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Rogerio N Kondo1, Antônio C Petrus2, Gonçalo R Silva2, Rodrigo A de Medeiros3, Mariana de Castro Faidiga4, Isadora Franco4, Naja Nabut4
1 From the Hospital Universitário, State University of Londrina, Londrina, Paraná, Brazil
2 Evangelical Hospital of Londrina, Londrina, Paraná, Brazil
3 Private Laboratory – Londrina, Londrina, Paraná, Brazil
4 Pontifical Catholic University of Londrina, Londrina, Paraná, Brazil
Correspondence Address:
Rogerio N Kondo
Hospital Universitário, State University of Londrina, Londrina, Paraná
Brazil
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/ijd.ijd_577_22
How to cite this article:Sir,
A 59-year-old male patient, with a recent diagnosis of a straight-sigmoid transitional tumour, underwent a contrast-enhanced computed tomography of the abdomen. The lesions evolved with umbilicated papules, plaques, vegetative nodules, vesicles, pustules, and haemorrhagic blisters on the face and trunk. There was a rapid evolution in the number and sizes of lesions, with a significant increase in papules with the formation of thick crusts on them and purulent secretion, including occlusion of the eyelids and obstruction of the nostrils, preventing nasal breathing [Figure 1]a and [Figure 1]b. He also presented haemorrhagic blisters on the forearms [Figure 1]c. Its glomerular filtration rate was around 37.7 ml/min.
Figure 1: (a) Papules and umbilicated plaques (5th day after iodine exposure) (b) Crusty and vegetative plaques (8th day after iodine exposure) (c) Haemorrhagic blistersHe underwent several debridement of the lesions, and biopsy of lesions of the face and temporal region. Several diagnostic hypotheses were raised by a large team of dermatologists from Centro de Estudos Dermatológico Roberto Schnitzler (CEDROS), among the main ones: Paraneoplastic syndrome (Muir–Torre syndrome), Lymphoma, Kaposi's disease, Erythema multiforme, Sweet's disease, Linear IgA (immunoglobulin A) dermatitis, Leprosy (Lucio's phenomenon). The histopathological examination showed basket-braided stratum corneum, acanthosis, ballooning, reticular degeneration, areas of epidermal necrosis, extravasation of red blood cells, significant fibrinoid degeneration of blood vessels, and perivascular and interstitial infiltrate consisting of lymphocytes, histiocytes, neutrophils, and few eosinophils, noting leukocytoclasia [Figure 2]a and [Figure 2]b. In the histological sections stained by PAS (Periodic Acid-Schiff), no pathogenic fungi were observed. In the sections stained by Fite-Faraco, there was no BAAR (bacilos álcool-ácido resistentes). There was also no herpetic cytopathic effect.
Figure 2: (a) (Panoramic) and (b) (in detail): Leukocytoclastic vasculitis: fibrinoid degeneration of blood vessels and nuclear debrisHistory of iodinated contrast use, acute renal failure, and histopathological findings of leukocytoclastic vasculitis led to the diagnosis of ID.
Iododerm (ID) may present as an acneiform eruption, but may have other forms of elementary lesions: papules or umbilicated plaques, vegetative plaques, nodules, vesicles, and haemorrhagic blisters.[1] There is no pathognomonic lesion for ID.
Lesions in umbilicated papules and erythematous plaques that appear suddenly can mimic other dermatoses such as cryptococcosis and Sweet's syndrome.[2],[3] In the present case, some papules in areas of sebaceous glands resembled sebaceous adenomas. As the patient had colon cancer, the hypothesis of Muir–Torre syndrome was raised.[4] However, with the appearance of other more exuberant lesions, led to the thought of other hypotheses.
Studies believe in the hypothesis of delayed hypersensitivity via iodine that would work as a hapten, triggering an inflammatory process, especially in areas with a greater number of sebaceous glands.[1] Renal failure would be another contributing factor, as the half-life of iodine is maintained for longer hours than in the population with preserved urinary clearance.[5]
Histopathological findings are nonspecific and include a polymorphonuclear infiltrate with few eosinophils and mast cells and the presence of follicular inflammatory infiltrate and leukocytoclastic vasculitis. In chronic lesions, pseudoepitheliomatous hyperplasia may occur.[5]
The diagnosis of ID is made by the clinical and anatomopathological association, considering that there are no diagnostic criteria or a pathognomonic feature.[5] Bromine and fluorine can also cause haloderm.[1]
Treatment consists of suspending the component with iodine, improvement in renal function, and administering a systemic corticosteroid.[1]
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
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