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TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE最新文献

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EVALI Masquerading as Cannabinoid Hyperemesis Syndrome EVALI伪装成大麻素呕吐综合征
Pub Date : 2021-01-01 DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2142
J. Spoons, S. Treat, M. McNabney, J. Horner, N. Smith
In mid-2019, cases of acute eosinophilic pneumonia caused by the vaporization and inhalation of tetrahydrocannabinol (THC) containing products began to rapidly appear. E-cigarette or vaping product useassociated lung injury, or EVALI as it became known, was eventually linked to substances such as vitamin E used in illicit manufacture of THC containing vaping products. A previously healthy 20 year old male presented with complaints of worsening nausea, vomiting, abdominal pain, fevers, and dry cough of several months. Symptoms began 3 months prior with periods of intractable nausea and vomiting that lasted from 24 hours to 1 week without complete resolution. An extensive outpatient workup was completed by gastroenterology without definitive diagnosis, including endoscopy. The patient had attempted therapy with ondansetron, phenergan, metoclopromide, cannabidiol (CBD) gummy candies, vaporized CBD and THC without success. Physical exam was remarkable for nystagmus on far lateral gaze, prompting concern for a central cause of his persistent nausea and vomiting. Chest x-ray was unremarkable, and laboratory examination was remarkable for mild leukocytosis. Neurology was consulted and MRI brain was unremarkable. Seventy-two hours after admission, with supportive care, his nausea and vomiting had improved, but he developed new fever of 101.9°F. CT angiogram of the thorax revealed diffuse ground glass opacities with an upper lobe predominance and opacification in the lower lobes without pulmonary embolism. COVID-19 nasal swab was obtained, and treatment for community acquired pneumonia was started empirically. CRP was elevated to 34.9 mg/dl, urine L. pneumophila, S. pneumoniae, respiratory virus PCR panel, H. capsulatum, Aspergillus antigen, Fungitell assay, and COVID-19 PCR testing, with subsequent repeat, were negative. On the 4th day of admission, he became short of breath with increasingly worse cough leading to desaturation in the low 80%'s requiring 6 L oxygen via nasal cannula. Pulmonology was consulted, and given his THC exposure, negative laboratory testing and CT thorax appearance, a diagnosis of EVALI was made. Prednisone (0.5 mg/kg) was started, and over the next 72 hours, the patient's cough improved with continued supportive care. He was discharged to complete a 15 day prednisone taper. The rapid rise in cases lead to nationwide reporting of manufacturing processes and consumer awareness, which has subsequently lead to a decrease in the number of reported EVALI cases. Our patient's presentation with prolonged gastrointestinal distress left an initially broad differential and reminds us to discuss vaping of THC-containing products with all patients with vaping exposure.
2019年年中,因汽化和吸入含四氢大麻酚(THC)产品引起的急性嗜酸性肺炎病例开始迅速出现。电子烟或电子烟产品相关的肺损伤(EVALI)最终与非法生产含有四氢大麻酚的电子烟产品中使用的维生素E等物质有关。既往健康的20岁男性,主诉恶心、呕吐、腹痛、发烧和干咳加重数月。症状开始于3个月前,难治性恶心和呕吐持续24小时至1周,但未完全缓解。广泛的门诊检查由胃肠病学完成,没有明确的诊断,包括内窥镜检查。患者曾尝试用昂丹司琼、非那根、甲氧氯丙胺、大麻二酚(CBD)软糖、蒸发CBD和四氢大麻酚进行治疗,但均未成功。体格检查有明显的远侧视眼球震颤,引起了对他持续恶心和呕吐的中心原因的关注。胸部x线检查无明显异常,实验室检查有轻度白细胞增多。求诊神经学,MRI脑无明显异常。入院72小时后,在支持性护理下,他的恶心和呕吐有所改善,但他出现了101.9°F的新发烧。胸部CT血管造影示弥漫性磨玻璃影,以上肺叶为主,下肺叶混浊,无肺栓塞。获得COVID-19鼻拭子,开始经验性社区获得性肺炎治疗。CRP升高至34.9 mg/dl,尿嗜肺乳杆菌、肺炎链球菌、呼吸道病毒PCR、荚膜乳杆菌、曲霉抗原、真菌细胞试验和COVID-19 PCR检测均为阴性,随后重复。入院第4天,患者出现呼吸急促,咳嗽加重,导致低80%血饱和度下降,需通过鼻插管给氧6l。咨询肺科,结合患者四氢大麻酚暴露、实验室检测阴性及胸部CT表现,诊断为EVALI。开始使用强的松(0.5 mg/kg),在接下来的72小时内,患者的咳嗽在持续的支持治疗下得到改善。他出院完成15天的强的松逐渐减少治疗。病例的迅速增加导致全国范围内报告生产过程和消费者意识,这随后导致报告的EVALI病例数量减少。我们的患者表现为长期的胃肠不适,这在最初留下了广泛的差异,并提醒我们与所有有电子烟接触的患者讨论含四氢大麻酚的电子烟产品。
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引用次数: 1
A Case of Bilateral Radiation Pneumonitis and Post Radiation Pulmonary Fibrosis One Month After Unilateral Lung Radiation 单侧肺放射1个月后双侧放射性肺炎及放射后肺纤维化1例
Pub Date : 2021-01-01 DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2151
X. Ying, R. Wozniak, H. Swerdloff, R. Kalil, T. Wong
Introduction: Radiation induced pulmonary fibrosis typically develops between 6-12 months after completion of radiation therapy (RT), and typically affects only the irradiated lung. We present a rare case of bilateral radiation induced pulmonary fibrosis occurring only one month after completion of unilateral RT. Case Presentation: A 75-year-old male with pleural mesothelioma treated with five cycles of neoadjuvant carboplatin and pemetrexed followed by thoracotomy, pleurectomy, decortication and six weeks of RT (28 fractions, total 50.4 Grays) (Figure 1A) presented 33 days after completing RT with five days of dyspnea and dry cough. Vitals were notable for oxygen saturation of 86% on room air with improvement to 97% on 4 L/min via nasal cannula. Review of his pre-RT computed tomography (CT) demonstrated left-sided bronchiectasis and basilar ground glass attenuation representing post-inflammatory changes (Figure 1B). Repeat CT 27 days after completion of RT showed new bilateral diffuse ground-glass opacities with left upper and lower lobe fibrosis (Figure 1C);CT upon current presentation revealed increased ground-glass opacities and bilateral fibrosis (Figure 1D). Blood cultures, SARSCoV-2 PCR, respiratory pathogen panel (including influenza A/B and respiratory syncytial virus), cryptococcal antigen, galactomannan and 1,3-beta-d-glucan were all unrevealing. Transthoracic echocardiogram revealed septal E/e' ratio 12.6 and estimated pulmonary artery systolic pressure 30 mmHg, and serum b-type natriuretic peptide level was 48 pg/ml. Detailed reconciliation confirmed he was not taking any new medications, including statins. Hypersensitivity pneumonitis panel was negative. His working diagnosis was radiation induced lung injury with features of both early pneumonitis and late fibrosis. Therapy with short-acting bronchodilators and systemic corticosteroids was initiated with significant clinical improvement;patient was discharged home on hospital day six off oxygen. Discussion: Radiation induced lung injury can generally be divided into acute and late phases. The former is commonly known as radiation pneumonitis and manifests as ground-glass opacities 4-12 weeks after completion of RT, and the latter presents as bronchiectasis and fibrosis 6-12 months later. Ours is a rare case of pneumonitis and fibrosis that developed within one month of completing RT. Additionally, this patient developed pneumonitis and fibrosis of his right lung, which did not receive any radiation;very few cases of pneumonitis on the nonirradiated lung have been reported. Immunologically mediated lymphocytic alveolitis has been proposed as a mechanism for contralateral spread of radiation fibrosis. Our patient showed significant clinical improvement with initiation of corticosteroids with the plan for a long, slow outpatient taper based on clinical response.
