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At the age of 28 she started a recurrent spring symptomatology in chest and upper arms that was classified by the clinical context, normal autoimmune profile and the study of skin biopsy of PLE. Due to the lack of response to corticosteroids and photoprotection, treatment was started with chloroquine, which was removed by itching and general discomfort. In 2009, at the age of 34, a photobiological study confirmed the PLE after finding papular response to UVB and UVA. Because of the intensity of the PLE and during the spring and summer of that year she was treated with azathioprine, with good response. In the spring of 2010 there was no response to azathioprine and it was decided to restart antimalarials (hydroxychloroquine 200<span class="elsevierStyleHsp" style=""></span>mg/12<span class="elsevierStyleHsp" style=""></span>h). After 24<span class="elsevierStyleHsp" style=""></span>h, the patient reported malaise, irritability, diarrhea, dyspnea with minimal exertion, dry cough and blurred vision. On physical examination bibasilar dry crackles were observed, and chest X-ray showed a bilateral interstitial pattern predominantly in the bases, which was confirmed by chest CT. Arterial blood gas analysis performed with a fraction of inspired oxygen to 31% showed: 68<span class="elsevierStyleHsp" style=""></span>mmHg arterial oxygen pressure; 28<span class="elsevierStyleHsp" style=""></span>mmHg arterial carbon dioxide pressure; 29<span class="elsevierStyleHsp" style=""></span>mEq/l bicarbonate, and pH of 7.49. The basic analysis was within normal limits. Serology was negative for hepatitis A, B and C viruses, the Epstein–Barr virus, herpes simplex virus I and II, the HIV, cytomegalovirus, Mycoplasma pneumoniae, Coxiella burnetii, Brucella, toxoplasma and treponema, as well as antinuclear, anti-DNA, antineutrophil cytoplasmic antibodies, anti-Ro/SS-A, anti-La/SS-B, anti-Sm, anti-RNP, anti-Scl-70, anti Jo 1, anti-PL7, anti-PL12, anticentromere, anti-Ku and anti-PM/Scl antibodies. The following tumor markers: alpha-fetoprotein, CEA, Ca 19.9 and Ca-125 were normal. Bronchoscopy showed normal endobronchial tree, microbiological cultures were negative and cytology showed no malignant cells; in bronchoalveolar lavage it was reported 67% lymphocytes, with a predominance of CD4 (45%), and 18% neutrophils. The echocardiogram showed no heart disease. Suspecting DILD secondary to hydroxychloroquine, it was decided to discontinue treatment; and high flow oxygen therapy was introduced and methylprednisolone at 40<span class="elsevierStyleHsp" style=""></span>mg/8<span class="elsevierStyleHsp" style=""></span>h doses with a decreasing drug schedule, experiencing rapid clinical and blood gas improvement. A month later, an X-ray confirmed the decreased interstitial lung pattern and oral corticosteroids were withdrawn. After 3 years of follow-up, the patient was asymptomatic and without evidence of lung disease.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Hydroxychloroquine is an antimalarial 4-aminoquinoline,<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> which is absorbed orally, reaching peak plasma concentration at 4–8<span class="elsevierStyleHsp" style=""></span>h; however, stable concentrations are not reached until after 4–6 weeks of continuous treatment, and thereafter they exert their actual therapeutic effect.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">5</span></a> The mechanism of action of hydroxychloroquine is not well known, but may act through various routes, causing different effects such as: photoprotector, anti-inflammatory, antiproliferative, immunomodulatory, antihyperlipidemic and antiplatelet.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> Most frequent side effects<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">6</span></a> of antimalarial agents are gastrointestinal and dermatological (hair graying, alopecia, blue-gray mucocutaneous pigmentation, rashes), although the most feared and dangerous are ophthalmological. Therefore, regular eye examinations are recommended. Other less common side effects have been reported, including impaired liver function, hematologic effects, cardiomyopathy, neuromuscular and central nervous system function. No cases of pulmonary involvement have been reported.</p><p id="par0020" class="elsevierStylePara elsevierViewall">There is a number of drugs capable of casing respiratory system disorders, but a literature search conducted between 1995 and today, which followed two strategies (hydroxychloroquine OR chloroquine AND interstitial lung disease [MeSH terms] AND adverse effects [MeSH subheading]), has shown no previous study describing DILD during treatment with hydroxychloroquine. Nor the website showing the drugs and type of injury that can occur in the lung (<a id="intr0010" class="elsevierStyleInterRef" href="http://www.pneumotox.com/">www.pneumotox.com</a>) shows said side effect of the antimalarial agent. The adverse reaction was notified to the National Pharmacovigilance System. The drugs as a cause of DILD are 3% of all DILDs.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">7</span></a> Diagnosis is difficult and requires a high index of suspicion, based on the temporal relationship between exposure to suspected drug and the onset of symptoms and/or radiographic abnormalities. Applying the Naranjo causality algorithm, the adverse effect that appears should be regarded as probable (6 points), especially considering re-exposure to an antimalarial agent, which further supports the relationship. In our case, the patient clinical history, the clinical and radiologic improvement on drug withdrawal, exclusion of other causes of lung disease, such as infection, tumor infiltration or heart failure, and stability in the clinical follow-up confirm the etiologic role of hydroxychloroquine in DILD within a hypersensitivity symptomatology to the drug.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Català Pérez R, Azón Masoliver A, Hernández Flix S. Enfermedad pulmonar intersticial inducida por hidroxicloroquina. Med Clin (Barc). 2015;145:415–416.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:7 [ 0 => array:3 [ "identificador" => "bib0040" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Photodermatoses" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "H.W. Lim" 1 => "J.L. Hawk" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "LibroEditado" => array:5 [ "titulo" => "Dermatology" "paginaInicial" => "1333" "paginaFinal" => "1336" "edicion" => "2.<span class="elsevierStyleSup">a</span> ed." 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Foucher" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1159/000079633" "Revista" => array:6 [ "tituloSerie" => "Respiration" "fecha" => "2004" "volumen" => "71" "paginaInicial" => "301" "paginaFinal" => "326" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/15316202" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/23870206/0000014500000009/v2_201605020201/S2387020616001868/v2_201605020201/en/main.assets" "Apartado" => array:4 [ "identificador" => "43309" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/23870206/0000014500000009/v2_201605020201/S2387020616001868/v2_201605020201/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020616001868?idApp=UINPBA00004N" ]
