Granular cell tumours are rare, mostly benign masses that arise from Schwann cells. Their pathophysiology is poorly understood, but the lesions are often seen in the breast, tongue, and skin. In this case report, we discuss a 34-year-old patient with recurrent pneumonia. The patient had several comorbidities, and was intubated due to respiratory distress and eventually placed on tracheostomy. During the procedure, she was noted to have a right middle lobe endobronchial lesion. It was excised and identified as a granular cell tumour. The patient was later weaned off the ventilator and discharged without any complications.

Severe lupus pneumonitis is a rare and life-threatening complication of systemic lupus erythematosus (SLE), characterized by its rapid progression and high mortality rate. This case report describes the clinical trajectory and therapeutic management of a young Aboriginal female with established lupus nephritis who developed severe lupus pneumonitis. Despite her stable renal condition under long-term immunosuppressive treatment, she experienced acute respiratory distress, leading to her admission to the intensive care unit and subsequent mechanical ventilation. The diagnostic process was complicated by the difficulty in obtaining tissue biopsies, necessitating reliance on clinical judgement and radiological evidence to formulate a diagnosis. The patient was treated with pulsed intravenous methylprednisolone followed by rituximab infusions, resulting in significant clinical and radiological improvement. This case highlights the importance of early and intensive immunosuppressive therapy in the management of severe lupus pneumonitis and underscores the utility of a multidisciplinary approach in overcoming diagnostic ambiguities. Furthermore, it contributes to the growing body of evidence supporting the efficacy of rituximab in severe lupus pneumonitis cases, offering insights into potential therapeutic avenues when conventional management strategies are inadequate or unsuitable.

BACKGROUND: Multidrug-resistant tuberculosis is a type of tuberculosis that is resistant to at least the first-line antituberculosis drugs namely, rifampicin and isoniazid. However, most of these studies were limited only to a single hospital. Therefore, this study aimed to identify the determinants of multidrug-resistant tuberculosis among adults undergoing treatment for tuberculosis in the Tigray region of Ethiopia.
METHODS: Hospital-based unmatched case-control study was conducted from 1 April 2019 to 30 June 2019. A simple random sampling method was used to select the required sample size. Variables at a p value less than 0.25 in bivariate analysis were entered into a multivariable analysis to identify the determinant factors of multidrug-resistant tuberculosis. Finally, the level of significance was declared at p<0.05.
RESULTS: Rural residence (adjusted OR (AOR) 2.54; 95% CI 1.34 to 4.83), HIV (AOR 4.5; 95% CI 1.4 to 14.2), relapse (AOR 3.86; 95% CI 1.98 to 7.5), return after lost follow-up (AOR 6.29; 95% CI 1.64 to 24.2), treatment failure (AOR 5.87; 95% CI 1.39 to 24.8) were among the determinants of multidrug-resistant tuberculosis.
CONCLUSIONS: Rural residence, HIV, relapses, return after lost follow-up and treatment failure were the identified determinant factors of multidrug-resistance tuberculosis.

Mycobacterium thermoresistibile is a thermotolerant nontuberculous mycobacterium which can rarely result in human infection. Although immunosuppression has been identified as a risk factor for infection, it is possible that mycobacterial laboratories may have previously under-recognized M. thermoresistibile as standard mycobacterial incubation temperatures are suboptimal for culture of this organism. Here, we present a case of severe M. thermoresistibile pneumonia associated with achalasia requiring life support in the intensive care unit. We speculated that the interplay between specific host and environmental risk factors contributed to acquisition of infection. Infection with this fastidious organism required prolonged treatment with multiple antimicrobials and adjunctive therapeutic drug monitoring which led to clinical cure despite residual lung injury. We also reviewed literature documenting cases of human infection with M. thermoresistibile. The diagnosis of M. thermoresistibile requires a high degree of clinical suspicion considering its association with immunosuppressive conditions, postulated environmental inoculation and eponymous culture growth characteristics.

In cases of Sweet\'s syndrome with pulmonary involvement, fever of unknown origin, and macrocytic anaemia, VEXAS syndrome can be considered in the differential diagnosis. A 67-year-old man who was taking prednisolone for a fever of unknown origin and Sweet\'s syndrome was referred to us because of an abnormal chest shadow. Computed tomography revealed a nonfibrotic hypersensitivity pneumonitis-like opacity, and blood test results indicated macrocytic anaemia. His pulmonary symptoms spontaneously improved but again exacerbated approximately 1 month later. Methylprednisolone pulse therapy improved his condition, but he had recurring fever flare and pulmonary involvement post-treatment. A peripheral blood UBA1 gene test planned at a specialized institution was not performed, making the diagnosis difficult. We attempted careful tapering of methylprednisolone, but his macrocytic anaemia led to pancytopenia and he unfortunately died of sepsis due to neutropenia.