放射诱导的肺纤维化通常发生在放射治疗(RT)完成后6-12个月,通常只影响被照射的肺。我们报告了一例罕见的双侧放射引起的肺纤维化病例,仅在单侧放疗完成一个月后发生。病例描述:一位75岁男性胸膜间皮瘤患者接受了5个周期的新辅助卡铂和培美曲塞治疗,随后进行了开胸、胸膜切除术、去皮术和6周的放疗(28个部分,总计50.4灰色)(图1A),在完成放疗后33天出现了5天的呼吸困难和干咳。呼吸室内空气时血氧饱和度可达86%,经鼻插管4升/分钟后可达97%。CT检查显示左侧支气管扩张和基底部磨玻璃衰减代表炎症后的变化(图1B)。RT完成后27天重复CT显示新的双侧弥漫性磨玻璃影伴左上肺叶和下肺叶纤维化(图1C);目前表现的CT显示磨玻璃影增加,双侧纤维化(图1D)。血培养、SARSCoV-2 PCR、呼吸道病原体检测(包括流感A/B和呼吸道合胞病毒)、隐球菌抗原、半乳甘露聚糖和1,3- β -d-葡聚糖均未发现。经胸超声心动图显示肺动脉E/ E比12.6,肺动脉收缩压30 mmHg,血清b型利钠肽48 pg/ml。详细的核对证实他没有服用任何新的药物,包括他汀类药物。超敏性肺炎阴性。他的工作诊断是放射性肺损伤,具有早期肺炎和晚期纤维化的特征。开始使用短效支气管扩张剂和全身性皮质类固醇治疗,临床明显改善;患者在住院第6天出院回家。讨论:放射性肺损伤一般可分为急性期和晚期。前者通常被称为放射性肺炎,在放疗完成后4-12周表现为磨玻璃样混浊,后者在6-12个月后表现为支气管扩张和纤维化。我们的病例是一例罕见的在完成放疗后一个月内出现肺炎和纤维化的病例。此外,该患者在未接受任何放疗的情况下出现右肺肺炎和纤维化,未接受放疗的肺很少有肺炎的报道。免疫介导的淋巴细胞性肺泡炎被认为是放射性纤维化对侧扩散的一种机制。我们的病人在开始使用皮质类固醇后表现出显著的临床改善,并计划根据临床反应进行长期、缓慢的门诊减药。
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引用次数: 0
Multifocal Pneumonia During a Pandemic 大流行期间的多灶性肺炎
Pub Date : 2021-01-01 DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2117
L. Ramírez, A. Mahgoub, U. Naqvi, A. Thota, J. Meharg
Intro: In patients with advanced melanoma, immune checkpoint inhibitors (ICPIs) have demonstrated a substantial advantage when compared to cytotoxic chemotherapies. By augmenting the immune response with these medications, immune-related adverse effects can occur, and often include dermatological toxicity, hepatotoxicity, endocrinopathies, and much more rarely, pneumonitis. Case Presentation: An 80-year-old with past medical history of bronchial asthma, hypertension, 30 pack year smoking history discontinued over 2 decades ago, and metastatic melanoma (MM) on neoadjuvant nivolumab presented to our hospital in September of 2020 with 5 days of worsening shortness of breath. He denied any fever, cough, chest discomfort, palpitation, nausea, vomiting, epigastric/abdominal pain, leg pain, or palpitations. He had been diagnosed with stage IIIc MM in March of 2020 and underwent surgical resection of his left hallux and had completed 5 cycles of immunotherapy with Nivolumab. On admission, the patient had sinus tachycardia to 115, respiratory rate of 18 bpm, normotensive, oxygen saturation 80% on room air, improved to 94% on 4L nasal cannula. Laboratory studies were remarkable for acute kidney injury with Creatinine 1.7mg/dl (1.1 baseline), procalcitonin less than 0.05 ng/dl, elevated D-Dimer to 2.6mg/L, complete blood count, and comprehensive metabolic panel unremarkable. Viral serologies and sputum cultures resulted negative. Chest x-ray demonstrated extensive multifocal bilateral airspace. CTPA revealed severe diffuse bilateral airspace disease concerning for infectious, versus noninfectious pneumonia or a neoplastic process. He subsequently underwent bronchoscopy with BAL of RLL/LLL and RLL brush biopsy, which was negative for malignancy and infectious etiologies, including COVID-19. The patient was diagnosed with grade 3 nivolumab induced pneumonitis, and treated with high dose steroids, and empiric antibiotics. His condition improved, steroids were tapered, and he was discharged on day 13. Discussion: Pneumonitis is a rare, life-threatening complication in patients being treated with nivolumab. When severe symptoms are present and hospitalization and oxygen supplementation are indicated, treatment includes discontinuation of the immunotherapy agent, high dose steroids, prophylactic antibiotics, and additional immunosuppressive therapy if no response to During the midst of a global pandemic, findings of multifocal pneumonia are presumed to be SARS-CoV-2 until proven otherwise. Despite the burden many physicians have faced amid the COVID-19 pandemic, maintaining a broad differential until the diagnosis is made for accurate treatment.
