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REPLY
Splenectomy-Induced Portal Hypertension and Pulmonary Hypertension
Marius M. Hoeper, MD, and
Jost Niedermeyer, MD
16 November 1999 | Volume 131 Issue 10 | Page 793
IN RESPONSE:
We thank Teramoto and colleagues for their comments. Their suggestions about possible mechanisms for the development of pulmonary hypertension after splenectomy are inconclusive. First, the development of portal hypertension after splenectomy is rare, and coexistence of portal hypertension and pulmonary hypertension was thoroughly excluded by Doppler ultrasonography in all our patients. No evidence suggests that abnormal pulmonary vasodilatation as part of the hepatopulmonary syndrome plays any role in splenectomy-associated pulmonary hypertension. Hypoxic vasoconstriction is not a feature of the hepatopulmonary syndrome, and respiratory acidosis is almost never involved.
Teramoto and colleagues also stressed the role of impaired regional NO synthetase expression for the development of the hepatopulmonary syndrome and pulmonary hypertension. Although increased levels of exhaled NO have been demonstrated with intrapulmonary vascular dilatation (1, 2), the situation is less clear for pulmonary hypertension (3, 4). However, the conclusion that splenectomy does not always cause pulmonary hypertension because hypoxia inhibits NO production (and therefore abnormal pulmonary vasodilation) is not supported by scientific evidence and contradicts clinical experience. Most patients who have had splenectomy are normoxic and will probably never develop pulmonary vascular disease. According to our experience and from the correspondence we received after our paper was published, the risk for pulmonary hypertension after splenectomy seems especially high in patients with hemolytic disorders, such as spherocytosis or thalassemia. Therefore, we think it is reasonable to assume that the prolonged presence of abnormal erythrocytes in the circulation is involved in the pathogenesis of postsplenectomy pulmonary hypertension. The exact mechanism, however, remains speculative.
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Author and Article Information
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Hannover Medical School; 30623 Hannover, Germany (Hoeper)
Hannover Medical School; 30623 Hannover, Germany (Niedermeyer)
1. Rolla G, Brussino L, Colagrande P, Dutto L, Polizzi S, Scappaticci E, et al. Exhaled nitric oxide and oxygenation abnormalities in hepatic cirrhosis Hepatology. 1997;26:842-7.[Medline]
2. Krowka MJ. Hepatopulmonary syndrome. Current concepts in diagnostic and therapeutic considerations Chest. 1994;105:1528-37.[Free Full Text]
3. Giaid A, Salch D. Reduced expression of the endothelial nitric oxide synthase in patients with pulmonary hypertension N Engl J Med. 1995;333:214-2.[Abstract/Free Full Text]
4. Mason NA, Springall DR, Burke M, Pollock J, Yacoub MH, Polak JM. High expression of endothelial nitric oxide synthase in plexiform lesions of pulmonary hypertension J Pathol. 1998;185:313-8.[Medline]
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[ABSTRACT][Full Text]
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