Gus Tisdale, Anand Mahadevan and Richard H. Matthews
Report and Discussion
T-Cell Lymphoma of the Rectum in a Patient with AIDS and Hepatitis C: A Case
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T-Cell Lymphoma of the Rectum in a Patient with AIDS
and Hepatitis C: A Case Report and Discussion
GUS TISDALE,aANAND MAHADEVAN,bRICHARD H. MATTHEWSb
aDivision of Hematology and Oncology, Department of Medicine, Boston University and Boston Veterans
Health Affairs Medical Centers, Boston, Massachusetts, USA; bDepartment of Radiation Oncology,
Beth Israel/Deaconess Medical Center, Harvard Medical School and Boston Veterans Health Affairs
Medical Centers, Boston, Massachusetts, USA
Key Words. T-cell lymphoma · AIDS · Multimodal treatment · Hepatitis C
Primary T-cell non-Hodgkin’s lymphoma (NHL) occur-
ring in the context of acquired immune deficiency syn-
drome (AIDS) is uncommon. Here, we report and
discuss such a case presenting in the rectum, and review
relevant literature. Although typical in some respects,
the case is, in other ways, somewhat unusual for an
AIDS-related NHL (ARL); ARL tends to be B cell and
advanced stage and our case was T cell and stage IE.
In addition, the patient suffered from concomitant
cirrhosis related to hepatitis C. Chemotherapeutic
options for ARL were limited early in the AIDS epi-
demic due to poor tolerability. Although this has largely
been mitigated by the advent of highly active antiretro-
viral therapy, our patient eventually suffered complica-
tions of chemotherapy, apparently related more to his
liver disease than to either his lymphoma or AIDS, that
ultimately brought about his demise. The Oncologist
The Oncologist 2005;10:292–298
Correspondence: Richard H. Matthews, M.D., Ph.D., Beth Israel/Deaconess Medical Center, Harvard Medical School, 330
Brookline Avenue, Boston, Massachusetts 02215, USA. Telephone: 617-232-9500, ext 4457 or ext 5628; e-mail:
RHMatthews@comcast.net Received April 15, 2004; accepted for publication December 23, 2004. ©AlphaMed Press
The gastrointestinal (GI) tract generally is the most com-
mon site for extranodal non-Hodgkin’s lymphoma (NHL),
usually of the B-cell type. These NHLs may be Epstein-
Barr virus (EBV) related and have long been known to be
associated with immunodeficiency. Various immunodefi-
cient states, including ataxia telangectasia, Wiskott-Aldrich
syndrome, and X-linked lymphoproliferative disorder, all
exhibit increased incidences of NHL. NHL is 60–100 times
more common in HIV-infected patients, and B-cell NHL is
an AIDS-defining illness. AIDS-related lymphomas
(ARLs) show a high incidence (about 95%) of extranodal
involvement, and >50% may be exclusively extranodal.
Most ARLs are of high grade, of B-cell lineage, advanced
stage, and are associated with B symptoms. ARL is usually
a late event in the course of AIDS, coming after some other
AIDS-defining illness . Almost all ARLs are of the B-
cell type and may be related to chronic B-cell stimulation in
HIV-infected patients. T-cell lymphomas are uncommonly
reported in AIDS patients; this could be due to the toxic
effect of HIV on T-cell survival. A registry survey of 6,788
cases of NHL with specified phenotype in AIDS patients
showed that only 1.4% were T-cell lymphomas . Here,
we present an unusual case of extranodal T-cell lymphoma
presenting in the rectum of an AIDS patient with chronic
hepatitis C virus (HCV) infection. We are aware of a case
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of Hodgkin’s disease presenting in the rectum of an HIV-
positive patient, but to the best of our knowledge, this is the
first report of T-cell NHL presenting in the rectum of an
AIDS patient as a solitary site .