在晚期黑色素瘤患者中,与细胞毒性化疗相比,免疫检查点抑制剂(icpi)已显示出实质性的优势。通过使用这些药物增强免疫反应,可能会发生与免疫相关的不良反应,通常包括皮肤毒性、肝毒性、内分泌病变,以及更罕见的肺炎。病例介绍:一名80岁的患者,既往有支气管哮喘、高血压病史,20多年前停止吸烟30年,并于2020年9月在新辅助纳沃单抗治疗下出现转移性黑色素瘤(MM),伴有5天呼吸急促加重。他否认有发热、咳嗽、胸部不适、心悸、恶心、呕吐、上腹痛、腿痛或心悸。他于2020年3月被诊断为IIIc期MM,接受了左拇切除术,并完成了5个周期的尼武单抗免疫治疗。入院时,患者窦性心动过速为115,呼吸频率为18次/分钟,血压正常,室内空气氧饱和度为80%,使用4L鼻插管后改善至94%。实验室研究表明,急性肾损伤的肌酐为1.7mg/dl(1.1基线),降钙素原低于0.05 ng/dl, d -二聚体升高至2.6mg/L,全血细胞计数和综合代谢组无显著差异。病毒血清学和痰培养结果为阴性。胸部x线显示广泛的双侧多灶空域。CTPA显示严重的弥漫性双侧空域疾病,与感染性肺炎或非感染性肺炎或肿瘤过程有关。随后,他接受了支气管镜检查,检查了RLL/LLL的BAL和RLL刷活检,结果显示恶性肿瘤和感染性病因(包括COVID-19)呈阴性。患者被诊断为3级纳武单抗引起的肺炎,并接受大剂量类固醇和经验性抗生素治疗。他的病情好转,类固醇逐渐减少,并于第13天出院。讨论:肺炎是接受纳武单抗治疗的患者中一种罕见的危及生命的并发症。当出现严重症状并需要住院治疗和补充氧气时,治疗包括停止免疫治疗剂、大剂量类固醇、预防性抗生素和如果对无反应的额外免疫抑制治疗。在全球大流行期间,多灶性肺炎的发现被推定为SARS-CoV-2,除非另有证明。尽管许多医生在COVID-19大流行期间面临着负担,但在做出诊断以进行准确治疗之前,仍要保持广泛的鉴别。
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引用次数: 0
Immunotherapy Induced Pneumonitis 免疫治疗引起的肺炎
Pub Date : 2021-01-01 DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2115
D. J. Shah, C. Cascio
INTRODUCTION: Pneumonitis is focal or diffuse inflammation of lung parenchyma. With recent advancements in oncology, immunotherapy is an emerging cause of pneumonitis. Atezolizumab is an immune checkpoint inhibitor (ICI) that targets PD-L1 to prevent the interaction with receptors PD-1 and B7-1, thus reversing T-cell suppression and can cause pneumonitis due to the inflammatory response. It has an incidence of up to 10%. Symptoms can include dyspnea (53%), cough (35%), fever (12%), and chest pain (7%). CASE: An 81-year-old male with unresectable hepatocellular carcinoma (HCC) on Atezolizumab-Bevacizumab, intra-lesional hematoma, and portal vein thrombosis presented with one day of dyspnea. In the ED, he was found to be hypoxic to 80% on room air. The examination was unremarkable except for bilateral crackles on auscultation. Laboratory tests including complete blood count, electrolytes, liver function tests, kidney function tests, and arterial blood gas were within normal limits. CT chest revealed bilateral multifocal airspace opacities. Due to the acute hypoxemic respiratory failure, he was transferred to the ICU for care. Blood cultures were sent. Antibiotic therapy with vancomycin, cefepime, and azithromycin was initiated for presumed community-acquired pneumonia. The patient continued to worsen clinically. All initial infectious workup was negative including blood cultures, tuberculosis and fungal workup, and respiratory viral pathogen PCR. COVID-19 and influenza PCR was negative thrice. Of note, the patient completed his second cycle of immunotherapy with Atezolizumab-Bevacizumab, four days prior to admission. He was started on methylprednisolone 2mg/kg/d on hospital day (HD) 5 for likely ICI-induced pneumonitis. Despite steroid therapy, no clinical improvement was noted. He was additionally given a single dose of infliximab 5mg/kg to which he improved clinically initially. However, he later grew Aspergillus in his bronchoalveolar lavage and passed away from multi-organ failure on HD 22. DISCUSSION: We describe a case of HCC with hematoma. Given the risk of bleeding with first-line therapy (Sorafenib), a combination of Atezolizumab-Bevacizumab was used instead. ICI-induced pneumonitis is a diagnosis of exclusion with no specific clinical picture or radiologic findings. Anti-VEGF antibodies like Bevacizumab are more likely to cause pulmonary hemorrhage than pneumonitis. ICI-induced pneumonitis is divided into 4 grades. This patient was categorized as Grade 3. The patient received infliximab as he did not respond to initial therapy consisting of empirical antibiotics and IV methylprednisolone. In patients on ICI, who present with respiratory symptoms, clinicians should have a high degree of suspicion for pneumonitis. Early diagnosis and treatment could potentially reduce mortality.
