Interstitial pneumonia with pulmonary parvovirus B19 infection

Li, Xueren; Chen, Xuefen; Zhang, Yuhua

doi:10.1016/j.medcli.2022.02.010

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(A) Diffuse ground-glass opacification (GGO) (arrows) and occasionally patchy consolidation (OP) (arrows) with a basilar predominance was seen on 19th August 2019. (B) Extensive OP and GGO (arrows) were shown after thoracoscopic lung biopsy. (C) The lesions (arrows) were significantly absorbed on 30th December 2019." ] ] ] "textoCompleto" => "Interstitial pneumonia (IP) is a heterogeneous disease characterized by fibrosis and inflammatory reaction of the parenchymal and interstitial lung tissue. It was believed that many viral infections can lead to pulmonary interstitial changes, including Epstein–Barr virus, Cytomegalovirus, Human herpesvirus-8, adenovirus, Hepatitis C, Transfusion-Transmitted virus, Human Immunodeficiency virus, Severe Acute Respiratory Syndrome, and Middle East Respiratory Syndrome.<a class="elsevierStyleCrossRef" href="#bib0005">1</a>Here, we reported a case of nonspecific interstitial pneumonia (NSIP) with pulmonary human parvovirus B19 (HPB19) infection. A thirty-five years old male patient was admitted in September 2019 with a history of cough, expectoration, and wheezing for one year. He had a history of ten years of smoking and exposure to metallic dust in the past. At the onset of the disease, he was diagnosed with pneumonia with respiratory failure and discharged with a better-improved condition with effective treatment. Six months before, he was diagnosed as IP and his condition improved regularly with anti-fibrosis, anti-inflammatory, and symptomatic treatment strategies. Because of the relapse of IP, he went to the hospital on 20th August 2019. His physical examination showed stable vital signs and auscultation detected Velcro in the lower of both lungs. Arterial blood gas analysis (inspired oxygen fraction, 21%) revealed a PH of 7.44, PaO2 of 71mmHg, and PaCO2 of 36mmHg. High-resolution computed tomography (HRCT) (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>A) showed diffuse ground-glass opacification, reticular opacities, and occasionally patchy consolidation with a basilar predominance on 19th August 2019. Forced expiratory volume in 1 second was 47.1%, forced vital capacity was 43.6%, and carbon monoxide diffusion capacity was 32% from pulmonary function tests. The bronchoalveolar lavage fluid (BALF) cell count showed 66.5% alveolar macrophages, 30.5% neutrophils, and 3% lymphocytes. The sequence of HPB19 infection was found in Next-generation sequencing (NGS) of BALF and Thoracoscopic lung biopsy (TLB). TLB showed NSIP with diffuse alveolar damage (DAD). Because lung lesions deteriorated on HRCT (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>B) on 4th September 2019 after TLB, he was transferred to intensive care units and treated with drugs and high-flow oxygen inhalation through the nose. HRCT showed that lung lesions in both sides were improved on 12th September 2019. He was discharged when the peripheral blood oxygen saturation increased to 96%. In the follow-up, the lesions in the lung on HRCT (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>C)were significantly absorbed on 30th December 2019.<elsevierMultimedia ident="fig0005"></elsevierMultimedia>The criterion of acute exacerbation of IP is in the light of the criteria of AE-IPF. The definition of AE-IPF was revised by Collard et al.,<a class="elsevierStyleCrossRef" href="#bib0010">2</a> which proclaimed trigger factors, such as infection and inhalation, could lead to acute exacerbation of diffuse lung injury. Infection often portends a more favorable prognosis after effective anti-infection. HPB19 might cause some diseases, including acute aplastic anemia, infectious erythema, arthritis, and purpura.<a class="elsevierStyleCrossRef" href="#bib0015">3</a> The capsid protein, a unique region of VP1 of HPB19 that extends outside the capsid of the virus, has a phospholipase A2 site and contains multiple antigenic determinants, which can stimulate the host to produce autoantibodies and induce and/or aggravate a variety of autoimmune diseases.<a class="elsevierStyleCrossRef" href="#bib0020">4</a> Since the first proposed by Arnold<a class="elsevierStyleCrossRef" href="#bib0015">3</a> in 1998, HPB19 associated interstitial lung disease had been reported. Cynthia et al.<a class="elsevierStyleCrossRef" href="#bib0025">5</a> studied nine IP patients with persistently high levels of serum antibodies of HPB19, three patients had the increase of epithelial factor, and infer that HPB19 was closely related to the pathogenesis and activity of the IP.In our case of NSIP with HPB19 infection, HPB19 DNA was detected by NGS both in BALF and lung biopsy. The pathological findings of surgical thoracoscopic lung biopsy showed fibrotic NSIP. We speculate that HPB19 might cause IP and the NSIP may be a common radiological and pathological pattern. Though the pathogenesis is not still clear, HPB19 may damage the lung tissue directly and stimulate the body to produce some autoantibodies to damage the lung. Therefore, we recommend that sample tests for B19 become a part of the routine work-up in the diagnosis and management of interstitial lung disease." 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(C) The lesions (arrows) were significantly absorbed on 30th December 2019." ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Association of COVID-19 and other viral infections with interstitial lung diseases, pulmonary fibrosis, and pulmonary hypertension: a narrative review" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "E. Atabati" 1 => "A. Dehghani-Samani" 2 => "S.G. 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Boeckler" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1111/j.1365-2230.2006.02087.x" "Revista" => array:6 [ "tituloSerie" => "Clin Exp Dermatol" "fecha" => "2006" "volumen" => "31" "paginaInicial" => "473" "paginaFinal" => "474" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16681615" "web" => "Medline" ] ] ] ] ] ] ] ] 4 => array:3 [ "identificador" => "bib0025" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "The role of microvascular injury in the evolution of idiopathic pulmonary fibrosis" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "C.M. Magro" 1 => "J. Allen" 2 => "A. Pope-Harman" 3 => "W.J. Waldman" 4 => "P. Moh" 5 => "S. 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