Partial splenic embolization for hypersplenism

Correspondence Partial Splenic Embolization for Hypersplenism To the Editor: We have read with considerable interest the article by Sangro et al ~ entitled "Partial Splenic Embolization for the Treatment of Hypersplenism in Cirrhosis." The authors have undoubtedly shown just w h a t was exp e c t e d - - t h a t partial splenic embolization leads to partial splenectomy. However, we are perturbed t h a t their excessive emphasis on the technical aspect has given somewhat short shrift to clinical medicine and medical ethics. We wish to make the following points to support our above statement. First, the authors have ignored the fact t h a t hypersplenism is usually clinically insignificant2 and therefore, the whole basis of using drastic measures to treat this condition is tenuous. Surely the authors have tried to weave the story of their technique around a clinical situation of interferon-induced cytopenia in patients with cirrhosis ofvirat origin. We would like to question the very necessity of such therapy at this late stage when there is little to be gained by eradicating the hepatitis infection; t h a t such patients can benefit from interferon has not been proved so far. Highly questionable on ethical grounds is the inclusion in the study of patients with asymptomatic thrombocytopenia, in whom neither surgery nor interferon therapy could be considered. Mere demonstration of low leukocyte and platelet counts in the absence of symptoms m a y not w a r r a n t any t r e a t m e n t because, although the number of circulating platelets and leukocytes is reduced, their function is often normal. 2 Prognosis and long-term survival of such patients are related to the severity of underlying disease r a t h e r t h a n to blood cell counts. 2 Second, the definition and proof of hypersplenism in the authors' cases can be questioned. The authors have used the term "hypersplenism" for reduction in one or more cellular elements of blood. However, they neither demonstrated presence of normal or hypercellular bone marrow nor excluded other causes of cytopenias, namely, folate deficiency, drug toxicity, and bone marrow hypoplasia. Third, the authors have placed a lot of importance on the withdrawal of interferon because of bone marrow depression. This is not a significant problem in clinical practice. The two main series quoted by the authors

mention that dose reduction in their patients was temporary and that these patients responded to treatment as frequently as those who received scheduled doses of interferon. 3'4 This is contrary to what Sangro et al 1 have mentioned in reference to these trials. Furthermore, it was shown that after i week of partial splenic embolization, aspartate transaminase and alanine transaminase levels decreased significantly. But no suitable explanation has been postulated to explain this improvement. Finally, the proportion of splenic tissue infarcted was estimated subjectively at the time of embolization. The same could have been assessed more objectively using scintigraphic techniques with radiolabeled red blood cells. We are reminded of w h a t Will Durant, 5 the famous modern philosopher, had to say about specialists in science, "The specialist puts on blinders in order to shut out from his vision all the world but one little spot, to which he glued his nose. Perspective was lost. Facts replaced understanding; and knowledge, split into a thousand isolated fragments, no longer generated wisdom." Should we not heed this warning. BRIJESH C. SHARMA RAKESH AGGARWAL SUBHASH R. NA~K

Department of Gastroenterology Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow, India REFERENCES

1. Sangro B, Bilbao I, Herrero I, Corella C, Longo J, Beloqui O, Ruiz J, et al. Partial splenic embolizationfor the treatment of hypersplenism in cirrhosis. HEPATOLOGY1993;18:309-314. 2. McCormickPA. The spleen, hypersplenism and other relationships between liver and spleen. In: McIntyrenN, BenhamouJP, Bircher J, Rizzeto M, Rhodes J, eds. OxfordTextbookof Clinical Hepatology. Oxford: University Press 1991:489-493. 3. Causse X, GodinotH, ChevallierM, ChossegrosP, ZoulimF, Ovzan D, Heyrand JP, et al. Comparisonof I or 3 MU of interferon alpha 2b and placebo in patients with chronicnonA,nonB hepatitis. Gastroenterology1991;101:497-502. 4. Perrillo RP, SchiffER, Davis GL, BodenheimerHC, Lindsay K, Payne J, DienstagJL, et al. A randomizedcontrolledtrial ofinterferon alpha 2b alone and after prednisolonewithdrawal for treatment of chronic hepatitis B. N Engl J Med 1990;323:295-301. 5. Durant W. The story of philosophy. Ed 2. 1993:viii.

Emergency Portacaval Shunt: A Perspective on the Perspective To the Editor: The editorial by Henderson and Grace 1 entitled "A Perspective on Emergency Portacaval Shunt" in the October 1994 issue of HEPATOLOGY raises questions about our randomized controlled trial (RCT) 2 t h a t dem a n d a response. The Patient Population. Henderson and Grace stated: "Any center conducting randomized controlled

trials has potential constraint on patient entry dictated by factors such as referral and practice patterns, and patient compliance. These must be clearly defined. ''1 Our paper clearly stated: "All patients with liver disease who entered the emergency room at the San Diego Veterans Administration Medical Center because of bleeding esophageal varices (41 patients), or in whom variceal hemorrhage developed during the course of hospitalization (two patients), were included in the

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