Pulmonary Langerhans Cell Histiocytosis Research Articles

Synchronous Pulmonary Langerhans Cell Histiocytosis and Multiple Cutaneous Reticulohistiocytomas With a Common BRAF-V600E/D Mutation Driver.

Histiocytoses constitute a group of heterogeneous disorders characterized by involvement of variable organs by neoplastic macrophage or dendritic cells. They may affect both adults and children with a predilection to the skin, bone, lungs, lymph nodes, and CNS. The coexistence of different types of histiocytoses in the same patient is an extremely rare phenomenon. We describe a very rare case of co-occurring pulmonary Langerhans cell histiocytosis with multiple cutaneous reticulohistiocytomas with a common BRAF-V600E mutation as the driver genetic event in both the lung and skin lesions. The presence of a common BRAF-V600E mutation provides evidence of their clonal relation and contributes to our understanding in the pathogenesis of multiple, co-occurring histiocytic proliferations.

Pulmonary Langerhans cell histiocytosis with multiple cavitary nodules after lung cancer surgery

AbstractPulmonary Langerhans cell histiocytosis (PLCH) is a subtype of Langerhans cell histiocytosis, a rare neoplastic disease characterized by lung involvement. Here, we present a case involving a patient with multiple cavitary nodules who was diagnosed with PLCH during surveillance after lung cancer surgery. A 74‐year‐old woman underwent right upper lobe resection surgery for right upper lobe lung adenocarcinoma, pStage IIA, 5 years ago. The patient underwent surveillance without adjuvant chemotherapy. During the fifth year of follow‐up, multiple nodules with cavitation were observed on computed tomography in both lung fields. Chemotherapy was considered to address the suspected recurrence of lung cancer; however, video‐assisted thoracoscopic surgery was performed due to the need for biomarker testing. Pathological examination led to the diagnosis of PLCH. This case emphasizes the importance of a proactive histological diagnosis to determine the appropriate treatment strategy, even in situations where lung cancer recurrence is clinically suspected.

Circulating monocytes decrease significantly following disease-directed therapy and may reflect disease expansion in Langerhans Cell Histiocytosis.

We aimed to examine the association between relative monocytosis and the recurrence of pulmonary Langerhans Cell Histiocytosis. Clinical, laboratory, radiographic and treatment data for 86 patients with a histopathological diagnosis of Langerhans Cell Histiocytosis over a 20-year duration. Parameters such as biological sex, age at diagnosis, time to diagnosis, molecular diagnostic data and imaging were collected. Treatment responses were assessed predominantly through radiography, with RECIST 1.1 criteria applied to MRI or CT scans and PERCIST utilized for serial PET imaging. Investigators also assessed peripheral blood absolute monocyte count at various time points, including initial diagnosis and the most recently available value. While peripheral blood absolute monocyte count between the earliest assessed timepoint and latest value did not differ, the mean value on progression (0.94K/µL), however, was significantly higher than that following re-institution of therapy (0.31, p = 0.000794. Our observation of relative monocytosis on LCH disease progression may be related to an increase in circulating LCH on disease progression or from increased monocyte production for later differentiation into mature dendritic cells that participate in MHC Class 1 upregulation. This trend is especially evident in pulmonary LCH which is incited by tissue trauma and irritation by environmental factors. The phenomena observed in our study parallel other non-LCH cohorts, specifically in published findings from our own group in patients with Rosai Dorfman and Erdheim Chester Disease. To further elucidate the molecular underpinnings of LCH and explore the etiology of this monocyte trend, expanded integrated genomic-transcriptomic sequencing analyses to evaluate the molecular character of LCH and ultimately clarify the origin of this monocyte trend are in progress. These studies are poised to offer invaluable insight to the molecular mechanisms underlying LCH, specifically as they pertain to monocyte signaling and differentiation.

