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Kaposi sarcoma
 

Kaposi sarcoma

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    Kaposi sarcoma Kaposi sarcoma Document Transcript

    • Clinical Nephrology, Vol. 71 – No. 2/2008 (214-216) Kaposi’s sarcoma in renal transplantation: Report of three cases E. Razeghi1, A. Hadadi2, P. Khashayar3 and G. Pourmand4 Case Report 1Nephrology, 2Infectious Diseases, 3Research and Development Center and ©2009 Dustri-Verlag Dr. K. Feistle 4Urology, Urology Research Center, Sina Hospital, Medical Sciences, ISSN 0301-0430 University of Tehran, Iran Kaposi’s sarcoma in renal transplantation Key words Abstract. Kaposi’s sarcoma (KS) is one the control subjects of the same ethnic origin transplant – Kaposi’s of the most common post transplant malig- [Bedan et al. 1999]. sarcoma – CMV infec- nancies. A variety of factors appears to con- tion Several studies have shown that in com- tribute to the development of KS including genetic factors, sex hormones, immunosup- parison to colorectal and breast cancer, KS is pression and oncogene viruses. We present 3 more prevalent in transplant recipients. It cases with concurrent KS and cytomegalo- should be noted that this tumor may be cured virus (CMV) infection in the first year after if the immunosuppressants are discontinued kidney transplantation. The suspicion on KS or reduced in this group of patients [Penn due to the skin lesions was confirmed by bi- opsy. The diagnosis of CMV infection was 2001]. made by detecting pp65 antigen in blood. The KS has a multi-centric origin and is char- KS lesions were limited to the skin in 2 pa- acterized by vascular and fibroblastic prolif- tients, while skin and gastrointestinal tract eration [Bedan et al. 1999]. Skin, conjunctiva were involved in 1 patient. Many factors are or oropharyngolaryngeal mucosa are in- reported to be involved in KS development, but the simultaneous occurrence of KS and volved in 58% of transplant patients with KS; CMV infection in our three cases suggested as for visceral disease mainly involving the CMV as an inducing factor for KS. gastrointestinal tract, lung and lymph nodes, they are reported to be present in about 42% of the patients [Bedan et al. 1999, Penn 2001]. The cause of post transplant KS remains Introduction unknown. Oncogenic viruses of the herpes type are believed to play an important etiolog- It is well established that organ transplant ical role [Brunner et al. 1995]. In kidney re- recipients receiving immunosuppressants cipients, the definite associating role of other have an increased risk for malignancy devel- viruses such as cytomegalovirus, the most opment [Boubenider et al. 1997]. common source of opportunistic infection, is Indeed, more than one in five patients ex- not yet clear [Moosa 2005]. periences malignancy within 15 years after We present 3 cases of kidney transplant kidney transplantation, this rate rises to more recipients who developed KS concurrently or than two in five patients within 20 years [Lon- shortly after cytomegalovirus infection in the Received don et al. 1995]. Malignancies related to vi- first year after transplantation. June 2, 2008; ruses occur more often in patients who have accepted in revised form undergone kidney transplantation compared June 24, 2008 with the general population [Brunner et al. Case 1 Correspondence to 1995, Kasiske et al. 2000, London et al. E. Razeghi, MD 1995]. Associate Professor of A 50-year-old man with end stage renal Nephrology, Urology Kaposi sarcoma (KS) is one of the most disease secondary to autosomal dominant Research Center, Sina common post transplant malignancies. An polycystic kidney disease received a living Hospital, Imam epidemiological study has shown a 400 -500 unrelated renal allograft. The CMV antibody Khomeini St. 11367- 46911, Tehran, Iran fold increase in the incidence of Kaposi sar- state prior to transplantation was positive in Effatl62@yahoo.com coma in this group of patients compared with both recipient (R+) and donor (D +).
    • Kaposi’s sarcoma in renal transplantation 215 He was prescribed a triple immunosup- At the 8th month after transplantation, she pressive regimen including cyclosporine presented with weakness, fatigue, thrombo- (Neoral), mycophenolate mofetil (MMF) and cytopenia, anemia and purpuric lesions. prednisolone. During the necessary work-up, the labora- Three months after transplantation, the tory data supported possible CMV infection patient presented with fever, fatigue, weak- and as a result ganciclovir was prescribed. ness and diarrhea. The diagnosis of CMV was One month later, she presented with purple made by detecting PP65 antigen and gan- lesions on the anterior side of both legs. Bi- ciclovir was prescribed. In the following opsy of the lesions confirmed KS. Cyclo- month, he developed diffuse reddish blue sporine maintenance therapy was reduced to plaques and papules on the skin, with no 2 mg/kg/day and radiotherapy was indicated. lymphadenopathy. Biopsy of the skin lesions After a few months the lesions regressed. confirmed the diagnosis of KS. Thoracic Gal- lium Scan was negative. Gastrointestinal en- doscopy and colonoscopy showed Kaposi- Discussion like mucosal lesions which were confirmed by biopsy. Kaposi’s sarcoma secondary to an immuno- Cyclosporine and mycophenolate mofetil suppressed state was first identified in 1969 in were stopped but KS did not regress and so kidney recipients. Since then, several cases of chemotherapy was started. KS were reported in patients receiving im- munosuppressives. This disease was also re- ported as the most frequent cancer following Case 2 kidney transplant in developing countries [Moosa 2005]. A 53-year-old man with endstage renal Two histologically characteristic