简介:肺炎是肺实质的局灶性或弥漫性炎症。随着肿瘤学的最新进展,免疫治疗是肺炎的一个新原因。Atezolizumab是一种免疫检查点抑制剂(ICI),靶向PD-L1以阻止与受体PD-1和B7-1的相互作用,从而逆转t细胞抑制,并可因炎症反应引起肺炎。它的发病率高达10%。症状包括呼吸困难(53%)、咳嗽(35%)、发烧(12%)和胸痛(7%)。病例:一名81岁男性患者接受阿特唑单抗-贝伐单抗治疗,患有不可切除的肝细胞癌(HCC),病变内血肿和门静脉血栓形成,表现为一天的呼吸困难。在急救室里,他被发现缺氧到室内空气的80%。除听诊双侧有裂纹外,检查无明显异常。实验室检查包括全血细胞计数、电解质、肝功能检查、肾功能检查和动脉血气检查均在正常范围内。胸部CT示双侧多灶性空域混浊。由于急性低氧性呼吸衰竭,他被转移到重症监护室治疗。送去了血液培养。对于假定的社区获得性肺炎,开始使用万古霉素、头孢吡肟和阿奇霉素进行抗生素治疗。患者临床情况继续恶化。所有最初的感染检查均为阴性,包括血液培养、结核和真菌检查以及呼吸道病毒病原体PCR。COVID-19和流感PCR 3次阴性。值得注意的是,患者在入院前4天完成了阿特唑单抗-贝伐单抗免疫治疗的第二个周期。他在住院日(HD) 5开始使用甲基强的松龙2mg/kg/d,可能是ici引起的肺炎。尽管类固醇治疗,没有临床改善。另外给予单剂量英夫利昔单抗5mg/kg,初步临床改善。然而,他后来在支气管肺泡灌洗液中生长曲霉,并于hd22因多器官衰竭而去世。讨论:我们报告一例肝细胞癌合并血肿。考虑到一线治疗(索拉非尼)的出血风险,使用Atezolizumab-Bevacizumab联合治疗。ici引起的肺炎是一种排除性诊断,没有特定的临床表现或放射学表现。抗vegf抗体如贝伐单抗比肺炎更容易引起肺出血。ci性肺炎分为4级。该患者被分类为3级。患者接受英夫利昔单抗治疗,因为他对由经验性抗生素和静脉注射甲基强的松龙组成的初始治疗没有反应。对于出现呼吸道症状的ICI患者,临床医生应高度怀疑是否患有肺炎。早期诊断和治疗有可能降低死亡率。
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引用次数: 0
A Case of Exogenous Lipoid Pneumonia in a Critically Ill Patient 危重患者外源性脂质性肺炎1例
Pub Date : 2021-01-01 DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2161
J. Sargi, J. Heaton, O. Adarkwah, G. Parhar, K. Zaman, N. Mesiha, F. Afroza, L. Gerolemou
Introduction:Lipoid pneumonia is a rare condition in which lipid molecules enter the alveoli. This condition usually manifests as hypoxemic respiratory failure after exogenous usage of different consumer products, including Vaseline, Vicks VapoRub and lip gloss, and occupational exposure in lubricant production, machine cleaning, and spray painting. We report a 79-year-old patient who presented with acute hypoxemic respiratory failure secondary to lipoid pneumonia. Case Presentation:A 79-year-old female with PMH of depression, chronic neck and back pain PTSD, HTN, HLD who presented to our institution with a chief complaint of non-productive cough and dyspnea on exertion for greater than a month. CXR showed diffuse bilateral interstitial opacities. CT imaging showed multifocal confluent geographic areas of ground-glass opacities in crazy paving patters, suggestive of alveolar pathology. Connective tissue disorders, respiratory cultures, and multiple COVID-19 tests were negative. BNP was normal. She initially required high flow oxygen with 80% FIO2. Steroids were started without improvement. The patient underwent bronchoscopy with BAL for suspected PAP, HP, and to rule out DAH. BAL showed lipid-laden macrophages on oil red o stain, and periodic acid shift stain was negative. The patient subsequently reported continuous Vicks vapor rub for many years, which was likely the reason for lipoid pneumonia development. Discussion:Lipoid pneumonia is a rare condition in which lipid molecules occupy intraalveolar space and are subsequently found in alveolar macrophages2. The exact mechanism is unknown;however, the pathogenesis and severity are related to the amount of inhaled materials used3. Lipoid pneumonia symptoms typically are chronic cough and progressive dyspnea on exertion. Recently, exogenous lipoid pneumonia has been linked to E-cigarettes usage4. Our case underlines the importance of keeping high clinical suspicion of lipoid pneumonia as a potential cause of dyspnea in patients with crazy paving patterns on CT scan. Taking a detailed history is essential in making the correct diagnosis.Conclusion Lipoid pneumonia is a rare diagnosis caused by inhaling different lipids containing materials. Physicians should be aware of this etiology as a possible differential diagnosis in patients admitted with acute hypoxemic respiratory failure.
简介:脂质肺炎是一种罕见的脂质分子进入肺泡的疾病。这种情况通常表现为外源使用不同的消费品,包括凡士林、维克斯喷雾和唇彩,以及在润滑剂生产、机器清洁和喷漆中职业暴露后的低氧性呼吸衰竭。我们报告一个79岁的病人谁提出急性低氧性呼吸衰竭继发于类脂性肺炎。病例介绍:一名79岁女性,伴有抑郁症、慢性颈部和背部疼痛、PTSD、HTN、HLD的PMH,主诉为非生产性咳嗽和用力时呼吸困难超过一个月。CXR显示双侧弥漫性间质混浊。CT表现为多灶融合的毛玻璃混浊区,呈疯狂铺路状,提示肺泡病变。结缔组织疾病、呼吸培养和多项COVID-19检测均为阴性。BNP正常。她最初需要80% FIO2的高流量氧气。开始使用类固醇后没有改善。患者行支气管镜BAL检查疑似PAP, HP,并排除DAH。BAL油红染色显示脂质巨噬细胞,周期性酸移染色为阴性。患者随后报告持续维克斯蒸汽摩擦多年,这可能是脂质肺炎发展的原因。讨论:脂质性肺炎是一种罕见的疾病,脂质分子占据肺泡腔,随后在肺泡巨噬细胞中发现2。确切的发病机制尚不清楚,但发病机制和严重程度与吸入物质的量有关。脂质性肺炎的典型症状是慢性咳嗽和用力时进行性呼吸困难。最近,外源性脂质肺炎与电子烟的使用有关。我们的病例强调了在CT扫描上出现疯狂铺路模式的患者中,对脂质肺炎作为呼吸困难的潜在原因保持高度临床怀疑的重要性。详细的病史是做出正确诊断的必要条件。结论脂质性肺炎是一种罕见的由吸入不同含脂物质引起的肺炎。医生应该意识到这一病因作为可能的鉴别诊断患者入院急性低氧性呼吸衰竭。
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引用次数: 0
Upadacitinib Associated Pneumocystis Jirovecii Pneumonia Upadacitinib相关性肺囊虫肺炎
Pub Date : 2021-01-01 DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2119
L. Jones, B. Stephens, S. Adams
Introduction:Upadacitinib is a new oral janus kinase (JAK) inhibitor that has been approved to treat rheumatoid arthritis. JAK inhibitors carry a black box warning for their association with severe infections especially when used in combination with other immunosuppressants. Although there is a strong association, there are very few reports of Pneumocystis jirovecii pneumonia (PJP) caused by upadacitinib. We describe a case of PJP due to upadacitinib use in rheumatoid arthritis. Case presentation: A 44-year-old woman with a history of rheumatoid arthritis presented with 2 weeks of dyspnea, dry cough and fever after recently starting upadacitinib. She was noted to be tachypneic, tachycardic and hypoxemic on admission. Initial laboratory tests were within normal limits and lactate dehydrogenase was 304. Respiratory viral panel and reverse transcription-polymerase chain reaction for severe acute respiratory syndrome coronavirus 2 were negative. Computerized tomography of the