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GENERAL CARE OF THE PATIENT WITH HIV AND CANCER
I. GENERAL. A malignancy develops in about 20% of patients with human immunodeficiency virus (HIV) during their lifetime, and is often the first clinical evidence of HIV infection. It is also responsible for 28% of AIDS patients’ deaths. The most common malignancies in this patient population are non-Hodgkin’s lymphoma, Kaposi’s sarcoma, and anogenital carcinoma. The incidence of other malignancies is also increased in HIV-infected patients, including Hodgkin’s lymphoma (HL), lung cancers, multiple myeloma, testicular tumors, hepatocellular carcinomas (HCCs), and childhood sarcomas. The frequency of non-AIDS–defining cancers has increased significantly over the last 15 years, and has been attributed to expansion of the HIV-infected population and aging. Most of these malignancies are associated with oncogenic viruses, including Epstein–Barr virus (EBV), human herpesvirus-8 (HHV8), and human papilloma viruses (HPV). When CD4 cell counts drop below 200 cell/mL, HIV-infected patients tend to experience greater toxicity with chemotherapy. Dose modifications and dose delays are common in this setting. Often, personalized dose modifications in lower performance status patients may be chosen by treating physicians. Providers need to be cognizant of any drug–drug interactions of highly active antiretroviral therapy (HAART) with antitumor therapies as well as supportive medications. Regular discussion between medical oncologists, infectious disease specialists, and radiation and surgical oncologists are essential. Maximizing nutritional status can assist in minimizing toxicity and accelerating recovery from therapy. Social work assistance is invaluable for these patients, who often have other financial, social, and personality difficulties.
II. DIAGNOSTIC STUDIES FOR HIV INFECTION should be considered in patients who are not known to be HIV infected, but who develop a malignancy that occurs at increased frequency with HIV infection. Many patients with HIV infection are unaware of their risk factors or deny their existence. HIV testing is recommended to all individuals presenting with aggressive B-cell lymphomas, Kaposi’s sarcoma, or anogenital carcinomas, as well as individuals with any malignancy who have higher than average risk for HIV (i.e., IV drug abusers, homosexuals or bisexuals, individuals with large numbers of sexual partners, and individuals from countries in Africa, southeast Asia, or parts of the Caribbean where HIV is especially prevalent). Appropriate pre- and posttesting counseling services should be available for these individuals. The screening HIV test is an enzyme-linked immunosorbent assay (ELISA), which, if positive, is confirmed by Western blot or plasma HIV RNA assay. The rapid, point-of-care, HIV antibody tests are an acceptable alternative to the ELISA and are in wide use. If HIV is diagnosed concurrently with such a malignancy, additional clinical evaluation of their HIV infection may be indicated. Plasma HIV RNA and CD4 should be determined during the evaluation of HIV-associated malignancies. However, it is important to recognize that chemotherapy can cause wide fluctuations of the CD4 count that may not be an accurate measurement of the immune status.
III. HAART will usually be recommended as concurrent therapy for the malignancy, and, in some cases, prophylaxis for opportunistic infections (OIs). Although issues of drug interactions and excessive toxicity must be considered, there is now considerable evidence supporting the concurrent use of HAART in all HIV-1-infected individuals.
A. HAART regimens include the use of at least three antiretroviral agents with nucleoside- or nucleotide-reverse transcriptase inhibitors (zidovudine, didanosine; didexoycytidine, stavudine, lamivudine, abacavir, and tenofovir emtricitabine) combined with nonnucleoside-reverse transcriptase inhibitors (nevirapine, delaviridine, efavirenz, rilpivirine, etravirine, and protease inhibitors (PIs); indinavir, ritonavir, nelfinavir, saquinavir, amprenavir, lopinavir plus ritonavir, atazanavir, tipranvir, fosamprenavir, and darunavir), fusion inhibitors (T-20, maraviroc), or integrase inhibitors (raltegravir, dolutegravir, and elvitegravir). Several nucleoside combination pills are available, including Combivir (zidovudine plus lamivudine), Epzicom (lamivudine plus abacavir), Trizivir (zidovudine plus lamivudine plus abacavir), or Truvada (tenofovir plus emtricitabine). A triple nucleoside regimen without a nonnucleoside or PI or integrase inhibitor or entry inhibitor is not appropriate. Combination pills that provide appropriate HAART combinations include Atripla (efavirenz plus tenofovir plus emtricitabine), Complera (rilpivirine plus tenofovir plus emtricitabine), and Stribild (elvitegraivr plus cobicistat plus tenofovir plus emtricitabine).
