A young man with acute respiratory distress syndrome: eosinophilia is not always “benign”

Ankur Jain; Pankaj Malhotra; Vikas Suri; Ritesh Agarwal; Amanjit Bal; Subhash Varma

doi:10.5045/br.2017.52.4.329

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Letter to the Editor

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Blood Res 2017; 52(4):

Published online December 31, 2017

https://doi.org/10.5045/br.2017.52.4.329

A young man with acute respiratory distress syndrome: eosinophilia is not always “benign”

Ankur Jain¹, Pankaj Malhotra^1*, Vikas Suri¹, Ritesh Agarwal², Amanjit Bal³, and Subhash Varma¹

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¹Department of Internal Medicine, Nehru Hospital, PGIMER, Chandigarh, India.

²Department of Pulmonary Medicine, Nehru Hospital, PGIMER, Chandigarh, India.

³Department of Histopathology, Nehru Hospital, PGIMER, Chandigarh, India.

Correspondence to : Pankaj Malhotra. Department of Internal Medicine, Nehru Hospital, PGIMER, Chandigarh 160012, India. hematpgi@gmail.com

Received: January 11, 2017; Accepted: April 11, 2017

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

FIGURES

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FIGURES
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Fig. 1.

(A) Chest X-ray (posteroanterior view) showing diffuse alveolar opacities with a normal cardiac shadow. (B) Chest X-ray 1 week after treatment with imatinib mesylate showing complete resolution of the infiltrates.

Fig. 2.

(A, B) Computed tomography scans showing confluent symmetrical central airspace shadows indicating pulmonary edema.

Fig. 3.

Photomicrographs showing (A) intra-alveolar Masson bodies indicating an organizing pneumonia pattern (hematoxylin and eosin, ×200), (B) Masson bodies (Masson's trichrome stain, ×200), (C) a few alveoli with fibrin balls (hematoxylin and eosin, ×200), and (D) an interstitial eosinophilic infiltrate (hematoxylin and eosin, ×400).

REFERENCES

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FIGURES
REFERENCES

Fowler, AA, Hamman, RF, Good, JT, et al. Adult respiratory distress syndrome: risk with common predispositions. Ann Intern Med, 1983;98;593-597.
Chusid, MJ, Dale, DC, West, BC, Wolff, SM. The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature. Medicine (Baltimore), 1975;54;1-27.
Roufosse, FE, Goldman, M, Cogan, E. Hypereosinophilic syndromes. Orphanet J Rare Dis, 2007;2;37.
Gotlib, J. World Health Organization-defined eosinophilic disorders: 2014 update on diagnosis, risk stratification, and management. Am J Hematol, 2014;89;325-337.
Gotlib, J, Cools, J, Malone, JM, Schrier, SL, Gilliland, DG, Coutré, SE. The FIP1L1-PDGFRalpha fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management. Blood, 2004;103;2879-2891.
Dulohery, MM, Patel, RR, Schneider, F, Ryu, JH. Lung involvement in hypereosinophilic syndromes. Respir Med, 2011;105;114-121.
Winn, RE, Kollef, MH, Meyer, JI. Pulmonary involvement in the hypereosinophilic syndrome. Chest, 1994;105;656-660.
Savage, N, George, TI, Gotlib, J. Myeloid neoplasms associated with eosinophilia and rearrangement of PDGFRA, PDGFRB, and FGFR1: a review. Int J Lab Hematol, 2013;35;491-500.

Article

Letter to the Editor

Blood Res 2017; 52(4): 329-332

Published online December 31, 2017 https://doi.org/10.5045/br.2017.52.4.329

A young man with acute respiratory distress syndrome: eosinophilia is not always “benign”

Ankur Jain¹, Pankaj Malhotra^1*, Vikas Suri¹, Ritesh Agarwal², Amanjit Bal³, and Subhash Varma¹

¹Department of Internal Medicine, Nehru Hospital, PGIMER, Chandigarh, India.

²Department of Pulmonary Medicine, Nehru Hospital, PGIMER, Chandigarh, India.

³Department of Histopathology, Nehru Hospital, PGIMER, Chandigarh, India.

Correspondence to:Pankaj Malhotra. Department of Internal Medicine, Nehru Hospital, PGIMER, Chandigarh 160012, India. hematpgi@gmail.com

Received: January 11, 2017; Accepted: April 11, 2017

Fig 1.

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Figure 1.

Blood Research 2017; 52: 329-332https://doi.org/10.5045/br.2017.52.4.329

Fig 2.

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Figure 2.

(A, B) Computed tomography scans showing confluent symmetrical central airspace shadows indicating pulmonary edema.

Blood Research 2017; 52: 329-332https://doi.org/10.5045/br.2017.52.4.329

Fig 3.

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Figure 3.

Blood Research 2017; 52: 329-332https://doi.org/10.5045/br.2017.52.4.329

References

Fowler, AA, Hamman, RF, Good, JT, et al. Adult respiratory distress syndrome: risk with common predispositions. Ann Intern Med, 1983;98;593-597.
Chusid, MJ, Dale, DC, West, BC, Wolff, SM. The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature. Medicine (Baltimore), 1975;54;1-27.
Roufosse, FE, Goldman, M, Cogan, E. Hypereosinophilic syndromes. Orphanet J Rare Dis, 2007;2;37.
Gotlib, J. World Health Organization-defined eosinophilic disorders: 2014 update on diagnosis, risk stratification, and management. Am J Hematol, 2014;89;325-337.
Gotlib, J, Cools, J, Malone, JM, Schrier, SL, Gilliland, DG, Coutré, SE. The FIP1L1-PDGFRalpha fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management. Blood, 2004;103;2879-2891.
Dulohery, MM, Patel, RR, Schneider, F, Ryu, JH. Lung involvement in hypereosinophilic syndromes. Respir Med, 2011;105;114-121.
Winn, RE, Kollef, MH, Meyer, JI. Pulmonary involvement in the hypereosinophilic syndrome. Chest, 1994;105;656-660.
Savage, N, George, TI, Gotlib, J. Myeloid neoplasms associated with eosinophilia and rearrangement of PDGFRA, PDGFRB, and FGFR1: a review. Int J Lab Hematol, 2013;35;491-500.