chest revealed diffuse multi-focal ground glass and consolidative opacities. The patient's respiratory status rapidly deteriorated, requiring admission to medical intensive care unit where she was initiated on invasive mechanical ventilation. A 1,3-beta-D-glucan serology test was positive and PJP polymerase chain reaction in bronchoalveolar lavage was positive. She was started on intravenous trimethoprim-sulfamethoxazole 400mg three times a day and intravenous methylprednisolone 500mg twice a day for three days. Her oxygen requirements rapidly improved and she was extubated on day 4 of admission. The patient was discharged without a supplemental oxygen requirement to complete a course of oral trimethoprim-sulfamethoxazole and prednisone. Discussion:JAK inhibitors are increasingly used for the treatment of rheumatoid arthritis and other autoimmune diseases. Other less selective JAK inhibitors such as tofacitinib and baricitinib have been associated with PJP in rheumatoid arthritis. Upadacitinib is a selective JAK1 inhibitor which is thought to give it an improved side effect profile compared to other less selective JAK inhibitors. This represents one of the first cases of PJP associated with the use of upadacitinib, a selective JAK1 inhibitor. PJP should be included in the differential diagnosis of patients treated with upadacitinib who present with fever, hypoxemia and pulmonary infiltrates. Awareness of this disease and its manifestations are critical to appropriate diagnostic evaluation and timely treatment.
Upadacitinib是一种新的口服janus激酶(JAK)抑制剂,已被批准用于治疗类风湿性关节炎。JAK抑制剂带有与严重感染相关的黑框警告,特别是与其他免疫抑制剂联合使用时。虽然有很强的相关性,但upadacitinib引起的肺囊虫肺炎(PJP)的报道很少。我们描述了一例PJP由于更新他替尼使用在类风湿关节炎。病例介绍:一名44岁女性,有类风湿关节炎病史,最近开始使用更新他替尼后出现2周呼吸困难、干咳和发烧。入院时发现她有呼吸急促、心动过速和低氧血症。初步化验结果在正常范围内,乳酸脱氢酶为304。呼吸道病毒面板和冠状病毒2型逆转录聚合酶链反应阴性。胸部电脑断层显示弥漫性多灶磨玻璃及实变影。病人的呼吸状况迅速恶化,需要送进医疗加护病房,在那里她开始接受有创机械通气。1,3- β - d -葡聚糖血清学试验阳性,支气管肺泡灌洗PJP聚合酶链反应阳性。开始静脉注射甲氧苄氨苄-磺胺甲恶唑400mg,每日3次;静脉注射甲基强的松龙500mg,每日2次,连用3天。她的氧气需求迅速改善,入院第4天拔管。患者出院时无需补充氧气以完成一个疗程的口服甲氧苄氨苄-磺胺甲恶唑和强的松。讨论:JAK抑制剂越来越多地用于类风湿关节炎和其他自身免疫性疾病的治疗。其他选择性较低的JAK抑制剂如托法替尼和巴西替尼与类风湿关节炎的PJP有关。Upadacitinib是一种选择性JAK1抑制剂,与其他选择性较低的JAK1抑制剂相比,Upadacitinib被认为具有更好的副作用。这是与选择性JAK1抑制剂upadacitinib相关的首批PJP病例之一。PJP应包括在upadacitinib治疗的患者的鉴别诊断中,这些患者表现为发热、低氧血症和肺部浸润。认识这种疾病及其表现对于适当的诊断评估和及时治疗至关重要。
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引用次数: 1
Palbociclib (Cyclin-Dependent Kinases CDK4 and CDK6 Selective Inhibitor) Induced Grade 3 Interstitial Pneumonitis 帕博西尼(细胞周期蛋白依赖性激酶CDK4和CDK6选择性抑制剂)诱导3级间质性肺炎
Pub Date : 2021-01-01 DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2118
R. Kunadharaju, A. Saradna, M. Ahmad, G. Fuhrer
Introduction: In postmenopausal women, Palbociclib is a selective cyclin-dependent kinase CDK4 and CKD6 inhibitor to treat hormone receptor-positive metastatic breast cancer in combination with Letrozole (Aromatase Inhibitor). We describe a case presenting with the rare side effect of Palbociclib induced interstitial pneumonitis. Case report: A 70-year-old Caucasian female was admitted to the hospital with complaints of progressive dyspnea, dry cough, epistaxis, pleuritic chest pain over one month. Her past medical history was significant for stage IIIC (pT3N3) invasive ductal breast cancer (ER-positive/PR-negative/HER2-negative) status post left segmental mastectomy and axillary lymph node dissection 17 years ago. She received adjuvant chemotherapy, followed by Anastrozole, for five years. She had a metastatic recurrence to bones, liver, and lymph nodes, which was ER-positive/PR-negative/HER2-negative, and was started on Palbociclib and Letrozole by the oncology team four months before admission. Upon presentation, she was noted to have hypoxia requiring four liters of oxygen via nasal cannula. On examination, she was in severe respiratory distress and had bilateral crackles on lung auscultation. CT chest with contrast revealed no pulmonary embolism and bilateral patchy interstitial opacities. Her lab work showed neutropenia, lymphopenia, and anemia. She had a thorough evaluation for viral (including COVID-19), bacterial, and fungal infection, heart failure, and autoimmune disorders, which were negative. Although diagnostic bronchoscopy was offered, she declined the procedure. She continued to have worsening hypoxemia and required a high flow nasal cannula (FiO2 70% and 50 liters of flow) for moderate ARDS, which was presumed to be secondary to drug-induced pneumonitis. Given the pattern of lung injury on CT, the subacute nature of her symptoms, and initial non-invasive evaluation, it was felt that infectious pneumonia was unlikely. She was managed conservatively with discontinuation of Palbociclib, and IV steroids were initiated (20 mg dexamethasone daily). Over 14 days during the hospital stay, her hypoxemia largely resolved, and she was successfully discharged to a rehabilitation facility. On the day of discharge, she was discharged on PO Prednisone dose 0.5mg/kg for six weeks along with oral Bactrim full dose three times a week for PJP prophylaxis. Discussion: Palbociclib is commonly associated with neutropenia, anemia, thrombocytopenia, fatigue, infection, and gastrointestinal side effects. Rarely Palbociclib is associated with interstitial pneumonitis (incidence <1%) due to unknown mechanisms. The early identification of this side effect and treatment with immediate cessation of the drug and corticosteroids could be a life-saving measure, as is the case with our patient.