Pulmonary involvement in children with Langerhans cell histiocytosis

Background. Pulmonary Langerhans cell histiocytosis (pLCH) is a rare disease, mostly a component of multisystemic LCH. We aimed to investigate the clinical features and treatment results in children with pLCH. Methods. We retrospectively reviewed the clinical, radiological, and treatment data of 37 patients with pLCH, diagnosed from 1974 to 2022. Results. 10% (n=37) of 367 patients with LCH had lung involvement. The median age was 1.8 years (range: 0.4 & 17.7) with a male-to-female ratio of 2.3. At admission 29.7% (n=11) presented with respiratory symptoms. Imaging showed a spectrum from nodular opacities to multiple cysts. All but one patient had multisystem disease. Twenty-nine received vinblastine-containing therapy. Ten-year event-free (EFS) and overall survival (OS) rates were 47.8% and 63.3%, respectively. In children younger and older than two years of age, the 10-year EFS was 53.3% vs. 40.2% and the 10-year OS was 58.7% vs. 68.8%, respectively. In children with and without risk organ involvement, 10-year EFS was 51.9% vs. 46.3% and 10-year OS was 51.9% vs. 73.7%. Conclusions. Lung and multisystem involvement are significant concerns in LCH, highlighting the need for careful management to reduce morbidity and mortality.

Living-donor lobar lung transplantation for pulmonary Langerhans cell histiocytosis complicated by extensive thrombi in central pulmonary arteries

BackgroundPulmonary Langerhans cell histiocytosis (PLCH) is a rare disorder characterized by the proliferation of Langerhans cells along the small airways, which causes nodular and cystic changes in the lung parenchyma. Lung transplantation can be a life-saving option for patients with severe respiratory failure or pulmonary hypertension. Herein, we present a case of successful lung transplantation in a patient with PLCH who developed unusually large thrombi in the central pulmonary artery.Case presentationA 47-year-old woman with 16-year history of PLCH with rapidly developing respiratory failure was admitted to our hospital for the evaluation of a lung transplant. Enhanced computed tomography revealed large thrombi in dilated central pulmonary arteries. Right heart catheterization revealed severe pulmonary hypertension, with a mean pulmonary artery pressure of 48 mmHg. The thrombi shrank markedly after 3 months of anticoagulation therapy. However, the respiratory status of the patient did not improve. We performed bilateral living-donor lobar lung transplantation with thrombectomy under extracorporeal membrane oxygenation for the remaining thrombi in the main pulmonary arteries. The dilated main pulmonary arteries of the recipient required direct plication for size mismatch. The patient survived in good condition for more than 2 years with no recurrence of thrombosis.ConclusionPreoperative anticoagulation therapy for massive thrombi in the pulmonary arteries was effective and led to safe lung transplantation.

Thoracic Frozen Section Pitfalls: Lung Adenocarcinoma Versus Selected Mimics.

Intraoperative (frozen section) analysis of lung lesions (nodules, masses, ground-glass opacities) can occasionally be diagnostically challenging. To describe selected pitfalls in thoracic frozen sections with a focus on the differential diagnosis between adenocarcinoma and its mimics, and to provide tips to prevent misinterpretation. Peer-reviewed literature and the author's experience. A common challenge in thoracic frozen sections is the differential diagnosis between lung adenocarcinoma and its mimics. Diagnostic difficulties arise because mimics of adenocarcinoma often entrap reactive lung epithelium that can appear atypical on frozen section slides. Entities that can be misinterpreted as adenocarcinoma include ciliated muconodular papillary tumor/bronchiolar adenoma, hamartoma, inflammatory myofibroblastic tumor, and pulmonary Langerhans cell histiocytosis. Knowledge of the key clinical, radiologic, and histologic features of these entities can help prevent overdiagnosis of adenocarcinoma. Pathologic findings that facilitate the distinction between adenocarcinoma and its mimics at frozen section include the appearance and contour of the lesion at low magnification, growth patterns, cilia, stromal features, shape of the epithelial cells (cuboidal versus columnar), nuclear features of malignancy (crowding, hyperchromasia, irregular contours), and abruptness of the junction between the lesion and adjacent uninvolved lung. Knowledge of the clinical context, imaging findings, and the surgical consequence of the intraoperative diagnosis can also prevent diagnostic errors. Finally, since adenocarcinomas of the lung are often relatively bland and lack the stromal desmoplasia seen in adenocarcinomas of other organs, familiarity with the morphologic spectrum of lung adenocarcinomas at frozen section analysis is important.

Pulmonary Langerhans Cell Histiocytosis Post-Hodgkin Lymphoma Completely Resolved With Vinblastine in a Heavy Smoker: Coincidence or Causation?