The patient was a 46-year-old gentleman who presented to
our facility with a 6-week history of rectal pain and hema-
tochezia in March 2001. His rectal pain was exacerbated by
bowel movements, but he denied constipation, weight loss,
fever, and chills or night sweats. His past medical history did
not include surgery or infection in the anorectal region. The
patient had transiently abused i.v. drugs in the 1980s and had
a history of alcohol abuse. In July 2000, he had suffered a
cavitary mycobacterial lung infection associated with a CD4
count of <5 cells/mm3and an HIV viral load (VL) of
>250,000 copies/ml. He was diagnosed as having AIDS and
was started on highly active antiretroviral therapy (HAART),
consisting of lamivudine (Epivir®; GlaxoSmithKline,
Philadelphia, PA, http://www.gsk.com), stavudine (Zerit®;
Bristol-Myers Squibb, Princeton, NJ, http://www.bms.com),
and efavirenz (Sustiva®; Bristol-Myers Squibb). He quit
using alcohol. The patient’s CD4 was 130 with an unde-
tectable VL by October 2000 (Table 1). His HCV antibody
level was repeatedly positive, and on October 31, 2000, his
HCV level was measured at 63.67 copies/ml in an assay
regarded as investigational. His hepatitis B virus (HBV)
status was assessed repeatedly, and was consistently nega-
tive. His liver function was assessed regularly in terms of
enzymes and bilirubin (Table 2). His alkaline phosphatase
and albumin levels were tabulated also but are not shown, as
there was less variation. The patient was a nonsmoker, was
married with no children, and remained fully active in his
usual work during his evaluation and treatment. Abdominal
computerized tomography (CT) scanning was performed due
293Rectal T-Cell Lymphoma
Table 1. Patient’s response to HAART
Date CD4 value CD4 % HIV viral load (copies/ml)
Table 2. Liver function tests in relation to therapy
DateSGPT, U/l (7–52)a
SGOT, U/l (10–45)a
Total bilirubin, mg/dl (0.2–1.2)a
1st cycle CHOP
2nd cycle CHOP
3rd cycle CHOP started next day
10/24/01 to 11/2/01 low pelvis XRT
11/17/01 NH4+ 72 µmol/l
aRange of normal values shown in parentheses.
Abbreviations: CHOP = cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy; SGOT = serum glutamic-oxaloacetic transaminase;
SGPT = serum glutamic-pyruvic transaminase; XRT = radiation therapy.
by guest on June 7, 2013
to a rising alpha-fetoprotein (AFP) level and abnormal liver
function tests (LFTs); this revealed dilation of the rectal vault,
and a rectal mass could not be excluded. Nodularity was noted
on rectal exam, which was biopsied. Pathology revealed nod-
ules of monomorphic intermediate lymphoid cells consistent
with lymphoma. Polymerase chain reaction (PCR) amplifica-
tion failed to show rearrangement of immunoglobulin heavy
chain genes. Immunohistochemistry confirmed the majority
of the lymphoid cells to be CD3+, CD43+with only scattered
CD20 elements, consistent with a peripheral T-cell lymphoma
of undetermined grade. The presence of CD3 antigen quali-
fied the lymphoma as T cell, whereas CD20 positivity would
have qualified it as B cell .
At his initial medical oncology clinic visit in May 2001,
the patient denied any B symptoms (weight loss, fever,
night sweats). He was afebrile and without regional or gen-
eralized lymphadenopathy. His LFTs were abnormal, with
aspartate aminotransferase and alanine aminotransferase
elevations of 276 U/l (normal 10–45) and 112 U/l (normal
7–52), respectively, alkaline phosphatase of 264 U/l (nor-
mal 30–115), and a total bilirubin of 2.1 mg/dl (normal
0.2–1.2). His lactate dehydrogenase (LDH) level was 255
U/l (normal 90–270) and his AFP was 16.6 ng/ml (normal
0–10). This would be judged as mild-moderate liver dys-
function . Bone marrow and cerebrospinal fluid (CSF)
examinations were normal, and a gallium scan was focally
positive in the rectum only. Thus, his clinical stage was
IEA, with an International Prognostic Index (IPI) of 0. He
was commenced on growth factor-supported combination
chemotherapy with CHOP (cyclophosphamide, doxoru-
bicin [Adriamycin®; Bedford Laboratories, Bedford, OH,
http://www.bedfordlabs.com], vincristine [Oncovin®; Eli
Lilly and Company, Indianapolis, IN, http://www.lilly.com],
and prednisone [Deltasone®; Pfizer Pharmaceuticals, New
York, NY, http://www.pfizer.com]), with the doxorubicin dose
reduced by 25% in cycles 1 and 2 due to his jaundice. In
addition, he received standard intrathecal cytarabine
(DepoCyt®; Enzon Pharmaceuticals, Inc., Bridgewater, NJ,
http://www.enzon.com) central nervous system (CNS) pro-
phylaxis. His first cycle resulted in anemia and fatigue, and he
developed worsening jaundice after the second cycle. A
delayed third cycle with a 25% reduced dose of doxorubicin
and a 50% reduced dose of vincristine was further complicated
by neuropathy and a further deterioration in liver function
(Table 2). He was referred for local field radiation therapy.