在绝经后妇女中,Palbociclib是一种选择性周期蛋白依赖性激酶CDK4和CKD6抑制剂,用于与来曲唑(芳香酶抑制剂)联合治疗激素受体阳性转移性乳腺癌。我们描述了一个病例与罕见的副作用帕博西尼诱导间质性肺炎。病例报告:一名70岁白人女性因进行性呼吸困难、干咳、鼻出血、胸膜炎性胸痛一个多月而入院。17年前左乳房切除术和腋窝淋巴结清扫后,她的既往病史对IIIC期(pT3N3)浸润性导管乳腺癌(er阳性/ pr阴性/ her2阴性)有重要意义。她接受了辅助化疗,随后服用阿那曲唑5年。她有骨、肝和淋巴结转移性复发,er阳性/ pr阴性/ her2阴性,入院前4个月肿瘤小组开始使用帕博西尼和来曲唑。入院时,医生注意到她缺氧,需要通过鼻插管吸氧4升。经检查,患者有严重呼吸窘迫,双侧肺听诊有脆音。胸部CT造影未见肺栓塞及双侧斑片状间质混浊。她的实验室检查显示中性粒细胞减少、淋巴细胞减少和贫血。她接受了病毒(包括COVID-19)、细菌和真菌感染、心力衰竭和自身免疫性疾病的全面评估,结果均为阴性。虽然提供了诊断性支气管镜检查,但她拒绝了这个程序。她的低氧血症持续恶化,需要高流量鼻插管(FiO2 70%和50升流量)治疗中度急性呼吸窘迫综合征,推测是继发于药物性肺炎。考虑到CT上肺损伤的类型、症状的亚急性性质以及初步的非侵入性评估,我们认为不太可能是感染性肺炎。患者接受保守治疗,停用帕博西尼,并开始静脉注射类固醇(每天20mg地塞米松)。在住院14天多的时间里,她的低氧血症基本得到解决,她成功地出院到康复机构。出院当天,患者予PO泼尼松剂量0.5mg/kg,连续6周,同时口服Bactrim全剂量,每周3次,预防PJP。讨论:帕博西尼通常与中性粒细胞减少、贫血、血小板减少、疲劳、感染和胃肠道副作用相关。由于未知的机制,帕博西尼很少与间质性肺炎(发病率<1%)相关。早期发现这种副作用并立即停用药物和皮质类固醇治疗可能是挽救生命的措施,就像我们的病人一样。
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引用次数: 1
A Case of Daptomycin Induced Acute Eosinophilic Pneumonia in a Patient with Septic Arthritis 达托霉素致脓毒性关节炎患者急性嗜酸性肺炎1例
Pub Date : 2021-01-01 DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2154
A. Mukherjee, K. Sankaramangalam
Introduction-Daptomycin is a unique lipopeptide antibiotic that exerts bactericidal action by cell membrane action potential disruption. It is used in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin resistant gram-positive organisms. However, acute eosinophilic pneumonitis (AEP) remains a rare life-threatening adverse effect of daptomycin therapy. Case-A 65-year-old gentleman with a history of diabetes mellitus presented with palpitations, dyspnea, and lethargy for four days. He did not have any fever but noted occasional nonproductive cough. He was discharged a week prior after a two-week hospitalization where he underwent treatment for MRSA septic knee arthritis, which was complicated by MRSA bacteremia and COVID-19 pneumonia. He was discharged on daptomycin and ceftaroline maintenance therapy. He was afebrile, but had tachycardia, tachypnea, and was hypoxic to 88% on room air. Pulmonary examination revealed bibasal decreased breath sounds. Investigations were notable for leukocytosis with peripheral eosinophilia of 27%. COVID-19 testing was negative twice. His chest-Xray revealed patchy bilateral opacities (Fig-1A), similar to his prior admission (Fig-1B). A computed tomography pulmonary angiogram showed bilateral, multifocal, irregular opacities (Fig-1C). Supplemental oxygen was started and daptomycin was promptly discontinued. Intravenous methylprednisolone was also initiated. Over the next two days, the patient improved significantly, was weaned off supplemental oxygen, and peripheral eosinophilia also improved. He was discharged after four days, on a prednisone taper and only ceftaroline was completed for a total of eight weeks. Discussion-Daptomycin induced AEP may present with dyspnea, fever, peripheral eosinophilia and bilateral multifocal pulmonary infiltrates, commonly within two to four weeks of drug exposure. 25% or more eosinophilia on bronchoalveolar lavage specimen is very specific. This adverse effect of daptomycin appears to be more time-dependent than dose-dependent. Daptomycin is inactivated by pulmonary surfactant, and this altered lipid biochemistry may precipitate T-helper-2 cell-mediated interleukin-5 elaboration. This triggers eosinophil recruitment and their pulmonary migration, resulting in the characteristic pulmonary inflammatory response. However, the exact mechanism remains unclear. We considered other differentials, including fungal or parasitic infections, recent COVID-19 pneumonia, and vasculitides;however, considering our patient's compatible presentation, and with a Naranjo algorithm score of six, daptomycin induced AEP was hypothesized to be the probable etiology. Management involves early recognition and discontinuation of daptomycin, with corticosteroids being used often to augment clinical recovery. The rarity of the presentation necessitates awareness and vigilance, as early discontinuation often results in an excellent prognosis and leads to future avoidance of daptomyc