The association among Langerhans cell histiocytosis, hematolymphoid malignancies, and heavy smoking has been addressed in medical literature to identify a possible potential link. Such occurrence can pose diagnostic challenges, as well as important clinical implications for disease progression and treatment approaches. We present pulmonary Langerhans cell histiocytosis instance in a 35-year-old male patient, with a 34-pack-year smoking history and nodular sclerosing Hodgkin lymphoma stage IIB who developed multiple bilateral lung nodules. The patient completed 6 cycles of doxorubicin (Adriamycin), bleomycin, vinblastine, and dacarbazine chemotherapy and radiotherapy 2 years earlier. CT chest scans revealed numerous micronodules scattered randomly throughout the upper and lower left lung lobes. Subsequent wedge resection exhibited cellular proliferation with grooved nuclei, eosinophilic cytoplasm, and surrounding inflammatory components. Immunohistochemical staining showed positive staining for S100 and CD1a confirming a diagnosis of pulmonary Langerhans cell histiocytosis. The patient responded to a 6-week treatment with vinblastine and prednisolone. A subsequent CT scan of the lungs revealed complete resolution after 3 years. This report underscores the importance of identifying pulmonary Langerhans cell histiocytosis in heavy smokers with Hodgkin lymphoma presenting with multiple nodular pulmonary lesions. For patients with Hodgkin lymphoma and a possible genetic predisposition, smoking may contribute to the overt development of pulmonary Langerhans cell histiocytosis. Therefore, smoking cessation and careful follow-up examinations are required. Further research is recommended to elucidate the underlying mechanisms of this intriguing association.

Pulmonary BRAF-driven Langerhans cell histiocytosis following selpercatinib use in metastatic medullary thyroid cancer.

RET mutations are implicated in 60% of medullary thyroid cancer (MTC) cases. The RET-selective tyrosine kinase inhibitor selpercatinib is associated with unprecedented efficacy compared to previous multi-kinase treatments. Langerhans cell histiocytosis (LCH) is a clonal histiocytic neoplasm usually driven by somatic BRAF mutations, resulting in dysregulated MAPK signalling. We describe a 22-year-old woman with metastatic MTC to regional lymph nodes, lung and liver. Tumour tissue harboured a somatic pathogenic RET variant p.(M918T) and selpercatinib was commenced. She experienced sustained clinical, biochemical and radiological responses. Two years later, she developed rapidly progressive apical lung nodules, prompting biopsy. Histopathology demonstrated LCH with a rare BRAF variant p.(V600_K601>D). The lung nodules improved with inhaled corticosteroids. We hypothesize that selective pressure from RET blockade may have activated a downstream somatic BRAF mutation, resulting in pulmonary LCH. We recommend continued vigilance for neoplasms driven by dysregulated downstream MAPK signalling in patients undergoing selective RET inhibition. Patients with RET-altered MTC can experience rapid disease improvement and sustained disease stability with selective RET blockade (selpercatinib). LCH is a clonal neoplasm driven by MAPK activation, for which the most common mechanism is BRAF mutation. Both MTC and pulmonary LCH are driven by dysregulated MAPK signalling pathway activation. We hypothesise that the RET-specific inhibitor selpercatinib may have caused the activation of dormant LCH secondary to selective pressure and clonal proliferation.

Abstract 2564: Circulating monocytes decrease significantly following disease-directed therapy and may reflect disease expansion in Langerhans cell histiocytosis