Initial plans were to treat the patient with 4,000 cGy in 20
fractions with parallel-opposed fields using 18-MV photons,
including the rectum and the adjoining pelvis. Conformal
field blocks were designed to reduce bowel toxicity. After
seven treatments (1,400 cGy), he was hospitalized with
mental status changes and liver failure, and his radiation
treatment was discontinued. After an episode of hemateme-
sis he went on to develop acute tubular necrosis leading to
multisystem failure and he died a few days later.
The progressive increase in NHL in recent years is only
partially explained by the AIDS epidemic. In a New Jersey
study, AIDS was associated more with the increase in NHL
in younger rather than older age groups . Combination
drug therapy for AIDS came into general use in 1995, and
the period of the mid-to-late 1990s saw marked reductions
in serious infections and deaths in AIDS patients. The inci-
dence of Kaposi’s sarcoma (KS) fell more sharply than that
of ARL in this period [7, 8]. Primary CNS lymphoma in
AIDS has been reduced in incidence about 20-fold since the
introduction of HAART, with systemic immunoblastic lym-
phomas diminishing to a lesser degree. Interestingly, these
effects on ARL incidence rates only become statistically
evident after about a year of therapy; our patient had perhaps
not started to benefit from HAART’s effects in preventing
ARL at the time of his diagnosis. The incidences of Burkitt’s
lymphoma and Hodgkin’s disease are unchanged since the
advent of HAART . A possible decline in ARL in the
HAART era is not as clear-cut as the decline in KS; depend-
ing on the series and mix of lymphoma types, it may even be
going up. NHL is AIDS defining in only 3% of cases, but
the cause of death in as many as 20% of cases . Low
CD4 counts have been linked to the occurrence of ARL .
HAART increases CD4 counts, decreases opportunistic
infections, and increases survival in AIDS patients .
Primary intestinal lymphomas in the general population
are of the T-cell type in 10%–34% of cases, and have been
described as presenting as rectal bleeding . In Western
countries, EBV appears not to play a pivotal role in the
pathogenesis of ARL, in contrast to the more direct link
evidenced by higher levels of EBV RNA transcripts in
tumors diagnosed in the Third World. The exact mecha-
nism of EBV involvement is not yet known , although
multiple related actions have been described .
Peripheral T-cell neoplasms by the Revised European-
American Classification of Lymphoid Neoplasms/World
Health Organization Classification of Lymphoid Neoplasms
are a family of lymphoid neoplasms, of which peripheral
T-cell lymphoma, not otherwise specified, is only one gen-
eral entity but is apparently the most appropriate designation
for our present case. Some of the other family members are
T-cell prolymphocytic leukemia, adult T-cell lymphoma/
leukemia (which is human T lymphotropic virus 1 positive),
mycosis fungoides, hepatosplenic gamma-delta T-cell lym-
phoma, and enteropathy-type T-cell lymphoma. This last
lymphoma has a GI location, but is usually found in the
Tisdale, Mahadevan, Matthews294
by guest on June 7, 2013
jejunum and is associated with a gluten-sensitive enteropa-
thy, and the disease generally follows a short, aggressive
course, with the patient expiring with multiple perforated
jejunal malignant ulcers .
Geographical variation has been observed in the associa-
tion between HCV and B-cell lymphomas [16, 17]. A recent,
large Italian series found 5 of 287 (0.31%) HCV-infected
patients with liver lesions had B-cell NHL, an approximate
12-fold higher incidence than in the general population .
