LETTER
Lung Dysfunction and Chronic Liver Disease
Paul A. Lange, MD, and
James K. Stoller, MD
1 February 1996 | Volume 124 Issue 3 | Pages 369-370
response: Dr. Brodkin points out the symptomatic and functional improvement that accompanied coil-spring embolization in the patient described by Felt and colleagues [1]. Although the published study did not describe the patient's improvement in dyspnea and exercise capacity, we agree that these unstated benefits shed a more optimistic light on the effect of the embolization. However, the modest improvement in oxygenation (an increase in room air PaO2 from 38 mm Hg to 53 mm Hg) and the persistence of orthodeoxia (despite the deployment of 22 coils in three separate procedures) does justify some reservations. Furthermore, as with liver transplantation for the hepatopulmonary syndrome, longer follow-up periods and larger patient samples among persons having embolization for the hepatopulmonary syndrome (rather than for other conditions such as hereditary hemorrhagic telangiectasia) are needed before the efficacy of embolization can be fully assessed.
Although a full discussion of portopulmonary hypertension was beyond the scope of our review of the hepatopulmonary syndrome [2], the comments of Dr. Yoshida and colleagues provide a fascinating parallel to the hepatopulmonary syndrome. Specifically, initial pessimism about the reversibility of pulmonary hypertension after liver transplantation [3] has become glimmering optimism as experience has grown [4]. Similarly, as with efficacy assessments for treatment of the hepatopulmonary syndrome, caution is warranted in deriving conclusions about treatment efficacy from a collection of case reports. Certainly, these reports clearly show the possibility of reversing pulmonary hypertension after liver transplantation but do not allow an estimate of the probability of such improvement. For example, under-reporting of cases in which pulmonary hypertension (or the hepatopulmonary syndrome) was not reversed may lead to an inflated impression about the efficacy of liver transplantation (so-called publication bias [[5]).
Overall, the comments of Dr. Brodkin and Dr. Yoshida and colleagues remind us that systematic information about the efficacy of therapy for the hepatopulmonary syndrome and for portopulmonary hypertension is needed. A multicenter registry for patients with these complications of liver disease would be a good beginning.
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Author and Article Information
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Cleveland Clinic Foundation; Cleveland, OH 44106
1. Felt RW, Kozak BE, Rosch J, Duell BP, Barker AF. Hepatogenic pulmonary angiodysplasia treated with coil-spring embolization. Chest. 1987; 91:920-2.
2. Lange PA, Stoller JK. The hepatopulmonary syndrome. Ann Intern Med. 1995; 122:521-9.
3. Hamdani R, Chelluri L, Selby R, Kramer D, Kang Y, Wood S, Van Thiel D. Sudden death in patients with pulmonary hypertension undergoing orthotopic liver transplantation. AASLD Abstracts. Hepatology. 1991; 14:282A.
4. Koneru B, Ahmed S, Weisse AB, Grant GP, McKim KA. Resolution of pulmonary hypertension of cirrhosis after liver transplantation. Transplantation. 1994; 58:1133-5.
5. Bero LA, Glantz SA, Romnie D. Publication bias and public health policy on environmental tobacco smoke. JAMA. 1994; 272:133-6.
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