Potassium iodide (KI) is a useful drug in the dermatologic armamentarium. It is successfully used for inflammatory dermatoses, most notably erythema nodosum, subacute nodular migratory panniculitis, nodular vasculitis, erythema multiforme, and Sweet's syndrome. KI is also successfully used for cutaneous and lymphocutaneous sporotrichosis. The precise mechanism by which KI acts is unknown. Although many minor side effects are common with this drug, major side effects can occur in pregnant patients and those with a history of kidney or thyroid disease. This article reviews the pharmacology, mechanism of action, indications, contraindications, and adverse effects of KI as a therapeutic agent. (J Am Acad Dermatol 2000;43:691-7.)

Potassium iodide in dermatology: a 19th century drug for the 21st century-uses, pharmacology, adverse effects, and contraindications.

The above authors have founded a clinical study group known as the GEPPI (Groupe d'Etudes de la Pathologie Pulmonaire Iatrogene. Address: Professor Ph. Camus, Service de Pneumologie, CHU, BP 1542, F-21034 Dijon, France; fax: 33 3 80 29 32 51; e-mail: pneumo.dijon@ planetb.fr). The purpose of this group is to provide information regarding individual cases, collect and update literature on drug-induced lung disease, publish updated lists of offending compounds, and formulate warnings when new side-effects of drugs are recognized. Thus, the present table may be subjected to update in the future in this Journal. The number of drugs which have been shown to damage the respiratory system in some instances continues to increase. The clinical pattern of involvement from drugs is diverse and difficult to memorize accurately. Table 1 is designed to provide the information currently available on such drugs in a readily accessible form. A good way of obtaining broad information on druginduced respiratory disease is to refer to general articles and reviews on the topic. Many such papers have been available in the literature in the recent years [1–37]. Another method is to scrutinize the literature regarding any given drug. We considered that the preparation of a table listing most drugs capable of injuring the respiratory system was appropriate. The present table includes: 1) generic drug name (no trade name is provided); 2) clinical pattern of involvement, according to the types described in the legend; 3) a rough estimate of frequency of the adverse effect from each compound (*: isolated case reports which await confirmation; **: about 10 cases available; ***: 20–100 cases available; ****: >100 cases reported); 4) relevant references. Obviously, not all references for a given compound have been mentioned, because the overall list would have been too long. For example, references regarding pulmonary adverse effects from bleomycin total 114, and 135 for nitrofurantoin. No attempt has been made to validate the case histories quoted here. Often, most if not all drugs from the same pharmacological category are likely to induce the same adverse effect in the lung. As an example, angiotensin-converting enzyme (ACE) inhibitors may induce cough [38], β-blockers may induce bronchospasm [35], nonsteroidal anti-inflammatory drugs may induce bronchospasm or eosinophilic pneumonia [39], and ergoline drugs may induce chronic pleural thickening or effusion [40]. A few compounds have been listed despite the fact that they were recalled or withdrawn from the market earlier (e.g. aminorex, hexamethonium, mecamylamine, practolol or tryptophan). There are several reasons for this: 1) disease from drugs such as I-tryptophan leave long-term sequelae and patients may still be seen with persistent illness from the drug; 2) the clinical picture (e.g. bronchiolitis obliterans organizing pneumonia (BOOP)) from classic drugs, such as hexamethonium or meca-mylamine, may be seen with newer drugs, such as penicillamine, gold or amiodarone; and 3) clinical pictures long thought to have vanished (e.g. pulmonary hypertension from the appetite suppresant, aminorex) have regained interest because similar newer compounds (e.g. fenfluramine) may induce the same adverse effect [41]. Contraceptive pills may induce varied changes in the pulmonary circulation [42–44], but the aetiological link is too weak to make it possible to blame one particular formulation or brand. The field of drug-induced pulmonary infections and cancer, as well as the complications of illicit drug use and abuse have been deliberately omitted. This list of drugs is available on a continuously updated Web page at: http://www.pneumotox.com/lungdrug. For further comments, see the editorial in this issue of the Journal. CURRENT UPDATE

https://erj.ersjournals.com/content/erj/10/2/265.full.pdf

Drugs that may injure the respiratory system

Erythema nodosum is the most common type of panniculitis; it may be due to a variety of underlying infectious or otherwise antigenic stimuli. The pathogenesis remains to be elucidated, but both neutrophilic inflammation and granulomatous inflammation are implicated. Beyond treating underlying triggers, therapeutic options consist mainly of nonsteroidal anti-inflammatory drugs, symptomatic care, potassium iodide, and colchicine. Erythema induratum (nodular vasculitis) is a related but distinctly different clinicopathologic reaction pattern of the subcutaneous fat. It is classically caused by an antigenic stimulus from Mycobacterium tuberculosis but may be associated with several other underlying disorders. After appropriate antimicrobial treatment in tuberculous cases, therapy for erythema induratum is similar to options for erythema nodosum.

Erythema nodosum and erythema induratum (nodular vasculitis): diagnosis and management

Summary

A 72-year-old woman with chronic renal failure requiring haemodialysis developed acute ioderma twice, after receiving iodide contrast dye for radiological procedures. Iododerma was localized to the face, scalp and elbows and was associated with papular purpura of the legs. Histopathology of the skin lesions showed acute necrortzing vasculitis. During the second skin eruption the patient developed acute respiratory distress, which was treated with corticosteroids. During the first eruption asymptomatic infiltrates were present on chest X-ray which disappeared 2 months later. At the present time iododerma seems more frequent in patients with renal failure. Iodides may also be responsible for pulmonary abnormalities, which are sometimes asymptomatic. All these features may be due to leucocytoclastic vasculitis following iodide ingestion.

Iododerma and acute respiratory distress with leucocytoclastic vasculitis following the intravenous injection of contrast medium.

Three patients with vegetating iododerma as a result of potassium iodide therapy are presented. The first patient had polyarteritis nodosa, the second had monoclonal gammopathy of undetermined significance, and the third had multiple myeloma. Vegetating iododerma probably represents an idiosyncratic response to iodides; patients with polyarteritis nodosa and paraproteinemias may be predisposed.

Peterson Gh

Papers

Pulmonary edema and iododerma induced by potassium iodide in the treatment of asthma.