HCV is known to be lymphotropic as well as hepatotrophic,
and its transcripts can be detected in CD34+stem cells. It has
been hypothesized that chronic immune stimulation leads to
both mixed cryoglobulinemia and an increased incidence of
B-cell NHL .
The staging work-up of ARL should include CT scans of
the chest, abdomen, and pelvis since two-thirds of ARL
patients will have intra-abdominal disease in such areas as
lymph nodes, the GI tract, the liver, the kidney, or the adren-
als . Laparotomy would rarely be used for staging today;
in an earlier era its systematic employment disclosed that, in
clinical stage I and II supradiaphragmatic non-AIDS related
NHL, only 22.5% of diffuse lymphomas were advanced in
stage at laparotomy, whereas 61% of nodular or follicular
lymphomas were advanced in stage at laparotomy . 67-
Gallium scanning can be useful at staging or in follow-up in
deciding whether a residual mass is likely to be a viable
tumor or not . Since CNS or leptomeningeal involvement
complicates ARL in 15%–40% of cases, lumbar puncture is
often included in the work-up .
Adverse prognostic factors for ARL include a CD4 count
of <100, a Karnofsky Performance Status score of <70%,
age >35 years, stage III or IV disease, an elevated LDH
level, and a history of injection drug abuse, factors of which
our patient had just two, age 46 and an earlier history of
injection drug abuse . HCV positivity has been reported
to be much higher in injection drug abusers than in homo-
sexuals . Prognostic evaluations of NHL in the general
population have used the IPI, which incorporates Ann Arbor
stage, age, elevated LDH level, performance status, and
number of extranodal sites [22, 24]. According to this mea-
sure, our patient was at moderate risk for recurrence and
death from his NHL. However, survival rates for ARL have
been poor relative to results in the general population .
Several groups published studies circa 1989–1991 com-
paring modest numbers of T-cell lymphomas with diffuse
large B-cell lymphomas and came to the general conclusion
that they were prognostically somewhat similar [26–28]. In
1997, a group from the MD Anderson Cancer Center pub-
lished a study with larger patient numbers, arriving at the con-
clusion that the T-cell immunophenotype was an independent
adverse prognostic factor, in contrast to diffuse large B-cell
lymphoma . Presumably, our patient’s T-cell morphology
would be considered an adverse factor.
CHOP chemotherapy may be regarded as the standard reg-
imen to use for ARL, whether of the B- or T-cell type,
although several modified regimens and doses are in some use,
including CDE (cyclophosphamide, doxorubicin, etoposide
[Etopophos®, VePesid®; Bristol-Myers Squibb]), and EPOCH
(etoposide, prednisone, vincristine, cyclophosphamide, dox-
orubicin) . ARL patients should also be treated with
HAART, which maximally suppresses HIV-1. The present
National Comprehensive Cancer Network guidelines treat
peripheral T-cell lymphomas as they do diffuse large B-cell
lymphomas, that is, by a combination of CHOP chemotherapy
and involved-field radiation therapy . Several studies are
available to support the use of combined-modality therapy for
localized intermediate or high-grade NHL; the common spe-
cific entity treated is, however, diffuse large B-cell lymphoma
[30–32]. Published evidence is unclear as to the necessary
degree of anthracycline dose reduction in patients with
advanced liver cirrhosis ; we employed a minor reduction.
Another consideration, the vinca alkaloids, have been
observed to be neurotoxic in the setting of hepatotoxicity due
to reduced drug clearance ; our patient did experience a
degree of this. Successful antiviral treatment of viral hepatitis
reactivated by systemic chemotherapy has been described,
although the scenario of reactivation then reported successful
hepatitis treatment, is uncommon . A Japanese survey sug-
gests that chemotherapy regimens containing steroids (com-
mon in lymphoma treatment) may be associated with fatal
reactivation of hepatitis .
