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Background and Objective: Severe asthma phenotyping based on invasive and non-invasive bio-markers assists in a better understanding of heterogeneity of clinical presentations and thereby using targeted therapies. Therefore, the current study was conducted to evaluate phenotypes based on non-invasive bio-markers of severe asthma patients attending a tertiary care hospital in North India., Methods: This was a retrospective, observational study conducted on the patients who visited the respiratory department of a tertiary care hospital in North India. Patients aged 18 years and above diagnosed with severe asthma were classified into distinct phenotypes, namely, atopic asthma, eosinophilic asthma, and Type 2 low asthma. Patients with their clinical and functional parameters were classified based on the levels of bio-chemical and hematological results [such as total/specific IgE, blood absolute eosinophil count (AEC)], skin prick tests, history of allergy, and the presence of allergic symptoms., Results: Out of total 100 severe asthmatics, the majority of the patients had an eosinophilic asthma (49%) phenotype, followed by atopic (allergic) asthma (36%) and Type 2 low asthma (15%) phenotypes. However, it was found that 29% of these patients had overlap of both atopy and eosinophilia. The atopic phenotype showed allergic symptoms, positive skin prick tests, and elevated IgE levels. The eosinophilic phenotype had high AEC (≥300 cells/uL) and low IgE (< 30 IU/ml) levels. The Type 2 low phenotype showed low AEC and IgE levels along with the absence of allergic symptoms. However, among these 100 patients, overlapping traits of both atopy and eosinophilia were labelled as overlap phenotypes. 50% of type 2 low severe asthma cases had eosinophils >150 cells/cmm and were eligible for mepolizumab., Conclusions: Identification of severe asthma pheno-endotypes based on simple non-invasive bio-markers is feasible in Indian settings, and it is of utmost importance for future treatment planning in these patients with available biologicals. Overlap of eosinophilic and atopic endotypes in one-third cases would challenge physicians to choose upfront appropriate biologicals in our country. Type 2 low asthma was least common with only <10% cases of severe asthma being ineligible for any biological., Competing Interests: None

Literature on concurrent association of sarcoidosis with lymphoproliferative malignancies other than lymphoma e.g. multiple myeloma is meager. The rarity of the situation prompted us to report this patient who was a 51-year-old woman with a 2-years history of breathlessness, cough with expectoration, chest pain and backache. Initial evaluation revealed mild anemia, increased alkaline phosphatase with chest skiagram showing both lower zone non homogenous opacities with calcified hilar lymph nodes. CECT chest showed mediastinal with bilateral hilar lymphadenopathy, parenchymal fibrosis, traction bronchiectasis, ground glass opacities, septal and peribronchovascular thickening affecting mid and lower lung zones bilaterally. MRI Dorsolumbar spine was suggestive of marrow infiltrative disorder. EBUS FNA of intrathoracic nodes, EBB and TBLB confirmed sarcoidosis. PET CT revealed hyper metabolic activity in lung, multiple lymph nodes and lytic bone lesions. Serum protein electrophoresis and immunofixation revealed a monoclonal paraprotein, immunoglobulin IgG kappa type. Bone marrow biopsy revealed an increase in plasma cells (15%), but no granulomas. Diagnosis of Indolent or multiple myeloma with sarcoidosis was established. 12 cases of sarcoidosis and multiple myeloma have been reported in literature, and mostly preceding the onset of multiple myeloma by many years, in our case both were diagnosed concurrently.

A 47-year-old-female presented with dyspnea and unproductive cough for 4 months. General examination revealed pulsatile swelling in the midline below the thyroid cartilage present since childhood. Computed tomography-angiography of the neck showed right innominate artery dilated, elongated and coursing above downward, anterior to the trachea below the thyroid, compressing the trachea and origin of the right subclavian artery higher up. A case of anomalous innominate artery causing symptomatic compression of the trachea in adults is a rare entity.