Susan K. Mathai M.D.

Zeynalyan, A.A., Kolasani, B., Naik, C., Sigakis, C.J.G., Silhan, L. and Mathai, S.K. (2021). “Rapidly progressive respiratory failure after helminth larvae ingestion.” BMC Pulm Med 21(1): 422.

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BACKGROUND: Self-administration of helminths has gained attention among patients as a potential but unproven therapy for autoimmune disease. We present a case of rapidly progressive respiratory failure in a patient with systemic sclerosis (SSc) and pulmonary arterial hypertension (PAH) as a result of self-administration of parasitic organisms. CASE: A 45-year-old woman with a history of interstitial lung disease and PAH due to limited cutaneous SSc presented to pulmonary clinic with worsening dyspnea, cough, and new onset hypoxemia. Three months prior to presentation she started oral helminth therapy with Necator americanus as an alternative treatment for SSc. Laboratory evaluation revelaed eosinophilia and elevated IgE levels. IgG antibodies to Strongyloides were detected. High resolution computed tomography of the chest revealed progressive ILD and new diffuse ground glass opacities. Transthoracic echocardiogram and right heart catheterization illustrated worsening PAH and right heart failure. The patient was admitted to the hospital and emergently evaluated for lung transplantation but was not a candidate for transplantation due to comorbidities. Despite aggressive treatment for PAH and right heart failure, her respiratory status deteriorated, and the patient transitioned to comfort-focused care. CONCLUSION: Although ingestion of helminths poses a risk of infection, helminth therapy has been investigated as a potential treatment for autoimmune diseases. In this case, self-prescribed helminth ingestion precipitated fatal acute worsening of lung inflammation, hypoxemia, and right heart dysfunction, highlighting the risk of experimental helminth therapy in patients, especially those with underlying respiratory disease.

Naik, C.A., Mathai, S.K., Sandkovsky, U.S., Ausloos, K.A., Guileyardo, J.M., Schwartz, G., Mason, D.P., Gottlieb, R. and Grazia, T.J. (2021). “Acute myocardial infarction secondary to mucormycosis after lung transplantation.” IDCases 23: e01019.

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We present a case of a 57-year-old man who underwent bilateral lung transplantation for idiopathic pulmonary fibrosis. His immediately post-operative course was complicated by fever and cardiac arrest. Despite supportive care and broad-spectrum antibiotics, he experienced continued clinical decline. Autopsy results indicated angioinvasive mucormycosis and coronary arteritis resulting in acute myocardial infarction as the cause of death.

Mathai, S.K., Cardwell, J., Metzger, F., Powers, J., Walts, A.D., Kropski, J.A., Eickelberg, O., Hauck, S.M., Yang, I.V. and Schwartz, D.A. (2020). “Preclinical Pulmonary Fibrosis Circulating Protein Biomarkers.” Am J Respir Crit Care Med 202(12): 1720-1724.

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Idiopathic pulmonary fibrosis (IPF) is characterized by progressive, irreversible scarring of the lung parenchyma that can require invasive diagnostic testing (1). Interstitial lung abnormalities (ILAs) have been described in the general population (2). Among asymptomatic first-degree relatives of patients with familial interstitial pneumonia (FIP), 14% have radiologic ILAs and 35% have interstitial abnormalities on biopsy (3). In the Framingham population, fibrotic ILAs were present in 1.8% of subjects ≥50 years of age (4) and associated with increased risk of death (5, 6), suggesting ILAs may be a harbinger of IPF. [No abstract; excerpt from article].

Mathai, S. K., J. Cardwell, F. Metzger, J. Powers, A. D. Walts, J. A. Kropski, O. Eickelberg, S. M. Hauck, I. V. Yang and D. A. Schwartz (2020). “Preclinical Pulmonary Fibrosis (PrePF) Circulating Protein Biomarkers.” Am J Respir Crit Care Med Aug 5. [Epub ahead of print.].

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Idiopathic pulmonary fibrosis (IPF) is characterized by progressive, irreversible scarring of the lung parenchyma that can require invasive diagnostic testing. Interstitial lung abnormalities (ILA) have been described in the general population. Among asymptomatic first-degree relatives of Familial Interstitial Pneumonia (FIP) patients, 14% have radiologic ILA and 35% have interstitial abnormalities on biopsy. In the Framingham population, fibrotic ILA were present in 1.8% of subjects ≥50 years of age and associated with increased risk of death (5, 6), suggesting ILA may be a harbinger of IPF. [No abstract; excerpt from article].

Bailey, K. L., H. Smith, S. K. Mathai, J. Huber, M. Yacoub, I. V. Yang, T. A. Wyatt, K. Kechris and E. L. Burnham (2020). “Alcohol Use Disorders Are Associated With a Unique Impact on Airway Epithelial Cell Gene Expression.” Alcohol Clin Exp Res Jun 11. [Epub ahead of print.].

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BACKGROUND: Alcohol use disorders (AUDs) and cigarette smoking both increase risk for the development of community-acquired pneumonia (CAP), likely through adverse effects on proximal airway mucociliary clearance and pathogen recognition. Smoking-related alterations on airway gene expression are well described, but little is known about the impact of AUDs. We measured gene expression in human airway epithelial cells (AECs), hypothesizing that AUDs would be associated with novel differences in gene expression that could alter risk for CAP. METHODS: Bronchoscopy with airway brushings was performed in participants with AUDs and controls to obtain AECs. An AUD Identification Test was used to define AUD. RNA was extracted from AECs, and mRNA expression data were collected on an Agilent micro-array. Differential expression analyses were performed on the filtered and normalized data with correction for multiple testing. Enrichment analyses were performed using clusterProfiler. RESULTS: Expression data from 19 control and 18 AUD participants were evaluated. After adjustment for smoking, AUDs were associated with significant differential expression of 520 AEC genes, including genes for ribosomal proteins and genes involved in protein folding. Enrichment analyses indicated significant differential expression of 24 pathways in AUDs, including those implicated in protein targeting to membrane and viral gene expression. Smoking-associated AEC gene expression differences mirrored previous reports, but differed from those associated with AUDs. CONCLUSIONS: AUDs have a distinct impact on AEC gene expression that may influence proximal airway function independent of smoking. Alcohol-associated alterations may influence risk for CAP through modifying key mechanisms important in protecting proximal airway integrity.