features disease secondary to diabetes mellitus re- of KS are known to be proliferation of ceived a living unrelated renal allograft. The angiomatous lesions and of spindle shaped CMV state before transplantation was docu- cells [Itkura et al. 1990]. The cause of post mented to be R+, D+. transplant KS remains unknown. Some fac- He received an immunosuppressive regi- tors such as genetic predisposition and onco- men consisting of cyclosporine (Neoral), genic viruses particularly herpes viruses are MMF and prednisolone. He returned to hos- reported to be involved in addition to the im- pital with diffuse purple skin lesions and con- munosuppression therapy [Regumey et al. stitutional complaints after 5 months. Biopsy 1998]. of the lesions confirmed KS and immuno- Genetic differences are based on ethnical histological assay for PP65 confirmed CMV differences; for instance, compared with the infection. Thoracic computerized tomogra- normal population, HLA-A2 is more frequent phy and gastrointestinal endoscopy were both in KS patients of Saudi Arabia because of the negative. Antiviral therapy was started and higher prevalence of HHV-8 in this group immunosuppressive drugs were reduced. [Moosa 2005]. Recovery to some extent was first re- According to epidemiologic, serologic ported however the skin lesions reappeared and geographic studies and the histological after a few months. So chemotherapy was findings, CMV is identified as a risk factor for recommended. Kaposi sarcoma [Itkura et al. 1990]. In an- other study carried out to reveal the relation between CMV infection and Kaposi’s sar- Case 3 coma in 64 patients with classic, endemic and epidemiologic KS, CMV -DNA was only A 43-year-old woman with endstage renal identified in 10 of the patients who had AIDS disease of unknown etiology received a renal and in neither of classic or endemic cases. allograft. She received the immunosuppres- This study did not confirm the distribution sive drugs including cyclosporine, azathio- and location of infected CMV cells as a major prine and prednisolone. The CMV state was pathologic stimulant factor for KS. In other reported to be R+, D+ before transplantation. words, similar to other immuno-suppressed
    • Razeghi, Hadadi, Khashayar and Pourmand 216 patients, CMV was identified as an opportu- Itkura H, Toriyama K, Uzuta F et al. Kaposis sarcoma. Gan to Kagaku Ryoho. 1990; 17: 620-626. nistic infection in these patients [Chakala- Kasiske BL, Vazquez MA, Harmon WE et al. Recommen- rouski et al. 1992]. dations for the outpatient surveillance of renal trans- In our patients, KS developed concur- plant recipient American society of transplantation. rently or shortly after CMV infection which JAM Soc Nephrol 2000; II (Suppl 15): 51-86. London NJ,Farmery SM, Will EJ et al. Risk of neoplasia was similar to other studies [Seigal et al. in renal transplant patients. Lancet 1995; 346: 1990]. 403-406. In a study reactivation of cytomegalovirus Moosa MR. Kaposis Sarcoma in kidney transplant recipi- ents: a 23-year experience. QKM. 2005; 98: 205-214. was reported in the serologic tests when KS Penn I. Neoplasms in renal transplant recipients. In: was diagnosed [Vlasic-Matas et al. 1994]. It Massry SG, Glassock RJ (eds.) Massry and Glassocks is possible that CMV infection secondary to textbook of nephrology, 4th edition. Philadelphia: the considerable pharmacological immuno- Lippincott Williams Wilkins; 2001. pp. 1672-1677. Regumey N, Tamm M, Wemli M et al. Transmission of hu- suppression was the cause making our pa- man herpes virus and infections from renal transplant tients more susceptible to develop KS. donors to recipients. N Engl J Med. 1998; 339: In neither of the patients presented in this 1358-1368. article, there was no sign of regression fol- Seigal B, Levinton-Kriss S, Schiffer A et al. Kaposi sar- coma in immunosuppression. Possibly the result of a lowing the immunosuppressive medication. dual viral infection. Cancer. 1990; 65: 492-498. It is possible that the unresponsiveness of our Vlasic-Matas J, Rumboldt Z, Puizina-Ivic N et al. Kaposi patients was due to the severity of disease or sarcoma in patients with kidney transplantation. Lijec Vjesn. 1994; 116: 95-97. other factors. In addition, the presence of other factors (particularly HHV8) could neither be excluded nor discussed in order to define their hypothetical pathogenic role. The association of CMV and KS suggests CMV as an inducing factor in KS. However it is not possible to completely rule out other factors especially herpes Type 8 and their pathologic role. Association of KS and CMV infection in these three patients suggests the role of CMV in developing Kaposi sarcoma. Finally, simultaneous CMV infection as the most important opportunistic infection indi- cates the severe immunosuppressive condi- tion in patients. As a result it is recommended to check the CMV state in patients with KS lesions, because the infection is treatable. Reference Bedan PL, Risichella IS, strumia R et al. Kaposis sar- coma in renal transplant recipients: pathogenetic rela- tion between the reduced density of Langerhans cells and cyclosporine therapy. J Nephrol. 1999; 12: 193-195. Boubenider S, Hiesse C, Goupy C et al. Incidence and consequences of post-transplantation lymphoproli- ferative disorders. J Nephrol. 1997; 10: 136-145. Brunner FP, Landis P, Selwood NH. Malignancies after renal transplantation: The EDTA-ERA registry expe- rience European Dialysis and Transplantation Associ- ation – Europeran Renal Association. Nephrol Dial Transplant. 1995; 1 (Suppl 1): 74-80. Chakalarouski C, Lang P, Buisson C et al. Monoclonal immunoglobulins in patients with renal transplants: characterization evolution and risk factors. Transpl Int. 1992; 5 (Suppl 1): 23-25.