Pulmonary Alveolar Proteinosis (PAP) is a rare lung disease characterized by excessive accumulation of surfactant lipids and proteins in alveoli and terminal airways. It is caused by impaired GM-CSF signaling [1]. Surfactant is synthesized and secreted by alveolar type II epithelial cells, and removed by uptake and catabolism by these cells, and the alveolar macrophages. Patients with PAP usually describe gradual onset of progressive exertional dyspnea and non-productive cough. However, an asymptomatic presentation is observed in up to 25% of cases, even in the presence of diffuse radiographic changes. Three recognized subtypes exist. Autoimmune PAP is associated with neutralizing GM-CSF autoantibodies and accounts about 90% of cases. Secondary PAP may occur in the context of any disease that reduces the abundance or functionality of alveolar macrophages, resulting in impaired surfactant clearance. Congenital PAP is the result of genetic mutations that disrupt GM-CSF signaling, including mutations in the α- or β-chains of the GM-CSF receptor [1-3].

This case shown here represents a rare situation where the breast implant is spontaneously and inadvertently migrated from its submammary position via the thoracic wall into the ipsilateral pleural cavity after performing an ipsilateral thoracotomy due to atypical wedge resection of the right upper lobe four months ago. Intraoperatively, the implant has been neither dislodged nor manipulated in any way. In the literature, there are some sparse case descriptions where such breast implant migrations are encountered after VATS procedure (video-assisted thoracoscopy) [2] and open thoracotomy surgery [3]. Interestingly, our case report is quite similar to those which was published by Dutch colleagues in 2014 [4]. Considering the etiology and pathomechanism of such an implant migration as shown here, there is a common agreement that both a leakage of the implant´s fibrous capsule and an operative transection of the intercostal thoracic wall are prerequisite to create a potential migrating pathway to allow implants moving towards the pleural cavity [5]. Additionally, it is believed that the negative pressure within the pleural cavity also alleviates the unidirectional herniation by “sucking in the implant” into the interpleural space [6]. Sometimes, external repetitive pressures such as stretching massages may cause or trigger such an implant dislocation. Furthermore, there are cases described in which, seemingly, implant migration does occur without known preceding thoracic surgery [7]. Eventually, there are cases published in the literature with intrapleural spreading of disrupted breast implant debris [8]. With our patient, thanks to the absence of any discomfort or pain, it was concluded after agreed statement of an interdisciplinary round table discussion not to remove the dislocated implant surgically because of potential intercostal tissue damage and subsequent pain to await. More astonishing, the clinicians involved in this case wondered the fact that the missed implant of her right breast remained either unnoticed or has been completely neglected by the female patient. In this short communication, we present a rare and unusual case of an obviously vanishing breast implant which is found to be inadvertently migrated into the adjacent pleural space after undergoing thoracic surgery. According to common legal policy at our institution, an approval for case reports is generally provided as it was obtained in this particular case.

Despite the fact, that lung cancer is more common among older smoking men, however it may also develop among young women without a smoking anamnesis. We report here a history of a non-smoking woman, 40 years old, with a diagnosis of lung adenocarcinoma at IV stage. Despite the fact, the woman received three lines of palliative chemotherapy, the disease progressed. After the sample of the tumor was tested by genetic approach, ROS1 mutation was detected, and the patient was treated with a ROS1 inhibitor, Crizotinib. Sharp improvement was observed already after the first week of treatment. After one-month adenocarcinoma shrink, and specific supraclavicular lymph nodes disappeared. Unfortunately, due to problems with financing the treatment was stopped, after what the disease began to progress rapidly, and the patient died after a month due to brain metastasis. This case is noteworthy also because the patient was first diagnosed a thrombophilia with thrombi present in deep calf veins, left heart ventricle and lungs Adenocarcinoma was discovered occasionally when during video-assisted thoracoscopic surgery biopsy specimen was taken from suspicious mass in the lower lobe of the right lung. This story reminds us that lung carcinoma may start with a paraneoplastic syndrome, like thrombophilia as in this case and finding of adenocarcinoma of the lung in young, non-smoking persons is indicative for possible ROS1 gene mutation. In such cases early treatment with ROS1 protein-tyrosine kinase inhibitors should be started as soon as possible.