Abstract Introduction: Langerhans Cell Histiocytosis (LCH) is a rare disorder characterized by clonal hematopoietic cell expansion forming eosinophilic granulomas. Treatment approaches vary based on disease severity. Despite established therapies, assessing treatment response, particularly regarding peripheral blood monocytes, lacks comprehensive markers. Methods: We studied 76 LCH patients, collecting data on demographics, diagnostic methods, and treatment responses. Peripheral blood absolute monocyte counts were analyzed at key time points, including disease onset, progression, and post-therapy reinstatement, using statistical tests for comparison. Results: Analyzing data from 76 patients (average age: 38), we found diverse disease presentations, with common imaging modalities being CT (37), PET (29), and MRI (22). Complete responses were observed in 17 of 49 patients, with 11 undergoing local therapy. Conversely, 5 patients with pulmonary LCH and chronic tobacco use showed persistent progression. Notably, peripheral blood monocyte counts did not differ between initial and latest assessments, but on disease progression, the mean count (0.94 K/µL) significantly exceeded that following therapy reinstatement (0.31, p=0.000794). Results: Analyzing data from 76 patients (average age: 38), we found diverse disease presentations, with common imaging modalities being CT (37), PET (29), and MRI (22). Complete responses were observed in 17 of 49 patients, with 11 undergoing local therapy. Conversely, 5 patients with pulmonary LCH and chronic tobacco use showed persistent progression. Notably, peripheral blood monocyte counts did not differ between initial and latest assessments, but on disease progression, the mean count (0.94 K/µL) significantly exceeded that following therapy reinstatement (0.31, p=0.000794). Discussion: LCH is proposed to result from dysregulated hematopoiesis, leading to sequential somatic mutations during monocyte differentiation leading to clonal expansion of CD1A and CD207+ histiocytes. Our finding of increased monocyte count during disease progression may suggest elevated circulating LCH or heightened monocyte production for subsequent differentiation, potentially contributing to MHC Class 1 upregulation. This phenomena mirrors published findings from our own group in patients with Rosai Dorfman and Erdheim Chester Disease. To further elucidate the molecular underpinnings of LCH and explore the etiology of this monocyte trend, genetic sequencing analysis is in progress. Ultimately, monitoring peripheral blood monocyte dynamics could offer valuable insights into LCH progression and treatment response. Citation Format: Haadi Ali, Sam Reynolds, Sabrina Wilcox, Naina Chipalkatti, Asra Ahmed. Circulating monocytes decrease significantly following disease-directed therapy and may reflect disease expansion in Langerhans cell histiocytosis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 2564.

Pediatric pulmonary Langerhans cell histiocytosis complicated by recurrent hemopneumothoraces

Langerhans cell histiocytosis is a rare disease of clonal proliferation and deposition of immature dendritic cells in various tissues, including the lungs, causing inflammation and organ destruction. We report a case of a 4-year-old girl with refractory multisystem Langerhans cell histiocytosis complicated by recurrent bilateral hemopneumothoraces in a pediatric tertiary hospital in Cape Town, South Africa. Video-assisted thoracoscopy revealed chronic inflammation of her pleura, with pleural fibrosis seen on histology. Despite pleurodesis, she continued to have recurrent hemopneumothoraces until she was started on a hydroxyurea-containing regimen with a good response.

Isolated Pulmonary Langerhans Cell Histiocytosis in a Child

Abstract A 4-year-old boy presented with a history of chronic cough for the past 1 year that was progressing for the last 2 weeks. History of intermittent fever with breathlessness was there. The child had received antibiotics, nebulization, and oral steroids, but was never prescribed inhaled steroids, as no wheeze was documented. As the X-ray chest was not showing any significant findings, a computerized tomography chest was done that showed septal thickening, and reticulonodular pattern bilaterally without bronchiectasis or mediastinal lymphadenopathy. Bronchoscopy was done and the lavage fluid found CD1a and S-100-positive cells suggestive of pulmonary Langerhans cell histiocytosis. There was no other organ involvement.

Clinical-radiological-pathological correlation in pulmonary hypertension with unclear and/or multifactorial mechanisms.

Ever since the second world symposium on pulmonary hypertension (PH) held in Evian, France, in 1998, PH has been classified into five major clinical groups. Group 5 PH includes a variety of distinct conditions with unclear and/or multifactorial underlying pathologies. Management of these patients is challenging as the number of patients within these groups is often small, not all individuals with certain underlying conditions are affected by PH and patients exhibit distinct symptoms due to different underlying diseases. Studies and clinical trials in these groups are largely lacking and mostly restricted to case series and registry reports. Nonetheless, the worldwide burden of group 5 PH is estimated to be significant in terms of the prevalence of some associated diseases. Group 5 PH encompasses six subgroups, including haematological disorders (inherited and acquired chronic haemolytic anaemia and chronic myeloproliferative disorders), systemic disorders (sarcoidosis, pulmonary Langerhans's cell histiocytosis and neurofibromatosis type 1), metabolic disorders (glycogen storage diseases and Gaucher disease), chronic renal failure with or without haemodialysis, pulmonary tumour thrombotic microangiopathy and fibrosing mediastinitis.