By general standards, our patient received appropriate
therapy, only to die from progression or reactivation of pre-
existing hepatic disease. Given the advantage of hindsight, an
alternative plan that might have given a better outcome for
our patient would be to have given only two cycles of CHOP
therapy with some reduction of anthracycline, and possibly
of steroid, followed by involved field radiotherapy to control
the identified disease, considering his stage I status. Two
more cycles after a rest period might then be considered. This
might (or might not) have altered the outcome. The hazard of
reactivation of HBV with cytotoxic therapy for NHL is more
clearly established. Cytotoxic and immunosuppressive ther-
apy enhances viral replication, with a consequent increase in
hepatocyte infection. When cytotoxic or immunosuppressive
drugs are withdrawn, immune function becomes restored,
resulting in destruction of infected hepatocytes, which
appears as acute hepatitis or hepatic failure [35, 36]. NHL
patients with hepatitis B surface antigen are particularly at
risk, with clinical hepatitis in 20%, with perhaps 3%–4%
mortality. The great majority of them, however, ultimately
295 Rectal T-Cell Lymphoma
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A reported series of 33 patients who were HCV positive and
were treated with cytotoxic chemotherapy for leukemias/lym-
phomas (26 had B-cell lymphomas) were followed and moni-
tored with LFTs. Eighteen of them encountered increases in
transaminase levels of a mild-moderate nature, occurring 2–3
weeks after withdrawal of chemotherapy. Only one of the 33
had a severe flare of hepatitis C. No patient died of liver failure,
and the final post-treatment levels of transaminases did not dif-
fer significantly from the pretreatment levels . Although fol-
lowing enzyme levels is the usual manner of gauging liver
dysfunction, some patients who, at liver biopsy, have signifi-
cant fibrosis or cirrhosis have fairly benign enzyme levels .
Stage of liver fibrosis with HCV infection has been found to be
worse with heavy alcohol consumption and male gender .
A study of cyclic chemotherapy for NHL in patients with either
HBV or HCV positivity associated a relevant number of hepati-
tis cases with HBV, but not with HCV . An Italian study of
NHL, with 37% of patients HCV positive, found that, with sim-
ilar chemotherapy regimens employed, there was no difference
in survival with HCV positivity . In contrast to the forego-
ing studies, Vento et al.  reported that two cases of NHL
patients who were HCV positive and treated with chemother-
apy developed severe hepatitis after chemotherapy was with-
drawn, and one of them died of liver failure; no denominator
was given. High-dose chemotherapy with autologous or allo-
geneic transplant may, in the future, be applicable in ARL
given that newer HAART regimens have improved patient tol-
erability of aggressive therapies [42, 43]. However, the pres-
ence of severe comorbidities, such as active liver disease, even
with preserved performance status, may remain a harbinger of
poor outcome for aggressive therapies. Bone marrow transplant
patients have been known to be at appreciable risk for reactiva-
tion of hepatitis C, and two hepatic deaths were reported in one
series of 11 patients . A second report also cited two deaths
related to bone marrow transplant following withdrawal of
immunosuppressive therapy . These were two acute
leukemia patients who contracted post-transfusion hepatitis
during chemotherapy for induction and consolidation.
Membranoproliferative glomerulonephritis is one of the extra-
hepatic manifestations that has been associated with HCV
When planning treatment for a particularly unusual lymphoma
presentation, such as this case of stage IE T-cell lymphoma of
the rectum in an HCV/HIV coinfected patient, one must apply
general principles, given the absence of applicable large series.
An overall management approach popular for some time for
early-stage, aggressive lymphomas is involved-field radiation
therapy combined with systemic chemotherapy such as CHOP
. In such a plan, the role of radiation therapy is to reduce
the risk of failure in the area of original gross disease, while
chemotherapy reduces the risk of failure at distant sites .
Optimal treatment of an AIDS patient also includes HAART.
Despite a preserved performance status and favorable tradi-
tional prognostication scores, the outcome may still be poor
when concomitant viral hepatitis and T-cell disease morphol-
ogy lessen disease responsiveness and hamper tolerability of
chemotherapy. A recent article suggests use of interferon-α
and ribavirin (Virazole®; Valeant Pharmaceuticals, Inter-
national, Costa Mesa, CA, http://www.valeant.com) to treat
HCV infection, but also notes problematic ribavirin interactions
with HAART drugs .
DISCLOSURE OF POTENTIAL CONFLICTS OF INTEREST
The authors indicated no potential conflicts of interest.
Tisdale, Mahadevan, Matthews296
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