Disclosure of interest : the authors declare that they have no conflicts of interest concerning this article.
References [1]
[2]
[3]
[4]
[5]
[6]
[7]
[8]
Hur H, Park AR, Jee SB, Jung SE, Kim W, Jeon HM. Perforation of the colon by invading recurrent gastro-intestinal stromal tumors during sunitinib treatment. World J Gastroenterol 2008;14:6096-9. Flaig TW, Kim FJ, La Rosa FG, Breaker K, Schoen J, Russ PD. Colonic pneumatosis and intestinal perforations with sunitinib treatment for renal cell carcinoma. Invest New Drugs 2009;27:83-7. Walraven M, Witteveen PO, Lolkema MP, van Hillegersberg R, Voest EE, Verheul HM. Antiangiogenic tyrosine kinase inhibition related gastrointestinal perforations: a case report and literature review. Angiogenesis 2011;14:135-41. Hoshino Y, Hasegawa H, Ishii Y, Endo T, Ochiai H, Okabayashi K et al. Two cases of bowel perforation associated with sunitinib treatment for renal cell carcinoma. Int J Clin Oncol 2012;17:412-6. Motzer RJ, Hutson TE, Tomczak P, Michaelson MD, Bukowski RM, Rixe O et al. Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N Engl J Med 2007;356:115-24. Peters NA, Richel DJ, Verhoeff JJ, Stalpers LJ. Bowel perforation after radiotherapy in a patient receiving sorafenib. J Clin Oncol 2008;26: 2405-6. Inoue T, Kinoshita H, Komai Y, Kawabata T, Kawa G, Uemura Y et al. Two cases of gastro-intestinal perforation after radiotherapy in patients receiving tyrosine kinase inhibitor for advanced renal cell carcinoma. World J Surg Oncol 2012;10:167. Albiges L, Oudard S, Negrier S, Caty A, Gravis G, Joly F et al. Complete remission with tyrosine kinase inhibitors in renal cell carcinoma. J Clin Oncol 2012;30:482-7. Jean-Sébastien Bladé1, Stéphane Bourgouin2, Émilie Romeo1, Laurys Boudin1, Jean-Pierre de Jauréguiberry1 1
HIA Sainte-Anne, service de médecine interne-oncologie, BP no 600, 83800 Toulon cedex 9, France 2 HIA Sainte-Anne, service de chirurgie viscérale et vasculaire, BP no 600, 83800 Toulon cedex 9, France
tome 43 > n811 > novembre 2014
Correspondence: Jean-Sébastien Bladé, HIA Sainte-Anne, service de médecine interne-oncologie, BP no 600, 83800 Toulon cedex 9, France. [email protected] Received 26 January 2014 Accepted 17 March 2014 Available online 3 July 2014 http://dx.doi.org/10.1016/j.lpm.2014.03.021 ß 2014 Elsevier Masson SAS Tous droits réservés.
Splenomegaly in haematological malignancies and portal hypertension Splénomégalie dans les hémopathies malignes et hypertension portale It is usually accepted that the sole condition of portal hyperafflux cannot explain the development of portal hypertension, in absence of other factors, as an intrinsic pathology of the liver or of the portal venous system, with consequently increased vascular resistances. The clinical condition of a homogeneous splenomegaly secondary to haematological malignancies can be considered an interesting model to study this problem. Observation We retrospectively examined clinical and radiological data of 20 patients, 15 males and 5 females, with a median age of 63 years (range 18–85 years), with a homogeneous splenomegaly secondary to haematological malignancy: chronic lymphocytic leukemia (7 cases), acute lymphoblastic leukemia (1 case), chronic myeloid leukemia (1 case), hairy cell leukemia (3 cases), splenic marginal zone lymphoma (4 cases), diffuse large B cell lymphoma (3 cases) and cutaneous follicular lymphoma (1 case). The liver function tests were normal in all the cases, and no signs of extramedullary haematopoiesis were demonstrated by haematological investigations. Our study has been chiefly based on the findings of contrastenhanced computed tomography and of ultrasonography, performed in every case before any treatment. The mean splenic volume calculated volumetrically with a software automatically contouring the spleen was 1610.22 cm3, ranging from 417.50 to 4728 cm3, being the mean normal value 214.6 cm3 [1]. The splenic artery and especially the splenic vein, at the hilum, appeared enlarged and tortuous, especially in cases of bigger splenomegaly. No signs of general or left-sided portal
1295
microvascular toxicity and therefore mucosal fragility. Bowel perforation under antiangiogenic TKI treatment is in most cases of early occurrence, in the first months (up to five months) if not the first weeks of treatment. Late event, as in our case, has just been reported in one case (thirteen months) [2]. Our case is peculiar in that the bowel perforation has been preceded by febrile diarrhoea, probably infectious, may be acting as a first hit on the mucosae paving the way to the subsequent perforation. Risk factors of bowel perforation under antiangiogenic TKI treatments are not known. However, in three cases linked with radiotherapy, all three with sorafenib, a possible radiosensitization is underlined [6,7]. At last, our case illustrates the issue of long-lasting antiangiogenic TKI treatments and the risk of late toxicity. It also illustrates the need of having guidelines concerning this small but existing subset of patients with MRCC in complete response under TKI treatments; a French group has already given clues: the interruption of TKI is possible with more than 60% of patients remaining in complete response with a median follow-up of about nine months [8].