Bronchoalveolar cytokine profile differentiates Pulmonary Langerhans cell histiocytosis patients from other smoking-related interstitial lung diseases

BackgroundPulmonary Langerhans cell histiocytosis (PLCH) is a rare interstitial lung disease (ILD) associated with smoking, whose definitive diagnosis requires the exclusion of other forms of ILD and a compatible surgical lung biopsy. Bronchoalveolar lavage (BAL) is commonly proposed for the diagnosis of ILD, including PLCH, but the diagnostic value of this technique is limited. Here, we have analyzed the levels of a panel of cytokines and chemokines in BAL from PLCH patients, in order to identify a distinct immune profile to discriminate PLCH from other smoking related-ILD (SR-ILD), and comparing the results with idiopathic pulmonary fibrosis (IPF) as another disease in which smoking is considered a risk factor.MethodsBAL samples were collected from thirty-six patients with different ILD, including seven patients with PLCH, sixteen with SR-ILD and thirteen with IPF. Inflammatory profiles were analyzed using the Human Cytokine Membrane Antibody Array. Principal component analysis (PCA) was performed to reduce dimensionality and protein–protein interaction (PPI) network analysis using STRING 11.5 database were conducted. Finally, Random forest (RF) method was used to build a prediction model.ResultsWe have found significant differences (p < 0.05) on thirty-two cytokines/chemokines when comparing BAL from PLCH patients with at least one of the other ILD. Four main groups of similarly regulated cytokines were established, identifying distinct sets of markers for each cluster. Exploratory analysis using PCA (principal component analysis) showed clustering and separation of patients, with the two first components capturing 69.69% of the total variance. Levels of TARC/CCL17, leptin, oncostatin M (OSM) and IP-10/CXCL10 were associated with lung function parameters, showing positive correlation with FVC. Finally, random forest (RF) algorithm demonstrates that PLCH patients can be differentiated from the other ILDs based solely on inflammatory profile (accuracy 96.25%).ConclusionsOur results show that patients with PLCH exhibit a distinct BAL immune profile to SR-ILD and IPF. PCA analysis and RF model identify a specific immune profile useful for discriminating PLCH.

Pediatric pulmonary multisystem langerhans cell histiocytosis: does lung lesion severity affect the outcome?

BackgroundThe pediatric pulmonary multisystem Langerhans cell histiocytosis (PPM LCH) is associated with either low risk or high risk organ(s). The nodulo-cystic lung lesions although pathognomonic, yet are very variable in severity and remain a source of controversy in certifying pulmonary LCH diagnosis. The study aimed to examine the prognostic value of clinical respiratory manifestations and radiological lung lesions severity. This is through associating a CT chest triad of bilateral, extensive and diffuse lesions. It is a retrospective study of 350 LCH patients who received systemic treatment at Children’s Cancer Hospital Egypt during the period from 2007 to 2020.ResultsSixty-seven patients (67/350–19.1%) had PPM LCH at presentation. Severe lung lesions were present in 24 of them. The median follow-up period was 61 months (IQR: 3.4–8.3). The 5-year overall survival (OS) and event free survival (EFS) was 89% and 56.6% respectively. The EFS, for severe radiological lesions triad was 38% ± 20.7 versus 66% ± 16.2 for non-severe lesions triad p 0.002, while for presence of chest X-ray changes 27% ± 22.344 versus absence of chest X ray changes 66% ± 14.7 p 0.001, for clinical respiratory manifestations 13% ± 13.9 versus none 62% ± 22.9 p < 0.001, for RO− with severe lung lesions 47% ± 30.4 versus RO− without severe lung lesions 69% ± 5.9 p 0.04. There was a tendency for the independent prognostic impact of severe lung involvement; aHR = 1.7 (95% CI 0.92–3.13, p = 0.09).ConclusionAlthough the lung is a low -risk organ per se in LCH, our study demonstrates a non negligeable prognostic impact of severe lung involvement in the risk stratification of pediatric LCH. This warrants further study and external validation.

Single-system pulmonary langerhans cell histiocytosis with only tracheobronchial involvement: a case report

BackgroundPulmonary Langerhans cell histiocytosis (PLCH) only with airway involvement manifested as diffuse thickening of the tracheobronchial walls is rare.Case report A 26-year-old male was admitted to the hospital with progressive wheezing, cough, and a source of blood in sputum after activity. He had no history of smoking. Chest computed tomography showed airway stenosis of different degrees with tracheobronchial wall thickening, and fiberoptic bronchoscopy demonstrated multiple nodular neoplasms in tracheobronchial, while the pulmonary parenchyma was normal. The patient’s condition partially improved after excision of partial lesions by fiberoptic bronchoscope. Histopathological results showed that CD1a and S-100 immunohistochemical staining was positive, and the molecular pathological results suggested that the BRAF V600E mutation, thus confirming the diagnosis of PLCH. The treatment of partial resection and systemic chemotherapy is effective. ConclusionsThe possibility of PLCH needs to be considered when diffuse tracheobronchial lesions without lung parenchyma involvement are encountered, which provides experience for early clinical diagnosis and adequate treatment.

