Amit Chopra
Albany Medical College
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Amit Chopra.
Expert Review of Clinical Immunology | 2016
Amit Chopra; Alexandros Kalkanis; Marc A. Judson
ABSTRACT Introduction: Numerous biomarkers have been evaluated for the diagnosis, assessment of disease activity, prognosis, and response to treatment in sarcoidosis. In this report, we discuss the clinical and research utility of several biomarkers used to evaluate sarcoidosis. Areas covered: The sarcoidosis biomarkers discussed include serologic tests, imaging studies, identification of inflammatory cells and genetic analyses. Literature was obtained from medical databases including PubMed and Web of Science. Expert commentary: Most of the biomarkers examined in sarcoidosis are not adequately specific or sensitive to be used in isolation to make clinical decisions. However, several sarcoidosis biomarkers have an important role in the clinical management of sarcoidosis when they are coupled with clinical data including the results of other biomarkers.
Thorax | 2017
Philip Svigals; Amit Chopra; James G. Ravenel; Paul J. Nietert; John T. Huggins
We compared the accuracy of pleural ultrasound versus chest CT versus chest radiograph (CXR) to determine radiographic complexity in predicting a complicated parapneumonic effusion (CPPE) defined by pleural fluid analysis. 66 patients with parapneumonic effusions were identified with complete data. Pleural ultrasound had a sensitivity of 69.2% (95% CI 48.2% to 85.7%) and specificity of 90.0% (95% CI 76.3% to 97.2%). Chest CT had a sensitivity of 76.9% (95% CI 56.3% to 91.0%) and specificity of 65.0% (95% CI 48.3% to 79.4%). CXR had a sensitivity of 61.5% (95% CI 40.6% to 79.8%) and specificity of 60.0% (95% CI 43.3% to 75.1%). Pleural ultrasound appears to be a superior modality to rule in a CPPE when compared with chest CT and CXR.
Current Opinion in Pulmonary Medicine | 2015
Amit Chopra; Marc A. Judson
Purpose of review Several studies have suggested an association between sarcoidosis and cancer, and between sarcoidosis and connective tissue diseases (CTDs). In this review, we discuss the evidence supporting and refuting these associations. Recent findings In terms of a cancer risk in sarcoidosis patients, the data are somewhat conflicting but generally show a very small increased risk. The data supporting an association between sarcoidosis and CTD are not as robust as for cancer. However, it appears that scleroderma is the CTD most strongly associated with sarcoidosis. Summary There are several important clinical and research-related implications of the association of sarcoidosis and CTDs. First, rigorous efforts should be made to exclude alternative causes for granulomatous inflammation before establishing a diagnosis of sarcoidosis. Second, the association between sarcoidosis and both cancer and CTDs may yield important insights into the immunopathogenesis of all three diseases. Finally, these data provide insight in answering a common question asked by sarcoidosis patients, ‘Am I at an increased risk of developing cancer?’ We believe that although there is an increased (relative) risk of cancer in sarcoidosis patients compared with the general population, that increased risk is quite small (low absolute risk).
Respiratory Medicine | 2014
Boris I. Medarov; Amit Chopra; Marc A. Judson
Portopulmonary hypertension (PoPH) is an often neglected form of pulmonary hypertension where pulmonary hypertension occurs in the presence of portal hypertension. PoPH is important to diagnose and treat as it may improve the patients quality of life and improve the outcome after liver transplantation. In this review, we discuss the clinical aspects of PoPH including its pathophysiology, diagnosis, treatment, and prognosis.
Thorax | 2016
Amit Chopra; Rahul G. Argula; Christopher Schaefer; Marc A. Judson; Terrill Huggins
An 83-year-old woman presented with a recurrent, right-sided pleural effusion. She had undergone three large volume thoracentesis in the past 2 years, which revealed a ‘clear appearing’ transudative effusion. She had a remote history of haemothorax, a complication from dual chamber pacemaker placement. A chest radiograph (figure 1A) showed a moderate sized, right pleural effusion. Pleural ultrasonography revealed an anechoic fluid collection. Approximately 1.2 L of yellow fluid was removed during thoracentesis. Pleural manometry performed during the thoracentesis revealed a biphasic pressure-volume (P-V) curve showing a steep increase in pleural space elastance at the terminal stages of drainage suggesting an unexpandable lung (figure 2). An air-contrast chest CT scan (figure 1B) showed abnormal visceral pleural thickening consistent with a …
Journal of Clinical Sleep Medicine | 2016
Amit Chopra; Molly Jung; Robert C. Kaplan; David W. Appel; Elizabeth Dinces; Sumitrajit Dhar; Phyllis C. Zee; Franklyn Gonzalez; David J. Lee; Alberto R. Ramos; Howard J. Hoffman; Susan Redline; Karen J. Cruickshanks; Neomi Shah
STUDY OBJECTIVE Sleep apnea (SA) may promote hearing impairment (HI) through ischemia and inflammation of the cochlea. Our objective was to assess an independent association between SA and HI in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) participants. METHODS We used data from the HCHS/SOL, a multicenter population-based study of self- identifying Hispanic/Latinos 18- to 74-y-old adults from four US urban communities. We performed home SA testing and in-clinic audiometry testing in all participants. SA was defined as an apnea-hypopnea index (AHI) ≥ 15 events/h. HI was defined as a mean hearing threshold > 25 dB hearing level in either ear at the frequencies: 3,000 to 8,000 Hz for high-frequency HI (HF-HI) and 500 to 2,000 Hz for low-frequency HI (LF-HI). Combined-frequency HI (CF-HI) was defined as both conditions present, and Any-HI was considered as HI in either low or high frequencies. RESULTS Of 13,967 participants, 9.9% had SA and 32.3% had Any-HI. Adjusted for risk factors for HI, those with SA had a 30% higher odds of Any-HI (95% confidence interval [CI] = 8% to 57%), 26% higher odds of HF-HI (CI = 3% to 55%), 127% higher odds of LF-HI (CI = 21% to 326%), and 29% higher odds of CF-HI (CI = 0% to 65%). A dose-response association was observed between AHI severity and Any-HI (versus no SA, OR for AHI ≥ 15 and < 30 = 1.22, CI = 0.96 to 1.54, and OR for AHI ≥ 30 = 1.46, CI = 1.11 to 1.91, p = 0.002). CONCLUSION SA is associated with HF-HI and LF-HI, independent of snoring and other confounders. COMMENTARY A commentary on this article appears in this issue on page 641.
