011;39(1):35-40. [Medline].

 
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The most common localization of the skin lesions in 12 patients with acrodermatitis chronica atrophicans (ACA). The number of ACA lesions in the particular body region is shown.
A 73-year-old female farmer with a cutaneous plaque on the sole of her right foot lasting for 6 months that, in the meantime, had extended onto the dorsum of her foot, her right leg, and the lower part of her right thigh. Infection of Borrelia burgdorferi was diagnosed with enzyme-linked immunosorbent assay, and acrodermatitis chronica atrophicans was confirmed histologically.
The external part of the right foot.
A 50-year-old male farmer was examined for cutaneous plaques on the dorsal side of his right hand lasting for 8 months that, in the meantime, had extended onto his right forearm and arm and had also developed on his right thigh. The patient complained of muscular weakness related to his right upper limb and periodic arthralgia. The neurologic examination demonstrated signs of right brachial plexus damage, confirmed by electromyography. Borrelia burgdorferi infection was diagnosed with enzyme-linked immunosorbent assay, indirect immunofluorescence assay (titer: 1:1,024), and Western blot. Histologic examination confirmed the diagnosis of acrodermatitis chronica atrophicans.
The typical inflammatory phase patches are seen on the right hand bone prominences.
A 68-year-old woman with a history of untreated erythema migrans on her left thigh 2 years previously. Ten months later, the plaque extended over the skin of her left buttock and became bluish with signs of livedo racemosa. Her forearms and breast were also involved. Borrelia burgdorferi infection was diagnosed with indirect immunofluorescence assay (1:4,096) and Western blot. Acrodermatitis chronica atrophicans was confirmed histologically. Because of intrathecal production of specific antibodies, diagnosis of asymptomatic neuroborreliosis was established.
After 30 days of treatment with ceftriaxone.
The livedo racemosa and acrodermatitis chronica atrophicans lesions on the left thigh and buttock before treatment.
The same patient after treatment.
A 69-year-old woman. The initial lesion developed on the dorsal side of her left hand 2 years previously and extended onto her left forearm and arm. A new erythematous lesion developed 2 months before on her right cheek beside the rosacea signs. Acrodermatitis chronica atrophicans was confirmed in the biopsy specimen taken from the skin of the forearm, and Borrelia burgdorferi infection was diagnosed with indirect immunofluorescence assay (1:2,048). The atrophic phase of acrodermatitis chronica atrophicans is visible on the hand, and the inflammatory phase is visible on the cheek.
The inflammatory phase of acrodermatitis chronica atrophicans can be seen with rosacea lesions on the cheek, the forehead, and the nose.
Fibrotic nodules on the left elbow.
A 48-year-old woman with a history of frequent tick bites and an initial inflammatory skin lesion on the left medial part of her ankle 2 years previously. The lesion extended onto the left leg and involved the knee. Fibrotic nodules developed in the medial part of the ankle and the knee. Moreover, she complained of balance disturbances and vertigo. Neurologic examination revealed the asymmetry of profound reflexes, bilateral lack of plantar reflexes with a tendency to the extensor plantar response (Babinski sign), ataxia, profound dysesthesia, and muscular atrophy of the left calf. Acrodermatitis chronica atrophicans was confirmed by histologic examination, and Borrelia burgdorferi infection was confirmed by a high specific antibody titer with indirect immunofluorescence assay (1:8,192); cerebrospinal fluid was not tested.
A 26-year-old female nurse recalled the onset of the disease on her right arm 4 years before. After 6 months, the plaques extended onto the right forearm and hand. The left arm and forearm were also involved 3 years previously. Induration of the skin of the right forearm was noted. Borrelia burgdorferi infection was diagnosed with indirect immunofluorescence assay (1:2,048) and confirmed by positive Western blot for both immunoglobulin M and immunoglobulin G antibodies.
Atrophic phase of acrodermatitis chronica atrophicans of the right upper limb with induration of the forearm.
A 68-year-old female jogger frequently exposed to ticks. Cutaneous plaques developed 4 years previously on her right lower limb and the right part of her trunk, including her breast and right upper limb. Typical extensive cigarette paper–like plaques, bluish or brownish red in color were evident. Fibrous nodules were found on her right elbow. Borrelia burgdorferi infection was confirmed with indirect immunofluorescence assay (1:1,024) and Western blot. Acrodermatitis chronica atrophicans was finally diagnosed by using histologic examinations.
A widespread acrodermatitis chronica atrophicans atrophic plaque on the back.
The atrophic skin lesions and fibrotic nodules of the right upper limb.
Biopsy specimen from the wrist of the patient shown in Image 4. The epidermis is slightly flattened. A zone of normal connective tissue can be seen below the epidermis. A patchy infiltrate consisting of lymphocytes and plasma cells is seen throughout the dermis. Telangiectasias are evident in the upper and deeper parts of the dermis.
A higher magnification. Telangiectatic vessels are surrounded by a cellular infiltrate in the upper dermis.
A higher magnification of the same biopsy specimen. Note the patchy cell infiltrate around the large vessels in the deep dermis.
 
 
 
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