Lettres à la rédaction
Lettres a` la re´ daction
Lettres a` la re´daction
hypertension were found in any case, in particular no dilated portal – or splenic – systemic collaterals. Intrinsic abnormalities of the liver, of the splenic vessels or of the mesenterico-portal axis were carefully excluded, as well as ascites, congestion and oedema of the splanchnic viscera. At the colour-coded Doppler ultrasound, the diameter of the portal vein was in a normal range.
Lymphangiome kystique du mésocôlon ascendant
Discussion
Les lymphangiomes kystiques (LK) sont des tumeurs conjonctivo-vasculaires malformatives, secondaires à une anomalie de développement embryologique du système lymphatique [1]. Les formes intra-abdominales de ces dysplasies bénignes, qui sont l’apanage de l’enfant, sont rares et se situent préférentiellement dans le mésentère [2,3]. Leur diagnostic est rarement porté à l’âge adulte [2,4]. Seuls quelques cas sporadiques ont été rapportés, surtout dans les formes localisées au niveau du mésocôlon [2,5,6]. Afin d’éviter les récidives et pour des raisons à la fois anatomique et topographique, la plupart des cas opérés ont nécessité une colectomie [2,6]. Nous décrivons l’observation d’un LK du mésocôlon ascendant, réséqué de façon conservatrice, mais curative.
These observations support our conviction that the sole condition of primary massive splenomegaly, with subsequent portal overflow, is not sufficient to induce a portal hypertension, in absence of concomitant or secondary disorders of the liver or of the portal system [2]. Therefore, when a condition of portal hypertension complicates splenomegaly in patients with haematological malignancies, further clinical and radiological examinations are indicated to investigate possible disorders of the liver or of the portal venous system [3,4]. Nevertheless, we agree that in case of arterio-portal fistula, a sudden and frank increase in the portal pressure and flow can induce a subsequent pre-sinusoidal portal hypertension, through arterialization and intimal hyperplasia of the portal venous branches [5]. Disclosure of interest : the authors declare that they have no conflicts of interest concerning this article.
References [1]
[2] [3]
[4]
[5]
Harris A, Kamishima T, Hao HY et al. Splenic volume measurement on computed tomography utilizing automatically contouring software and its relationship with age, gender, and antropometric parameters. Eur J Radiol 2010;75:97-101. Cichoz-Lach H, Celinski K, Slomka M, Kasztelan-Szczerbinska B. Pathophysiology of portal hypertension. J Physiol Pharmac 2008;59:231-8. Agarwal A, Jain M. Multidetector CT portal venography in evaluation portosystemic collateral vessels. J Med Imaging Radiother Oncol 2008;52:4-9. Zhao LQ, He W, Ji M et al. 64-row multidetector computed tomography portal venography of gastric variceal collateral circulation. World J Gastroenterol 2010;16:1003-7. Guzman EA, Mc Cahill LE, Rogers FB. Arterioportal fistulas: introduction of a novel classification with therapeutic implications. J Gastrointest Surg 2006;10:543-50. Antonio Manenti1, Fabio Forghieri2, Dario Colasanto3, Mario Luppi2 1
University of Modena, departments of surgery, via del Pozzo, 41100 Modena, Italy 2 University of Modena, departments of haematology, 41100 Modena, Italy 3 University of Modena, departments of radiology, 41100 Modena, Italy Correspondence: Antonio Manenti, University of Modena, departments of surgery, via del Pozzo, 41100 Modena, Italy. [email protected] Received 6 December 2013 Accepted 19 February 2014 Available online 13 June 2014
1296
http://dx.doi.org/10.1016/j.lpm.2014.02.024 ß 2014 Elsevier Masson SAS Tous droits réservés.