Case reports in pulmonology | 2015
Amit Chopra; Creticus P. Marak; Narendrakumar Alappan; Chang Shim
Hepatitis C virus infection is the leading cause of chronic liver disease in the United States of America. Pegylated interferon α and ribavirin combination is the mainstay of treatment. Severe pulmonary toxicities are rarely reported. We report here a case of severe form of organizing pneumonia secondary to pegylated interferon α therapy presenting as acute respiratory failure. Patient has near complete recovery with withdrawal of pegylated interferon α and steroid therapy. We report this case to raise the awareness of this rare but potentially life-threatening pulmonary complication of pegylated interferon α therapy.
Respirology | 2018
John T. Huggins; Fabien Maldonado; Amit Chopra; Najib M. Rahman; Richard W. Light
Unexpandable lung is a common complication of malignant pleural effusions and inflammatory pleural diseases, such as pleural infection (e.g. empyema and complicated parapneumonic effusion) and noninfectious fibrinous pleuritis. Unexpandable lung due to pleural disease may be because of an active pleural process, and is referred to as malignant or inflammatory lung entrapment.
Chest | 2018
Amit Chopra; Amit Nautiyal; Alexander Kalkanis; Marc A. Judson
A drug-induced sarcoidosis-like reaction (DISR) is a systemic granulomatous reaction that is indistinguishable from sarcoidosis and occurs in a temporal relationship with initiation of an offending drug. DISRs typically improve or resolve after withdrawal of the offending drug. Four common categories of drugs that have been associated with the development of a DISR are immune checkpoint inhibitors, highly active antiretroviral therapy, interferons, and tumor necrosis factor-α antagonists. Similar to sarcoidosis, DISRs do not necessarily require treatment because they may cause no significant symptoms, quality of life impairment, or organ dysfunction. When treatment of a DISR is required, standard antisarcoidosis regimens seem to be effective. Because a DISR tends to improve or resolve when the offending drug is discontinued, this is another effective treatment for a DISR. However, the offending drug need not be discontinued if it is useful, and antigranulomatous therapy can be added. In some situations, the development of a DISR may suggest a beneficial effect of the inducing drug. Understanding the mechanisms leading to DISRs may yield important insights into the immunopathogenesis of sarcoidosis.
The American Journal of the Medical Sciences | 2017
Adam Austin; Sidharth Navin Jogani; Paul Bradley Brasher; Rahul G. Argula; John T. Huggins; Amit Chopra
Abstract Urinothorax is an uncommon thoracic complication of genitourinary (GU) tract disease, which is most frequently caused by obstructive uropathy, but may also occur as a result of iatrogenic or traumatic GU injury. It is underrecognized because of a perceived notion as to the rarity of the diagnosis and the absence of established diagnostic criteria. Urinothorax is typically described as a paucicellular, transudative pleural effusion with a pleural fluid/serum creatinine ratio >1.0. It is the only transudate associated with pleural fluid acidosis (pH < 7.40). When the pleural fluid analysis demonstrates features of a transudate, pH <7.40 and a pleural fluid/serum creatinine ratio >1.0, a confident clinical diagnosis of urinothorax can be established. A technetium 99m renal scan can be considered a confirmatory test in patients who lack the typical pleural fluid analysis features or fail to demonstrate evidence of obstructive uropathy that can be identified via conventional radiographic modalities. Management of a urinothorax requires a multidisciplinary approach with an emphasis on the correction of the underlying GU tract pathology, and once corrected, this often leads to a rapid resolution of the pleural effusion.