Pulmonary mucormycosis is an uncommon pulmonary fungal disease, which is commonly seen in immunocompromised individuals. It is caused by fungi of class Zygomycetes. It constitutes the third most common invasive fungal infection following aspergillosis and candidiasis. Risk factors include patients with hematological malignancies, diabetes mellitus, and immunocompromised states. It is difficult to diagnose early due to non-specific clinical presentation and delay in treatment associated with greater mortality. As we know that Tuberculosis and HIV are highly prevalent in country like India. Post pulmonary tuberculosis is emerging as a risk factor for Pulmonary mucormycosis in the developing countries like India. Patients with non-resolving pneumonia are generally misdiagnosed as Pulmonary tuberculosis. The diagnosis of Pulmonary Mucormycosis is based upon demonstration of fungal hyphae in the clinical specimen. We highlight the importance of clinical suspicion in these cases for early diagnosis and early treatment initiation can reverse morbidity and mortality associated with Pulmonary Mucormycosis. We report 2 cases of Pulmonary mucormycosis present in post-pulmonary tuberculosis patients.

As we know that, Asthma and chronic obstructive pulmonary diseases are well characterized diseases, they can co-exist as asthma-COPD overlap (ACO). The co-existence of asthma-chronic obstructive pulmonary disease overlap (ACO) in chronic obstructive pulmonary disease (COPD) patients is often unrecognized. In patients with a primary diagnosis of COPD or Asthma, the identification of ACO has got implication for better prognosis and treatment. Such patients experience frequent exacerbations, poor quality of life, rapid decline in lung function and high mortality than COPD or Asthma alone. Inhalational steroids provide significant alleviation of symptoms in such patients and some studies suggest that the most severe patients may respond to biological agents indicated for severe asthma. Patients who have asthma with a COPD component tend to present with severe hypoxia because of Irreversible/fixed airway obstruction and impairment of the alveolar diffusion capacity by emphysematous changes. In contrast, patients with COPD who have an asthma component not only have exertional dyspnoea but also develop paroxysmal wheezing or dyspnoea at night or in the early morning. The criteria to diagnose asthma-COPD overlap (ACO) include positive bronchodilator response, sputum eosinophilia or previous diagnosis of asthma, high IgE and/or history of atopy. There is scarcity of literature available in country like India. We highlight the importance of identification of Asthma COPD overlap as different phenotype from COPD or asthma alone as it is challenging to diagnose ACO in India. We report 3 cases having both the features of asthma and COPD, later diagnosed with Asthma-COPD overlap.

Organizing pneumonia (OP), can be seen in association with lung injury, infection, drug intoxication, and connective tissue diseases. Patients of rheumatoid arthritis (RA) are prone to develop interstitial lung disease (ILD), but the pulmonary involvement usually occurs several years after the joint manifestations. Only in about 10% cases of RA, the initial manifestation of the disease can be in the form of interstitial lung disease. OP as the initial manifestation of RA is extremely uncommon occurrence. Here is presented a case of 52-year-old male who presented with OP as the initial manifestation of RA. On investigation, the RA factor and anti-CCP Antibodies were positive. Based on clinical, radiological and histopathological findings the diagnosis was established.

Cystic fibrosis is explained in this paper that suggests tackling the disease by elimination of the most significant sources of contamination.

