Halogenoderma 

Updated: Mar 26, 2021
Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD 

Overview

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. Fluoride-contaminated groundwater runs the risk of cutaneous and visceral adverse effects, a particular concern in Pakistan.[1]  Exposure to iodine, including radiographic contrast media, wound irrigation with povidone–iodine solution, iodide supplement use, and amiodarone intake may produce iododerma.[2]

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.[3] An infant also developed it from a calcium bromide–containing syrup for colic.[4]  Potassium bromide has also been linked.[5] When cardiac catheterization is performed with iodinated contrast material, vegetating cutaneous nodules can occur.[6]

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.[7] Perhaps, in some cases, these mediators may account for the histopathologic changes of leukocytoclastic vasculitis that are sometimes evident.[8]

Etiology

In past years when iodine was used as an expectorant, sedative, anti-inflammatory, and antithyroid agent, iododermas were more common. Nowadays, the administration of iodide-containing radiopaque contrast medium[9, 10] for cholecystography[11] and urography is the most common cause, especially in patients in renal failure. Acute iododerma due to iodinated contrast media has been well described.[12] Iodine I 131 treatment for hyperthyroidism[13] has also been reported to induce iododerma of the ankles and feet in approximately 2% of the treated patients.[14] . Oral potassium iodide for hyperthyroidism may produce an acneiform eruption of the face.[15] It may rarely develop after topical use of iodine following topical povidone-iodine application.[16]  Iododerma may occur from iodinated multivitamins.[17]

Bromoderma develops after an individual consumes bromide-containing drugs.[18, 19] For example, potassium bromide is frequently used as an anticonvulsant drug in the treatment of epilepsy. Bromocriptine is a dopamine agonist used for pituitary adenomas.[20] It has also been used as a sedative. It may produce bromoderma in infants too.[21]

Fluoride gel preparations, applied topically to the teeth, are prophylactically used as effective cariostatic agents in patients receiving radiation therapy.

Patient Education

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

 

Presentation

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.[22]

Bromoderma is rare and due to ingestion, inhalation, or contact with products containing bromides.[23]

Physical Examination

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.[9] Vegetating iododerma has also been reported to be associated with pulmonary infiltrates.[24] Some patients have had swelling of salivary glands (iodide mumps).[2, 25] Localized pustulosis had been reported after povidone-iodine sitz baths.[26]

Bromoderma is characterized by multiple, vegetative, ulcerating, and pustular lesions with elevated papillomatous borders, especially on the legs.[5, 27] 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.

 

DDx

Diagnostic Considerations

Also consider the following:

Differential Diagnoses

 

Workup

Laboratory 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.[28] 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.[29] 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. Iododerma may be viewed as a rare neutrophilic dermatosis.[2]

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

 

Treatment

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.