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Rodrigo Cartin-Ceba, MD; Karen L. Swanson, DO, FCCP; Michael J. Krowka, MD, FCCP
Author and Funding Information

From the Department of Medicine, Division of Pulmonary and Critical Care Medicine, Mayo Clinic (Drs Cartin-Ceba and Krowka); and Mayo Clinic (Dr Swanson).

Correspondence to: Rodrigo Cartin-Ceba, MD, Department of Medicine, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, 200 First St SW, Rochester, MN 55905; e-mail: cartinceba.rodrigo@mayo.edu


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;145(2):426-427. doi:10.1378/chest.13-2748
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To the Editor:

We thank Dr Salerno for his interest in our article1 and for his insightful comments. We agree with him that the low reported incidence of brain abscesses in patients with hepatopulmonary syndrome (HPS) compared with patients with hereditary hemorrhagic telangiectasia (HHT) is intriguing. Although surveillance bias may play a role because this complication is well-known in patients with HHT, we consider that different mechanistic factors are at play.

First, although intuitively one might consider that size and frequency do matter (pulmonary arteriovenous malformations [PAVMs] are usually larger and more frequent in HHT than in HPS), the literature does not fully support this observation. Initial small studies suggested that neurologic complications in patients with HHT (brain abscess and stroke) are more common in those with more severe or diffuse PAVMs.2,3 However, a cohort study of 219 consecutive patients with HHT and PAVMs showed no clear relationship between the risk of brain abscess or stroke with markers of PAVM severity, including diameter of the largest feeding vessel or degree of right-to-left shunt.4 As mentioned by Dr Salerno, a second potential mechanism has to do with the local microenvironment at the pulmonary vasculature level. The extensive accumulation of pulmonary intravascular macrophages that adhere to the pulmonary endothelium in animal models of biliary cirrhosis is very well known and is believed to be a compensatory mechanism due to the dramatic decrease in the phagocytic capacity of the liver that allows circulating bacteria to enter the pulmonary circulation.5 If a similar phenomenon occurs in humans, we speculate that the increased intravascular macrophage activity could play a role in better bacterial clearance, despite shunting. A third potential mechanism is the common use of antibiotic therapy to prevent spontaneous bacterial peritonitis in patients with HPS compared with patients with HHT. Long-term antibiotic use in these patients may help to further reduce transient bacteremia, decreasing the risk of brain abscesses. Furthermore, it has been shown in experimental models that the use of antibiotics, such as norfloxacin (commonly prescribed in patients with cirrhosis to prevent spontaneous bacterial peritonitis), reduces the severity of intrapulmonary shunting by decreasing the nitric oxide production of the pulmonary intravascular macrophages.6 We agree with Dr Salerno that further prospective studies which include the reporting of cerebrovascular events in the setting of HPS are needed to elucidate this important clinical question.

References

Cartin-Ceba R, Swanson KL, Krowka MJ. Pulmonary arteriovenous malformations. Chest. 2013;144(3):1033-1044. [CrossRef] [PubMed]
 
Moussouttas M, Fayad P, Rosenblatt M, et al. Pulmonary arteriovenous malformations: cerebral ischemia and neurologic manifestations. Neurology. 2000;55(7):959-964. [CrossRef] [PubMed]
 
Pierucci P, Murphy J, Henderson KJ, Chyun DA, White RI Jr. New definition and natural history of patients with diffuse pulmonary arteriovenous malformations: twenty-seven-year experience. Chest. 2008;133(3):653-661. [CrossRef] [PubMed]
 
Shovlin CL, Jackson JE, Bamford KB, et al. Primary determinants of ischaemic stroke/brain abscess risks are independent of severity of pulmonary arteriovenous malformations in hereditary haemorrhagic telangiectasia. Thorax. 2008;63(3):259-266. [CrossRef] [PubMed]
 
Miot-Noirault E, Faure L, Guichard Y, Montharu J, Le Pape A. Scintigraphic in vivo assessment of the development of pulmonary intravascular macrophages in liver disease: experimental study in rats with biliary cirrhosis. Chest. 2001;120(3):941-947. [CrossRef] [PubMed]
 
Rabiller A, Nunes H, Lebrec D, et al. Prevention of gram-negative translocation reduces the severity of hepatopulmonary syndrome. Am J Respir Crit Care Med. 2002;166(4):514-517. [CrossRef] [PubMed]
 

Figures

Tables

References

Cartin-Ceba R, Swanson KL, Krowka MJ. Pulmonary arteriovenous malformations. Chest. 2013;144(3):1033-1044. [CrossRef] [PubMed]
 
Moussouttas M, Fayad P, Rosenblatt M, et al. Pulmonary arteriovenous malformations: cerebral ischemia and neurologic manifestations. Neurology. 2000;55(7):959-964. [CrossRef] [PubMed]
 
Pierucci P, Murphy J, Henderson KJ, Chyun DA, White RI Jr. New definition and natural history of patients with diffuse pulmonary arteriovenous malformations: twenty-seven-year experience. Chest. 2008;133(3):653-661. [CrossRef] [PubMed]
 
Shovlin CL, Jackson JE, Bamford KB, et al. Primary determinants of ischaemic stroke/brain abscess risks are independent of severity of pulmonary arteriovenous malformations in hereditary haemorrhagic telangiectasia. Thorax. 2008;63(3):259-266. [CrossRef] [PubMed]
 
Miot-Noirault E, Faure L, Guichard Y, Montharu J, Le Pape A. Scintigraphic in vivo assessment of the development of pulmonary intravascular macrophages in liver disease: experimental study in rats with biliary cirrhosis. Chest. 2001;120(3):941-947. [CrossRef] [PubMed]
 
Rabiller A, Nunes H, Lebrec D, et al. Prevention of gram-negative translocation reduces the severity of hepatopulmonary syndrome. Am J Respir Crit Care Med. 2002;166(4):514-517. [CrossRef] [PubMed]
 
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