Introduction: the perennial pandemic: There are serious challenges posed by the SARS-CoV-2 virus and COVID-19 as the disease. With the persistence of the pandemic over one and half year, it is being feared that the COVID-19 may have become the new reality associated with human existence world over and the mankind may have to live with it for years or even decades. Further, the grievous nature of the disease is evolving further with genomic changes in the virus in form of mutations and evolution of variants, with enhanced infectivity and probably virulence. Acute and chronic phases of COVID-19: Epidemiologically, it is becoming clear that apart from the advanced age and pre-existing conditions, such as diabetes, cardiovascular, pulmonary, and renal diseases, certain constituent factors render some patients more vulnerable to more severe forms of the disease. These factors influence the COVID-19 manifestations, its course, and later the convalescence period as well as the newly defined ‘Long COVID phase. The substantial continuing morbidity after resolution of the infection indicates persisting multisystem effects of ‘Long Covid’. Lung damage associated with COVID-19: COVID-19 is primarily a respiratory disease presenting with a broad spectrum of respiratory tract involvement ranging from mild upper airway affliction to progressive life-threatening viral pneumonia and respiratory failure. It affects the respiratory system in various ways across the spectrum of disease severity, depending on age, immune status, and comorbidities. The symptoms may be mild, such as cough, shortness of breath and fevers, to severe and critical disease, including respiratory failure, shock, cytokine crisis, and multi-organ failure. Implications for the post-COVID care: Depending on the severity of respiratory inflammation and damage, as well as associated comorbidities, duration of injury and genetics, the progressive fibrosis leads to constriction and compression of lung tissues and damage to pulmonary microvasculature. Consequently, the COVID-19 patients with moderate/severe symptoms are likely to have a significant degree of long-term reduction in lung function. Depending on the severity of the disease, extensive and long-lasting damage to the lungs can occur, which may persist after resolution of the infection. Managing the long COVID’s challenges: Given global scale of the pandemic, the healthcare needs for patients with sequelae of COVID-19, especially in those with lung affliction are bound to increase in the near future. The challenge can be tackled by harnessing the existing healthcare infrastructure, development of scalable healthcare models and integration across various disciplines with a combination of pharmacological and non-pharmacological modalities. Following clinical and investigational assessment, the therapeutic strategy should depend on the disease manifestations, extent of damage in lungs and other organs, and associated complications.

Meigs syndrome is an uncommon presentation, where a benign ovarian neoplasia presents along with ascites and pleural effusion. About 1% of ovarian neoplasia can present as Meigs syndrome. Patients with Meigs’ syndrome and elevated serum CA-125 are not frequently reported. We report a case of a 50-year-old women who presented with shortness of breath, cough, weight loss of one and half month duration. Chest radiograph of the patient with clinical examination of patient confirms pleural effusion as cause of progressive shortness of breath. The presence of a pelvic mass and elevated serum CA-125, which raised the possibility of malignancy. After complete resection of tumor, the pathologic reports confirmed a benign ovarian neoplasia. We highlight the importance of suspicion, careful general examination, radiological assessment and histological tests to confirm the diagnosis of Meigs’ syndrome.

Chronic fatigue syndrome (CFS) is a poorly-understood respiratory condition that affects millions of individuals. Hyperbaric oxygen therapy (HBOT) is a treatment option being considered to address CFS as it is suggested to combat fatigue and increase oxygenation. HBOT provides two opportunities in advancing research of CFS: it may provide data on symptom amelioration and be utilized in the search for a biomarker. By either identifying biomarkers before using HBOT to compare epigenomes of patients before and after treatment or using HBOT to find epigenetic discrepancies between patients with and without treatment, matching epigenetic regulation with symptom amelioration may significantly advance the understanding of the etiology and treatment mechanism for CFS. EPAS1/HIF-2α is a leading candidate for an epigenetic biomarker as it responds differentially to hypoxic and normoxic conditions, which degrades more slowly in hypoxic conditions. Epigenetic regulation of EPAS1/HIF-2α in such differential conditions may be explored in HBOT experiments. In addition to HBOT as a promising treatment option for CFS symptoms, it may aid the identification of biomarkers in CFS. Further research into both outcomes is strongly encouraged.