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Author: Lajos Kemeny, MD, PhD, Professor and Head, Department of Dermatology and Allergology, Albert Szent-Gyorgyi Medical Center, University of Szeged, Hungary

Coauthor(s): Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School

Editors: Neil Shear, MD, Professor and Chief of Dermatology, Professor of Medicine, Pediatrics and Pharmacology, University of Toronto Faculty of Medicine; Head of Dermatology, Sunnybrook Women's College Health Sciences Center and Women's College Hospital, Canada; David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic; Jeffrey J Miller, MD, Associate Professor, Department of Dermatology, Penn State University, Milton S Hershey Medical Center; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center

Author and Editor Disclosure

Synonyms and related keywords: bromoderma, iododerma, fluoroderma, exposure to halogen-containing drugs or substances, skin eruptions

Background

Halogenodermas are skin eruptions that result after exposure to halogen-containing drugs or substances. The terms iododerma, bromoderma, and fluoroderma are used to describe skin lesions that occur after an individual consumes iodide-, bromide-, or fluoride-containing preparations.

Bromoderma is a cutaneous reaction caused by the use of products containing bromide. The administration of a syrup that contains sodium bromide is one cause (Bel, 2001). When cardiac catheterization is performed with iodinated contrast material, vegetating cutaneous nodules can occur.

Pathophysiology

Halogenoderma may represent a delayed hypersensitivity allergic response. In some studies, the results of lymphocyte transformation tests with iodinated human serum albumin have been positive, suggesting that iodine may act as a hapten.

Iodides can increase the movement of polymorphonuclear leukocytes into the areas of inflammation. Inflammatory mediators released from neutrophils might be responsible for the hyperproliferative and vegetative aspects of the skin lesions. Perhaps, in some cases, these mediators may account for the histopathologic changes of leukocytoclastic vasculitis that are sometimes evident (Vaillant, 1990).



History

  • Papulonodular eruptions, having an acneiform appearance, may occur after the ingestion of certain bromide and iodide preparations. The eruptions are less common with fluoride ingestion.
  • Fluoride gel preparations for the prophylaxis of postirradiation dental caries may cause fluorodermas when they are applied to the teeth (Blasik, 1979).

Physical

Bromoderma tends to be evident as pustules or vegetating plaques; sometimes, plaques with a periphery of pustules appear. In bromoderma, the pustules usually appear on the lower extremities. In iododerma, the pustules are more likely to occur on the face, they appear less papillomatous, and they may become ulcerated.

  • Iododerma is characterized by vesicular, pustular, hemorrhagic, suppurative, and/or ulcerative lesions that occur on the areas of the skin with the highest concentration of sebaceous glands, such as the face; however, the mucous membranes, the extremities, and the trunk can also be affected. Vegetating iododerma has also been reported to be associated with pulmonary infiltrates (Pranteda, 2004).
  • Bromoderma is characterized by multiple, vegetative, ulcerating, and pustular lesions with elevated papillomatous borders, especially on the legs. Bromoderma can appear as a follicular eruption on any hair-bearing body surface and can also occur in the butterfly area of the face.
  • Fluoroderma that develops after the skin is exposed to fluoride-containing preparations resembles iododerma; the papulonodular lesions are numerous and scattered.

Causes

  • In past years when iodine was used as expectorant, sedative, anti-inflammatory, and antithyroid agents, iododermas were more common. Nowadays, the administration of iodide-containing radiopaque contrast medium for cholecystography and urography is the most common cause, especially in patients in renal failure. Iodine I 131 treatment for hyperthyroidism has also been reported to induce iododerma of the ankles and feet in approximately 2% of the treated patients.
  • Bromoderma develops after an individual consumes bromide-containing drugs. For example, potassium bromide is frequently used as an anticonvulsant drug in the treatment of epilepsy.
  • Fluoride gel preparations, applied topically to the teeth, are prophylactically used as effective cariostatic agents in patients receiving radiation therapy.



Rosacea

Other Problems to be Considered

Pemphigus vegetans
North American blastomycosis
Sweet syndrome
Tertiary syphilis



Lab Studies

  • Serum or urine bromide and iodide levels should be measured.
  • Serum immunoelectrophoresis should be performed. Monoclonal gammopathy has been reported in some patients with iododerma and bromoderma. Therefore, serum immunoelectrophoresis should be considered.

Histologic Findings

Cutaneous halogenoderma produces a suggestive pattern of epidermal and dermal changes. Papillomatosis may be observed, sometimes to the level of pseudoepitheliomatous hyperplasia or acanthosis. Often, intraepidermal abscesses form with neutrophils, eosinophils, and, at times, necrotic or even acantholytic keratinocytes within them (Rosenberg, 1972). These epidermal changes tend to be more pronounced in bromoderma than in iododerma, in which case the epidermis may be more likely to become eroded or ulcerated.

The epidermal and dermal alterations in fluoroderma tend to be milder than those of the other 2 eruptions.

In the dermis, a dense infiltrate of mainly neutrophils and some leukocytoclasia may be initially observed around areas of dermal necrosis. True vasculitis may be present. Eosinophils may also be evident; at times, these may be numerous. Later, the infiltrate becomes more chronic, with a predominance of histocytes that have abundant cytoplasm and large nuclei.



Medical Care

Usually, no specific treatment is required.

  • Halogenoderma resolves 4-6 weeks after the causative factor is eliminated.
  • Diuretics may be used to speed bromide ion clearance.
  • The skin lesions may be treated with corticosteroids.

Diet

Patients with iododermas should avoid iodine in their diet.



Patient Education

  • Patients with iododermas should be instructed to avoid iodine in their diet, medications, and future radiographic studies.



Medical/Legal Pitfalls

  • Failure to make the diagnosis is a pitfall. Halogenoderma is frequently misdiagnosed because of its rare occurrence today.
  • Failure to inform patients to avoid iodine in their diets or medications, including over-the-counter products, is a pitfall.



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Halogenoderma excerpt

Article Last Updated: Mar 22, 2006