Try a new search

Format these results:

Searched for:



Total Results:


Outcomes after long-term mechanical ventilation of cancer patients

Haviland, Kelly; Tan, Kay See; Schwenk, Nadja; Pillai, Manju V; Stover, Diane E; Downey, Robert J
BACKGROUND:The probability of weaning and of long-term survival of chronically mechanically ventilated cancer patients is unknown, with incomplete information available to guide therapeutic decisions. We sought to determine the probability of weaning and overall survival of cancer patients requiring long-term mechanical ventilation in a specialized weaning unit. METHODS:A single-institution retrospective review of patients requiring mechanical ventilation outside of a critical care setting from 2008 to 2012 and from January 1 to December 31, 2018, was performed. Demographic and clinical data were recorded, including cancer specifics, comorbidities, treatments, and outcomes. Overall survival was determined using the Kaplan-Meier approach. Time to weaning was analyzed using the cumulative incidence function, with death considered a competing risk. Prognostic factors were evaluated for use in prospective evaluations of weaning protocols. RESULTS:Between 2008 and 2012, 122 patients required mechanical ventilation outside of a critical care setting with weaning as a goal of care. The cumulative incidence of weaning after discharge from the intensive care unit was 42% at 21 days, 49% at 30 days, 58% at 60 days, 61% at 90 days, and 61% at 120 days. The median survival was 0.16 years (95% CI, 0.12 to 0.33) for those not weaned and 1.05 years (95% CI, 0.60 to 1.34) for those weaned. Overall survival at 1 year and 2 years was 52 and 32% among those weaned and 16 and 9% among those not weaned. During 2018, 36 patients at our institution required mechanical ventilation outside of a critical care setting, with weaning as a goal of care. Overall, with a median follow-up of 140 days (range, 0-425 days; average, 141 days), 25% of patients requiring long-term mechanical ventilation (9 of 36) are alive. CONCLUSIONS:Cancer patients can be weaned from long-term mechanical ventilation, even after prolonged periods of support. Implementation of a resource-intensive weaning program did not improve rates of successful weaning. No clear time on mechanical ventilation could be identified beyond which weaning was unprecedented. Short-term overall survival for these patients is poor.
PMID: 32228554
ISSN: 1472-684x
CID: 4458182

Pulmonary toxicity

Chapter by: Pillai, Manju
in: DeVita, Hellman, and Rosenberg's cancer : principles & practice of oncology by DeVita, Vincent T; Lawrence, Theodore S; Rosenberg, Steven A (Eds)
Philadelphia : Wolters Kluwer, copyright 2019
pp. ?-?
ISBN: 1496394631
CID: 3799542


Lixon, A.; Pillai, M.; Abdulfattah, O.; Weinstein, M.
ISSN: 0161-8105
CID: 4458292

A Case of Unilateral Pleural Effusion with Large Thyroid Mass [Meeting Abstract]

Reid, E.; Pillai, M.
ISSN: 1073-449x
CID: 4458302


Mehta, Vishisht; Pillai, Manju
ISSN: 0012-3692
CID: 4458192

Rasburicase Induced Methemoglobinemia in a Patient with G6PD Deficiency- A Review of Pathophysiology and Treatment Considerations [Meeting Abstract]

Makkar, P.; Pillai, M. V.; Mehta, V.
ISSN: 1073-449x
CID: 4458202

Relapsing Pulmonary Nocardiosis From Various Species Within a Single Host [Meeting Abstract]

Gupta, Karan; Pillai, Manju
ISSN: 0012-3692
CID: 3534762

A Troubling Trifecta: Pulmonary Alveolar Proteinosis and Pneumocystis Pneumonia in Acute Myeloid Leukemia [Meeting Abstract]

Patel, Priya; Lee, Robert; Pillai, Manju; Stover, Diane
ISSN: 0012-3692
CID: 3534752

Ribosomal RNA gene sequencing for early diagnosis of Blastomyces dermatitidis infection [Case Report]

Morjaria, Sejal; Otto, Caitlin; Moreira, Andre; Chung, Romy; Hatzoglou, Vaios; Pillai, Manju; Banaei, Niaz; Tang, Yi-Wei; Figueroa, Cesar J
Prompt detection and identification of fungal pathogens at the genus and species level is critical in order to provide timely antifungal therapy. Here, we highlight the vital role of molecular diagnostics in achieving a fast and definitive diagnosis of disseminated blastomycosis in a diabetic patient presenting as a brain mass initially thought to be tumoral in nature. A broad-range PCR amplification and sequencing of the fungal ribosomal RNA genes on brain biopsy tissue obtained during elective craniotomy revealed a final microbial identification of Ajellomyces dermatitidis (telemorph of Blastomyces dermatitidis).
PMID: 26129971
ISSN: 1878-3511
CID: 3546982

α1-Antitrypsin activates protein phosphatase 2A to counter lung inflammatory responses

Geraghty, Patrick; Eden, Edward; Pillai, Manju; Campos, Michael; McElvaney, Noel G; Foronjy, Robert F
RATIONALE/BACKGROUND:α1-Antitrypsin (A1AT) was identified as a plasma protease inhibitor; however, it is now recognized as a multifunctional protein that modulates immunity, inflammation, proteostasis, apoptosis, and cellular senescence. Like A1AT, protein phosphatase 2A (PP2A), a major serine-threonine phosphatase, regulates similar biologic processes and plays a key role in chronic obstructive pulmonary disease. OBJECTIVES/OBJECTIVE:Given their common effects, this study investigated whether A1AT acts via PP2A to alter tumor necrosis factor (TNF) signaling, inflammation, and proteolytic responses in this disease. METHODS:PP2A activity was measured in peripheral blood neutrophils from A1AT-deficient (PiZZ) and healthy (PiMM) individuals and in alveolar macrophages from normal (60 mg/kg) and high-dose (120 mg/kg) A1AT-treated PiZZ subjects. PP2A activation was assessed in human neutrophils, airway epithelial cells, and peripheral blood monocytes treated with plasma purified A1AT protein. Similarly, lung PP2A activity was measured in mice administered intranasal A1AT. PP2A was silenced in lung epithelial cells treated with A1AT and matrix metalloproteinase and cytokine production was then measured following TNF-α stimulation. MEASUREMENTS AND MAIN RESULTS/RESULTS:PP2A was significantly lower in neutrophils isolated from PiZZ compared with PiMM subjects. A1AT protein activated PP2A in human alveolar macrophages, monocytes, neutrophils, airway epithelial cells, and in mouse lungs. This activation required functionally active A1AT protein and protein tyrosine phosphatase 1B expression. A1AT treatment acted via PP2A to prevent p38 and IκBα phosphorylation and matrix metalloproteinase and cytokine induction in TNF-α-stimulated epithelial cells. CONCLUSIONS:Together, these data indicate that A1AT modulates PP2A to counter inflammatory and proteolytic responses induced by TNF signaling in the lung.
PMID: 25341065
ISSN: 1535-4970
CID: 3534692