Cystic lymphangioma of the ascending mesocolon
Observation Un homme âgé de 65 ans, sans antécédent pathologique ni de traumatisme, consultait pour une douleur du flanc droit évoluant depuis deux semaines. La palpation du flanc droit révélait une masse intra-abdominale mobilisable, de consistance ferme. Le bilan biologique était normal. Le scanner abdomino-pelvien avec injection de produit de contraste mettait en évidence, au temps artériel et en coupe axiale, une formation kystique cloisonnée, à parois fines non rehaussées par le contraste, localisée dans la cavité abdominale en regard du côlon ascendant (figure 1). Le diagnostic de LK mésentérique était évoqué. Un traitement chirurgical par laparotomie était proposé. À l’exploration, on retrouvait l’origine mésentérique de la masse kystique développée à partir du mésocôlon ascendant (figure 2). Après dissection et ligature pas à pas des vaisseaux lymphatiques péritumoraux, nous avons constaté un accolement de la masse kystique avec la troisième portion du duodénum sans l’envahir. Une exérèse tumorale complète sans colectomie était réalisée. Le côlon ascendant était de bonne vitalité et conservé. Macroscopiquement, la tumeur était entourée d’une capsule fine, de couleur hétérogène, mesurant environ 8 cm de grand axe. À la coupe, il s’agissait d’une formation nodulaire multiple et kystique à contenu hémorragique et nécrotique. L’examen histologique de la tumorectomie permettait de confirmer le diagnostic d’un LK. Les suites opératoires étaient simples. À 18 mois, le patient était asymptomatique, aucune récidive n’était observée. Discussion Les LK du mésocôlon sont des formes topographiques rares de l’adulte dont la prise en charge peut être alourdie par la nécessité de colectomie [2]. Les cas rapportés intéressaient tome 43 > n811 > novembre 2014
References [1]
[2]
[3]
[4]
[5]
[6]
[7]
[8]
Hur H, Park AR, Jee SB, Jung SE, Kim W, Jeon HM. Perforation of the colon by invading recurrent gastro-intestinal stromal tumors during sunitinib treatment. World J Gastroenterol 2008;14:6096-9. Flaig TW, Kim FJ, La Rosa FG, Breaker K, Schoen J, Russ PD. Colonic pneumatosis and intestinal perforations with sunitinib treatment for renal cell carcinoma. Invest New Drugs 2009;27:83-7. Walraven M, Witteveen PO, Lolkema MP, van Hillegersberg R, Voest EE, Verheul HM. Antiangiogenic tyrosine kinase inhibition related gastrointestinal perforations: a case report and literature review. Angiogenesis 2011;14:135-41. Hoshino Y, Hasegawa H, Ishii Y, Endo T, Ochiai H, Okabayashi K et al. Two cases of bowel perforation associated with sunitinib treatment for renal cell carcinoma. Int J Clin Oncol 2012;17:412-6. Motzer RJ, Hutson TE, Tomczak P, Michaelson MD, Bukowski RM, Rixe O et al. Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N Engl J Med 2007;356:115-24. Peters NA, Richel DJ, Verhoeff JJ, Stalpers LJ. Bowel perforation after radiotherapy in a patient receiving sorafenib. J Clin Oncol 2008;26: 2405-6. Inoue T, Kinoshita H, Komai Y, Kawabata T, Kawa G, Uemura Y et al. Two cases of gastro-intestinal perforation after radiotherapy in patients receiving tyrosine kinase inhibitor for advanced renal cell carcinoma. World J Surg Oncol 2012;10:167. Albiges L, Oudard S, Negrier S, Caty A, Gravis G, Joly F et al. Complete remission with tyrosine kinase inhibitors in renal cell carcinoma. J Clin Oncol 2012;30:482-7. Jean-Sébastien Bladé1, Stéphane Bourgouin2, Émilie Romeo1, Laurys Boudin1, Jean-Pierre de Jauréguiberry1 1
HIA Sainte-Anne, service de médecine interne-oncologie, BP no 600, 83800 Toulon cedex 9, France 2 HIA Sainte-Anne, service de chirurgie viscérale et vasculaire, BP no 600, 83800 Toulon cedex 9, France
tome 43 > n811 > novembre 2014
Correspondence: Jean-Sébastien Bladé, HIA Sainte-Anne, service de médecine interne-oncologie, BP no 600, 83800 Toulon cedex 9, France. [email protected] Received 26 January 2014 Accepted 17 March 2014 Available online 3 July 2014 http://dx.doi.org/10.1016/j.lpm.2014.03.021 ß 2014 Elsevier Masson SAS Tous droits réservés.