达托霉素是一种独特的脂肽类抗生素,通过破坏细胞膜动作电位发挥杀菌作用。它用于治疗耐甲氧西林金黄色葡萄球菌(MRSA)和耐万古霉素革兰氏阳性菌。然而,急性嗜酸性粒细胞肺炎(AEP)仍然是达托霉素治疗中一种罕见的危及生命的不良反应。病例:65岁男性,有糖尿病史,出现心悸、呼吸困难、嗜睡4天。他没有发烧,但偶尔咳嗽。他在住院治疗两周后出院,当时他患有MRSA脓毒性膝关节炎,并伴有MRSA菌血症和COVID-19肺炎。出院时给予达托霉素和头孢他林维持治疗。他不发烧,但有心动过速,呼吸急促,室内空气缺氧至88%。肺部检查显示双基底呼吸音减少。白细胞增多,外周血嗜酸性粒细胞增多占27%。新冠病毒检测两次呈阴性。胸片示双侧斑片状影(图1a),与入院前相似(图1b)。计算机断层肺血管造影显示双侧,多灶,不规则影(图1c)。开始补充氧气,并立即停用达托霉素。同时开始静脉注射甲基强的松龙。在接下来的两天里,患者明显好转,不再补充氧气,外周嗜酸性粒细胞也有所改善。四天后,他出院,泼尼松逐渐减少,只有头孢他林完成了总共八周的治疗。达托霉素诱导的AEP可能表现为呼吸困难、发热、外周嗜酸性粒细胞增多和双侧多灶性肺浸润,通常在药物暴露2至4周内发生。支气管肺泡灌洗标本呈25%或以上嗜酸性粒细胞增多是非常特异的。达托霉素的这种不良反应似乎是时间依赖性大于剂量依赖性。达托霉素被肺表面活性剂灭活,这种改变的脂质生物化学可能沉淀T-helper-2细胞介导的白介素-5精化。这触发了嗜酸性粒细胞的募集和它们的肺迁移,导致特征性的肺部炎症反应。然而,确切的机制尚不清楚。我们考虑了其他的差异,包括真菌或寄生虫感染,最近的COVID-19肺炎和血管增生;然而,考虑到我们的患者的相容表现,并且Naranjo算法得分为6分,我们假设达托霉素诱导的AEP是可能的病因。治疗包括早期识别和停用达托霉素,并经常使用皮质类固醇来增加临床恢复。罕见的表现需要引起注意和警惕,因为早期停药通常会导致良好的预后,并导致未来避免使用达托霉素,而漏诊可能会危及生命。
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引用次数: 1
Deceptive Lungs: Is it Brentuximab Induced Pneumonitis or Pneumonia 欺骗性肺:是Brentuximab引起的肺炎还是肺炎
Pub Date : 2021-01-01 DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2123
A. Syeda, T. Mohammed, M. Mir
Introduction: Pulmonary toxicity can be a lethal side effect associated with many newer anti-cancer agents especially immune checkpoint inhibitors. In the times of ever-growing patient population on precision oncology therapies, timely identification of drug induced lung injury can be challenging. Here we highlight pulmonary toxicity as an adverse effect of brentuximab vedotin (BV). Case Report: A 70-year-old male, former smoker with a recent diagnosis of advanced stage classic Hodgkin's lymphoma recently started on BV, presented with two days of progressive dyspnea, fever and productive cough. He denied exposure to sick contacts and recent travel. Of note, he was hospitalized ten days earlier for suspected pneumonia and had completed a course of antibiotics. Vital signs were notable for temperature 101.7°F, heart rate 110 beats/minute, respiratory rate 30 breaths/minute and oxygen saturation of 90% on 6L of oxygen. Physical examination was noteworthy for bibasilar rhonchi. Lab workup was unremarkable and COVID-19 test was negative. Imaging studies displayed new bilateral basal infiltrates on CXR and CT scan of the chest demonstrated new alveolar opacities involving the lower lobes, and interval improvement was noted in the upper lobe opacities. He was treated for presumed pneumonia with broad spectrum antibiotics. However, his oxygen requirements continued to increase, necessitating a further infectious and rheumatologic workup which was negative. After thorough diagnostic evaluation, in the absence of other plausible etiology, the patient's symptoms were attributed to pneumonitis secondary to the chemotherapeutic agent BV. Henceforth, intravenous steroids were initiated which resulted in clinical improvement. Further treatment with BV was withheld and he was discharged on a steroid taper. One month later, a subsequent CT scan of the chest demonstrated complete resolution of bilateral alveolar opacities. Discussion: BV is a CD30 directed antibody-drug conjugate used in advanced or refractory classic Hodgkin's lymphoma. It is known to cause a higher rate of pulmonary toxicity when combined with bleomycin containing regimens with a reported incidence of 40%, hence this combination is contraindicated. However, the incidence of pneumonitis is noted to be only 5% in patients receiving BV in combination with non-bleomycin regimens, which was the case in our patient in lieu of his two back-to-back hospitalizations after receiving two cycles of BV. The exact mechanism of action is unclear but is probably due to hypersensitivity pneumonitis. Although it is a diagnosis of exclusion, a high degree of suspicion is crucial for prompt cessation of the drug in order to prevent adverse outcomes.
