TL;DR: The ulceration, pseudoepitheliomatous hyperplasia and abscess formation do support an iododerma‐like eruption of a 42‐year‐old male who developed multiple pinpoint pustules on both lower extremities.
Abstract: Iododerma is a rare skin eruption that is usually induced by the systemic use of iodide-containing radiographic contrast medium or treatment with oral potassium iodide therapy. Iododerma has also rarely been reported to occur following topical application of iodine. We herein report the case of a 42-year-old male who developed multiple pinpoint pustules on both lower extremities. Three days after the eruption began, the patient started applying topical 10% povidone-iodine solution to the lesions. During this treatment, the lesions enlarged into multiple 2-9-cm pus-filled bullae, limited to the treated areas. Lesional bacterial culture swab and Gram stain were negative. Blood cultures were also negative and the patient's white blood cell count was normal. A punch biopsy specimen revealed pseudoepitheliomatous hyperplasia and dermal-epidermal separation with epidermal necrosis and underlying abscess formation. A superficial and deep perivascular, interstitial and perifollicular infiltrate containing numerous neutrophils, with abscess formation and eosinophils was also seen. This histology was consistent with iododerma and the patient's lesions involuted following cessation of topical iodine use, leaving only post-inflammatory hyperpigmentation. In summary, our patient likely had a folliculitis that was then treated with topical povidone-iodine that led to iododerma. Although it remains possible that the reaction was an unusual contact hypersensitivity response, the ulceration, pseudoepitheliomatous hyperplasia and abscess formation do support an iododerma-like eruption.
TL;DR: A 60-year-old white woman developed lesions of the conjunctiva and skin consistent with iododerma and one of the skin lesions disclosed pseudoepitheliomatous hyperplasia associated with acute and chronic inflammation.
TL;DR: A very unusual case of iododerma is described, which has long been thought that the basis of these eruptions has been hypersensitivity, and the role of allergy in the pathogenesis of such reactions is established.
Abstract: ORALLY ingested potassium iodide solution is frequently used in asthma and chronic bronchitis as an expectorant. The administration of iodides not uncommonly results in a large variety of dermatologic abnormalities known collectively as iododerma. These may include lesions that are vesicular, pustular, hemorrhagic, or urticarial. It has long been thought that the basis of these eruptions has been hypersensitivity, but such a mechanism has been difficult to prove. Within the past few years, however, several attempts to establish the role of allergy in the pathogenesis of such reactions have been successful.1 2 3 This paper describes a very unusual case of iododerma . . .
TL;DR: A robust case of iododerma from exposure to iodinated contrast dye in the setting of renal insufficiency is presented, and no findings are pathognomonic for this condition.
Abstract: INTRODUCTION Iododerma is a rare eruption caused by the inadvertent accumulation of iodine. Published sources of iodine excess producing iododerma include oral and intravenous iodinated contrast dyes, potassium iodide, amiodarone, and topical wound care products such as povidone iodine and iodoform gauze or in expectorants. Iododerma is more common in patients with renal dysfunction because of the impaired renal clearance and accumulation of iodine. One study of patients with endstage renal disease who received iodinated contrast documented that the plasma half-life of the contrast was increased to 23 hours compared with 2 hours in those with normal kidney function. The pathophysiology of iododerma is currently unknown, but it is speculated to be the induction of a delayed hypersensitivity reaction via iodine acting as a hapten. Here we present a robust case of iododerma from exposure to iodinated contrast dye in the setting of renal insufficiency. No findings are pathognomonic for this condition; thus, meticulous clinical evaluation and investigation of exposure history are required to make the diagnosis.