Splenomegaly in haematological malignancies and portal hypertension Splénomégalie dans les hémopathies malignes et hypertension portale It is usually accepted that the sole condition of portal hyperafflux cannot explain the development of portal hypertension, in absence of other factors, as an intrinsic pathology of the liver or of the portal venous system, with consequently increased vascular resistances. The clinical condition of a homogeneous splenomegaly secondary to haematological malignancies can be considered an interesting model to study this problem. Observation We retrospectively examined clinical and radiological data of 20 patients, 15 males and 5 females, with a median age of 63 years (range 18–85 years), with a homogeneous splenomegaly secondary to haematological malignancy: chronic lymphocytic leukemia (7 cases), acute lymphoblastic leukemia (1 case), chronic myeloid leukemia (1 case), hairy cell leukemia (3 cases), splenic marginal zone lymphoma (4 cases), diffuse large B cell lymphoma (3 cases) and cutaneous follicular lymphoma (1 case). The liver function tests were normal in all the cases, and no signs of extramedullary haematopoiesis were demonstrated by haematological investigations. Our study has been chiefly based on the findings of contrastenhanced computed tomography and of ultrasonography, performed in every case before any treatment. The mean splenic volume calculated volumetrically with a software automatically contouring the spleen was 1610.22 cm3, ranging from 417.50 to 4728 cm3, being the mean normal value 214.6 cm3 [1]. The splenic artery and especially the splenic vein, at the hilum, appeared enlarged and tortuous, especially in cases of bigger splenomegaly. No signs of general or left-sided portal
1295
microvascular toxicity and therefore mucosal fragility. Bowel perforation under antiangiogenic TKI treatment is in most cases of early occurrence, in the first months (up to five months) if not the first weeks of treatment. Late event, as in our case, has just been reported in one case (thirteen months) [2]. Our case is peculiar in that the bowel perforation has been preceded by febrile diarrhoea, probably infectious, may be acting as a first hit on the mucosae paving the way to the subsequent perforation. Risk factors of bowel perforation under antiangiogenic TKI treatments are not known. However, in three cases linked with radiotherapy, all three with sorafenib, a possible radiosensitization is underlined [6,7]. At last, our case illustrates the issue of long-lasting antiangiogenic TKI treatments and the risk of late toxicity. It also illustrates the need of having guidelines concerning this small but existing subset of patients with MRCC in complete response under TKI treatments; a French group has already given clues: the interruption of TKI is possible with more than 60% of patients remaining in complete response with a median follow-up of about nine months [8].
Lettres à la rédaction
Lettres a` la re´ daction
Lettres a` la re´daction
hypertension were found in any case, in particular no dilated portal – or splenic – systemic collaterals. Intrinsic abnormalities of the liver, of the splenic vessels or of the mesenterico-portal axis were carefully excluded, as well as ascites, congestion and oedema of the splanchnic viscera. At the colour-coded Doppler ultrasound, the diameter of the portal vein was in a normal range.
Lymphangiome kystique du mésocôlon ascendant
Discussion
Les lymphangiomes kystiques (LK) sont des tumeurs conjonctivo-vasculaires malformatives, secondaires à une anomalie de développement embryologique du système lymphatique [1]. Les formes intra-abdominales de ces dysplasies bénignes, qui sont l’apanage de l’enfant, sont rares et se situent préférentiellement dans le mésentère [2,3]. Leur diagnostic est rarement porté à l’âge adulte [2,4]. Seuls quelques cas sporadiques ont été rapportés, surtout dans les formes localisées au niveau du mésocôlon [2,5,6]. Afin d’éviter les récidives et pour des raisons à la fois anatomique et topographique, la plupart des cas opérés ont nécessité une colectomie [2,6]. Nous décrivons l’observation d’un LK du mésocôlon ascendant, réséqué de façon conservatrice, mais curative.