肺毒性可能是与许多新的抗癌药物特别是免疫检查点抑制剂相关的致命副作用。在精确肿瘤治疗的患者人数不断增长的时代,及时识别药物性肺损伤可能具有挑战性。在这里,我们强调肺毒性作为brentuximab vedotin (BV)的不良反应。病例报告:一名70岁男性,前吸烟者,最近诊断为晚期经典霍奇金淋巴瘤,最近开始BV,表现为两天进行性呼吸困难,发烧和咳嗽。他否认曾接触过病人,也否认最近有过旅行。值得注意的是,他在十天前因疑似肺炎住院,并完成了一个疗程的抗生素治疗。体温101.7°F,心率110次/分钟,呼吸频率30次/分钟,6L氧饱和度90%,生命体征显著。双基底隆齐的体格检查值得注意。实验室检查无显著差异,COVID-19检测为阴性。影像学检查显示新的双侧基底浸润,胸部CT扫描显示新的肺泡混浊累及下肺叶,上肺叶混浊有所改善。他被诊断为肺炎,接受了广谱抗生素治疗。然而,他的需氧量继续增加,需要进一步的感染和风湿病检查,结果为阴性。经过彻底的诊断评估,在没有其他合理病因的情况下,患者的症状归因于化疗药物BV继发肺炎。此后,静脉注射类固醇导致临床改善。他停止了进一步的BV治疗,出院时使用类固醇减量治疗。一个月后,胸部CT扫描显示双侧肺泡混浊完全消失。讨论:BV是一种CD30导向的抗体-药物偶联物,用于晚期或难治性经典霍奇金淋巴瘤。已知与含博来霉素的方案联合使用会导致更高的肺毒性发生率,据报道发生率为40%,因此这种联合使用是禁忌的。然而,在接受BV联合非博莱霉素治疗的患者中,肺炎的发病率仅为5%,这就是我们的患者在接受两个BV周期后连续两次住院的情况。确切的作用机制尚不清楚,但可能是由于过敏性肺炎。虽然这是一种排除诊断,但高度怀疑对于迅速停止药物以防止不良后果至关重要。
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引用次数: 2
Think It Twice Before You Give Piperacillin-Tazobactam 服用哌拉西林-他唑巴坦前要三思
Pub Date : 2021-01-01 DOI: 10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2160
L.A. Vazquez Zubillaga, A. Rivera-Diaz, O. Cantres
Piperacillin-tazobactam is a Beta-lactam and beta-Lactamase combination antibiotic very commonly used to treat infections, specially in critically ill patients. The most common adverse effects related to its use are mostly gastrointestinal and allergic. Lung infiltration with pulmonary eosinophilia is a very rare event, but when occurs has significant morbidity and mortality. For this reason, physicians should be aware of this possible reaction. This is a case of a 43 year-old woman with medical history of Morbid Obesity who presented to the emergency department complaining of severe stabbing right upper quadrant pain associated with nausea and non-bloody emesis after a heavy meal. Abdominal computed tomography (CT) revealed acute cholecystitis. She was initially treated with piperacillin-tazobactam, intravenous volume expansion and pain medication. The patient underwent cholecystectomy the next day. After surgery, the patient was complained of dyspnea. Arterial blood gases revealed respiratory acidosis and significative hypoxemia. Chest CT revealed bilateral consolidation and ground glass opacities with predominance of upper lobes. Laboratory was unremarkable, without leukocytosis, or eosinophilia, normal procalcitonin, and blood cultures and COVID-19 test were negative. A bronchoscopy was performed to obtain cultures, cell count and cytology analysis. Results showed negative negative microbiology cultures. Cellular differential counts of bronchoalveolar lavage showed a predominance of eosinophils (26% of total cell count. There was no peripheral eosinophilia, and eosinophilia work up, including parasitic infection evaluation was negative. Rheumatologic serologies work-up was also negative. The patient did not received other medications during her short admission, and initial admission X ray was completely normal. Piperacillintazobactam was discontinued and the patient was started in systemic steroids with rapid resolution of hypoxemia after the first 48hrs. Those findings suggested that piperacillin-tazobactam was most likely the cause of Acute Eosinophilic Pneumonia in this patient, after she was started for the treatment for acute cholecystitis. Piperacillin-tazobactam has been rarely associated to acute eosinophilic pneumonia. It may present as an acute hypoxemic respiratory failure as seen in few case reports. Presentation can occur any time during piperacillintazobactam, therapy, usually after days or weeks of therapy. High suspicion of the diagnosis in patients with pneumonia treatment with poor response to antibiotics or multi lobar disease, during therapy with piperacillintazobactam help to identify the diagnosis. Bronchoalveolar lavage with cellular differential > 25% confirm the diagnosis in a patient with no other etiology for pulmonary eosinophilia. Discontinuation of the medication and systemic steroids is the treatment of choice, usually with favorable rapid response.
哌拉西林-他唑巴坦是一种β -内酰胺和β -内酰胺酶联合抗生素,通常用于治疗感染,特别是危重患者。最常见的不良反应是胃肠道和过敏反应。肺浸润伴嗜酸性粒细胞增多是一种非常罕见的疾病,但一旦发生,其发病率和死亡率都很高。因此,医生应该意识到这种可能的反应。这是一个43岁的女性病例,有病态肥胖病史,她到急诊科就诊,主诉大餐后右上腹剧烈刺痛,伴有恶心和非血性呕吐。腹部电脑断层扫描显示急性胆囊炎。她最初接受哌拉西林-他唑巴坦、静脉容量扩张和止痛药治疗。病人在第二天接受了胆囊切除术。手术后,患者主诉呼吸困难。动脉血气显示呼吸性酸中毒和明显的低氧血症。胸部CT示双侧实变及磨玻璃影,以上肺叶为主。实验室检查无异常,无白细胞增多、嗜酸性粒细胞增多,降钙素原正常,血培养及COVID-19检测阴性。进行支气管镜检查以获得培养物、细胞计数和细胞学分析。结果微生物培养呈阴性。支气管肺泡灌洗的细胞差异计数显示嗜酸性粒细胞占优势(占总细胞计数的26%)。外周血无嗜酸性粒细胞增多,嗜酸性粒细胞增多,包括寄生虫感染评价阴性。风湿病血清学检查也为阴性。患者入院时间短,未接受其他药物治疗,入院初X线完全正常。停用哌拉西林他唑巴坦,患者开始全体性类固醇治疗,低氧血症在最初48小时后迅速消退。这些结果提示,在该患者开始接受急性胆囊炎治疗后,哌拉西林-他唑巴坦最有可能是导致急性嗜酸性粒细胞性肺炎的原因。哌拉西林-他唑巴坦很少与急性嗜酸性肺炎相关。在少数病例报告中可表现为急性低氧性呼吸衰竭。在哌拉西林他唑巴坦治疗期间,症状可发生在任何时间,通常在治疗数天或数周后。对肺炎治疗中抗生素反应较差或多叶性疾病的患者诊断高度怀疑,在治疗期间使用哌拉西林他唑巴坦有助于鉴别诊断。支气管肺泡灌洗伴细胞分化;25%的病例确诊为无其他病因的肺嗜酸性粒细胞增多症。停药和全身性类固醇是治疗的选择,通常有良好的快速反应。
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引用次数: 1
期刊
TP36. TP036 WHAT DRUG CAUSED THAT? CASE REPORTS IN DRUG-INDUCED LUNG DISEASE
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