Hepatopulmonary syndrome (HPS) is the triad of liver disease, hypoxia and intrapulmonary shunt. In this case report, we describe an immunocompromised female with a background of common variable immunodeficiency (CVID) who presented with haemoptysis and dyspnoea. Investigations demonstrated significant hypoxaemia and intrapulmonary right-to-left shunting. Further evidence revealed advanced liver cirrhosis, and a diagnosis of HPS was made. This extremely rare association of CVID and HPS is one of the few cases reported in the literature.

Chronic interstitial lung abnormalities have been described in sickle cell disease (SCD) and attributed to repetitive episode of acute chest syndrome. We report a series of 22 cases of diffuse cystic lung disease in SCD with a case-control study to hunt for mechanism. On pathological analysis of a surgical lung biopsy of the index case, the bronchioles had the appearance of constrictive bronchiolitis. Pulmonary function test results revealed lower forced expiratory flow from 25% to 75% of vital capacity in cases versus controls. These findings suggest a bronchiolar mechanism that was not associated with more acute chest syndrome.

Patients with interstitial lung disease (ILD) are known to develop an acute exacerbation (AE) after surgery. Previous studies have evaluated the predictors of postoperative AE. However, it remains unclear whether the results of those studies can be generalised to patients with different types of ILD and/or extrapolated to those who undergo non-pulmonary surgery. This study aimed to elucidate the predictors of the development of AE after surgery with general anaesthesia in patients with ILD.
We conducted a nested matched case-control study of 700 patients from an initial cohort of 50 840 patients. We excluded those who underwent solid organ or bone marrow transplantation. The cases were patients with ILD who developed AE within 30 days postoperatively, whereas the controls did not develop AE. Each case (n=28) was matched with four controls (n=112) for sex, year of surgery and multiple operations within 30 days. Furthermore, a multivariable conditional logistic regression analysis was used to identify significant predictors, as indicated by a p value of <0.05.
After adjusting for potential confounders, the multivariable conditional logistic regression analysis identified honeycombing on CT (OR 3.09; 95% CI 1.07 to 8.92), a per cent predicted FVC <80% (OR 4.21; 95% CI 1.46 to 12.2) and an ARISCAT score ≥45 (OR 6.14; 95% CI 2.10 to 18.0) significantly associated with the development of postoperative AE.
We found that the three factors were independent predictors for the development of postoperative AE in patients with ILD. These predictors are advantageous because they can be readily evaluated before surgery by surgeons and anaesthesiologists even without consulting experienced pulmonologists.

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BACKGROUND: Pulmonary tumor thrombotic microangiopathy is a special type of tumor thromboembolism. We report the case of a patient who developed pulmonary tumor thrombotic microangiopathy with alveolar hemorrhage. Almost all patients with pulmonary tumor thrombotic microangiopathy die within 1 week of the onset of dyspnea; however, the prognosis in this case was better, with 10 weeks of survival from presentation.
METHODS: A 62-year-old Japanese man was referred to our hospital with a 4-week history of dyspnea on exertion and severe pulmonary hypertension. Five years previously, he had undergone distal gastrectomy for gastric cancer. He was afebrile, normotensive, and hypoxemic. A physical examination was unremarkable except for purpura on his upper extremities and trunk. Blood tests showed anemia and disseminated intravascular coagulation. Chest computed tomography revealed diffuse ground-glass opacities with emphysema in his upper lungs, moderate pleural effusions, mediastinal lymphadenopathy, and enlargement of the right ventricle and main pulmonary artery. A computed tomography pulmonary angiogram showed no evidence of pulmonary embolism. Lung perfusion scintigraphy showed multiple segmental defects. Although recurrence of gastric cancer was confirmed from the results of bone marrow biopsy, bronchoscopy was not performed due to bleeding diathesis. He was treated with corticosteroids, antibiotics, and platelet transfusion, following which resolution of the abnormal lung shadows and right ventricular pressure overload along with partial alleviation of respiratory failure was observed. Because of his poor performance status, he was eventually transited to palliative care and died 6 weeks after admission. Necropsy of the lung confirmed the diagnosis of pulmonary tumor thrombotic microangiopathy with alveolar hemorrhage.
CONCLUSIONS: Pulmonary tumor thrombotic microangiopathy should be considered in the differential diagnosis of patients with cancer who present with severe pulmonary hypertension. In pulmonary tumor thrombotic microangiopathy, local inflammation in pulmonary microvasculature may contribute to pulmonary hypertension, and regulation of inflammation using corticosteroids may help improve the prognosis.