Cladribine treatment in patients with pulmonary Langerhans cell histiocytosis.

Cladribine treatment in patients with pulmonary Langerhans cell histiocytosis.

Lung transplantation as a rescue option in childhood critical pulmonary Langerhans cell histiocytosis.

Lung transplantation as a rescue option in childhood critical pulmonary Langerhans cell histiocytosis.

Long-term outcomes among adults with Langerhans cell histiocytosis

AbstractAdvances in the treatment of Langerhans cell histiocytosis (LCH) have resulted in a growing survivor population. There is a lack of data on long-term outcomes among adults with LCH. We conducted a retrospective record review of 219 adults (aged ≥18 years) with LCH. Most common presentation was multisystem (34.2%), followed by single-system pulmonary (32%), unifocal (28.3%), and single-system multifocal (5.5%) LCH. Risk organ involvement (the liver, spleen, or bone marrow) was seen in 8.7% of cases, and 40 of 88 (45.5%) tested cases were BRAFV600E. At a median follow-up of 74 months, 5-year progression-free survival (PFS) was 58.3% and estimated median PFS was 83 months. Median overall survival (OS) was not reached; 5- and 10-year OS rates were 88.7% and 74.5%, respectively. Risk organ involvement was associated with worse PFS (hazard ratio [HR], 4.5) and OS (HR, 10.8). BRAFV600E was not associated with risk organ involvement or survival. When compared with matched unaffected US population, individuals with LCH had a significantly higher risk of overall mortality (standardized mortality ratio [SMR], 2.66), specifically among those aged <55 years at diagnosis (SMR, 5.94) and those with multisystem disease (SMR, 4.12). Second cancers occurred in 16.4% cases, including diverse hematologic and solid organ malignancies. LCH-associated deaths constituted 36.1% of deaths and occurred within 5 years of diagnosis. After 5 years, non-LCH causes of death, including second cancers, chronic obstructive pulmonary disease, and cardiovascular diseases, predominated. Our study highlights, to our knowledge, for the first time, that adults with LCH experience early and late mortality from non-LCH causes and the need for development of targeted survivorship programs to improve outcomes.

Effects of Smoking Marijuana on the Respiratory System: A Systematic Review.

The prevalence of marijuana use and its derivatives has surged over the past century, largely due to increasing legalization globally. Despite arguments advocating its benefits, marijuana smoking exposes the lungs to harmful combustion byproducts, leading to various respiratory issues such as asthma, pneumonia, emphysema, and chronic obstructive pulmonary disease. We embarked on an extensive literature search, utilizing PubMed/Medline, Scopus, Web of Science, and Google Scholar databases, identifying 200 studies. After the elimination of duplicates, and meticulous review of abstracts and full texts, 55 studies were included in our analysis. Current literature demonstrates that marijuana use negatively impacts lung function, triggering symptoms like chronic cough, sputum production, and wheezing, and diminishing FEV1/FVC ratio in spirometry tests. Moreover, prolonged or chronic marijuana use augments the risk of respiratory function impairment. While the carcinogenic effects of marijuana are still contested, a weak correlation between marijuana use and lung cancer has been observed in some studies. Additionally, instances of other pathologies linked to marijuana use have been reported, including the development of COPD, pulmonary bullae, spontaneous pneumothorax, pleuritic pain, chronic pulmonary aspergillosis, hemoptysis, and pulmonary Langerhans cell histiocytosis. The evidence underscores that marijuana use is detrimental to respiratory health. In light of the escalating trend of marijuana use, particularly among the youth, it is imperative to advocate public health messages discouraging its consumption.

Alpha 1-antitrypsin deficiency in pulmonary langerhans cell histiocytosis: A case report

The association between Pulmonary Langerhans Cell Histiocytosis (PLCH) and Alpha 1-Antitrypsin Deficiency (AATD) is currently undefined; in fact, the largest scientific study available in literature was performed on 50 patients.