These observations support our conviction that the sole condition of primary massive splenomegaly, with subsequent portal overflow, is not sufficient to induce a portal hypertension, in absence of concomitant or secondary disorders of the liver or of the portal system [2]. Therefore, when a condition of portal hypertension complicates splenomegaly in patients with haematological malignancies, further clinical and radiological examinations are indicated to investigate possible disorders of the liver or of the portal venous system [3,4]. Nevertheless, we agree that in case of arterio-portal fistula, a sudden and frank increase in the portal pressure and flow can induce a subsequent pre-sinusoidal portal hypertension, through arterialization and intimal hyperplasia of the portal venous branches [5]. Disclosure of interest : the authors declare that they have no conflicts of interest concerning this article.
References [1]
[2] [3]
[4]
[5]
Harris A, Kamishima T, Hao HY et al. Splenic volume measurement on computed tomography utilizing automatically contouring software and its relationship with age, gender, and antropometric parameters. Eur J Radiol 2010;75:97-101. Cichoz-Lach H, Celinski K, Slomka M, Kasztelan-Szczerbinska B. Pathophysiology of portal hypertension. J Physiol Pharmac 2008;59:231-8. Agarwal A, Jain M. Multidetector CT portal venography in evaluation portosystemic collateral vessels. J Med Imaging Radiother Oncol 2008;52:4-9. Zhao LQ, He W, Ji M et al. 64-row multidetector computed tomography portal venography of gastric variceal collateral circulation. World J Gastroenterol 2010;16:1003-7. Guzman EA, Mc Cahill LE, Rogers FB. Arterioportal fistulas: introduction of a novel classification with therapeutic implications. J Gastrointest Surg 2006;10:543-50. Antonio Manenti1, Fabio Forghieri2, Dario Colasanto3, Mario Luppi2 1
University of Modena, departments of surgery, via del Pozzo, 41100 Modena, Italy 2 University of Modena, departments of haematology, 41100 Modena, Italy 3 University of Modena, departments of radiology, 41100 Modena, Italy Correspondence: Antonio Manenti, University of Modena, departments of surgery, via del Pozzo, 41100 Modena, Italy. [email protected] Received 6 December 2013 Accepted 19 February 2014 Available online 13 June 2014
1296
http://dx.doi.org/10.1016/j.lpm.2014.02.024 ß 2014 Elsevier Masson SAS Tous droits réservés.
Cystic lymphangioma of the ascending mesocolon
Observation Un homme âgé de 65 ans, sans antécédent pathologique ni de traumatisme, consultait pour une douleur du flanc droit évoluant depuis deux semaines. La palpation du flanc droit révélait une masse intra-abdominale mobilisable, de consistance ferme. Le bilan biologique était normal. Le scanner abdomino-pelvien avec injection de produit de contraste mettait en évidence, au temps artériel et en coupe axiale, une formation kystique cloisonnée, à parois fines non rehaussées par le contraste, localisée dans la cavité abdominale en regard du côlon ascendant (figure 1). Le diagnostic de LK mésentérique était évoqué. Un traitement chirurgical par laparotomie était proposé. À l’exploration, on retrouvait l’origine mésentérique de la masse kystique développée à partir du mésocôlon ascendant (figure 2). Après dissection et ligature pas à pas des vaisseaux lymphatiques péritumoraux, nous avons constaté un accolement de la masse kystique avec la troisième portion du duodénum sans l’envahir. Une exérèse tumorale complète sans colectomie était réalisée. Le côlon ascendant était de bonne vitalité et conservé. Macroscopiquement, la tumeur était entourée d’une capsule fine, de couleur hétérogène, mesurant environ 8 cm de grand axe. À la coupe, il s’agissait d’une formation nodulaire multiple et kystique à contenu hémorragique et nécrotique. L’examen histologique de la tumorectomie permettait de confirmer le diagnostic d’un LK. Les suites opératoires étaient simples. À 18 mois, le patient était asymptomatique, aucune récidive n’était observée. Discussion Les LK du mésocôlon sont des formes topographiques rares de l’adulte dont la prise en charge peut être alourdie par la nécessité de colectomie [2]. Les cas rapportés intéressaient tome 43 > n811 > novembre 2014
