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
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:
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.
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consequences of post-transplantation lymphoproli-
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