B. Benefits of HAART include a lower incidence of development of HIV-associated malignancies, especially primary CNS lymphoma and Kaposi’s sarcoma. Moreover, with HAART the onset of malignancies in individuals is at a higher level of CD4, there is improved tolerance of full-dose chemotherapy, improved response rates and duration of responses, and improved survival during treatment of their malignancy. Pharmacokinetic studies have suggested that metabolism and clearance of several cytotoxic chemotherapeutic agents is not affected by HAART, but caution is still recommended when high doses of chemotherapy are utilized, for example, during stem cell transplantation studies. Several antivirals are inducers and/or inhibitors of cytochrome Cyp3A4, including PIs, elvitegravir (component of Stribild), and, to a lesser extent, nonnucleoside-reverse transcriptase inhibitors. Thus, adverse interactions may occur with targeted chemotherapeutic agents that are also Cyp3A4 inhibitors or inducers (e.g., dasantinib, imatinib, nilotinib, erlotinib, gefitinib, everolimus, sunitinb, sorafenib, and pazopanib).
C. Specific recommendations for combining HAART with chemotherapy include avoiding the nucleoside analog zidovudine, in light of excessive neutropenia and anemia. Moreover, the PI atazanavir, which causes hyperbilirubinemia in almost one-third of patients, can also be problematic when anthracyclines or vinca alkaloids are utilized. Some authors have also suggested that HAART regimens, including PIs, may be associated with more myelosuppression when combined with chemotherapy than those lacking PIs, although this remains controversial. Caution is recommended in the use of antiretrovirals associated with neurotoxicity (e.g., didanosine, stavudine, and dideoxcytidine) together with chemotherapy regimens including vinca alkaloids, especially in individuals with preexisting HIV-associated neuropathy. PIs commonly cause gastrointestinal (GI) toxicities. It should also be recognized that nucleoside inhibitors may cause lactic acidosis, abacavir may cause a multisystem hypersensitivity reaction, emtricitabine occasionally causes hyperpigmentation of the palms and soles, etravirine causes a rash, nevirapine may cause liver toxicity, and efavirenz is frequently associated with central nervous side effects. Atazanavir, ritonavir-boosted lopinavir, and saquinavir are associated with prolongation of the QT interval, as are anthracyclines, arsenic trioxide, dasatinib, lapatinib, nilotinib, sunitinib, and tamoxifen. Therefore, because of the potential for sudden death, these combinations should be avoided. Well-tolerated regimens for a HAART-naïve patient who will receive chemotherapy would be Truvada (300 mg tenofovir plus 200 mg emtricitabine) once daily with Sustiva (600 mg) once daily, or Truvada once daily with raltegavir (400 mg) twice daily. A preferred initial PI-based regimen for a HAART-naive patient is ritonavir (100 mg)-boosted darunvair (800 mg) once daily with Truvada once daily.
D. Initiation of HAART therapy should be accompanied by liver function tests; amylase and lipase as baseline values since several antiretrovirals (e.g., didanosine) can cause pancreatitis; an HIV genotype test to identify drug-resistant mutations; fasting glucose and lipid profile since PIs may cause dyslipidemias and glucose intolerance; a serologic tests for syphilis, hepatitis A, B, and C viruses, toxoplasmosis, cytomegalovirus (CMV) assays; glucose-6-phosphate dehydrogenase testing in case dapsone will be needed; cervical Papanicolaou smear, opthalmalogy examination, and anal and cervical screening for HPV if available; and tuberculin skin test, chest radiography, and an electrocardiogram since HIV may be associated with cardiomyopathy. Vaccinations for influenza, hepatitis A and B viruses, and Streptococcus pneumonia should also be considered.
E. Optimal care of the HIV-infected patient should be done in collaboration with an infectious disease specialist. During active treatment, repeat HIV RNA levels should be assessed, and after completion of therapy, both HIV RNA and CD4 counts should be obtained.
IV. PROPHYLAXIS FOR OPPORTUNISTIC INFECTIONS (OIs) is also indicated in individuals with depressed CD4 count. Since chemotherapy can also transiently affect the CD4 count, it has been suggested that OI prophylaxis recommendations be expanded in individuals receiving chemotherapy. Thus, if it is anticipated that the CD4 count will decline below 200/mm,3 prophylaxis for Pneumocystis jiroveci pneumonia (PCP) is recommended with bactrim thrice weekly, or in allergic patients, dapsone or atovaquone. If the CD4 count is anticipated to decline below 50/mm3, prophylaxis for Mycobacterium avium intracellulare (MAI) is also indicated with weekly azithromycin. In individuals with prior OI, who have a CD4 count above these cut-off values and have discontinued prophylactic antibiotics, resumption of prophylactic antibiotics concurrent with chemotherapy may be indicated. Special attention is also recommended in evaluating possible clinical signs of OI in the HIV-positive patient receiving chemotherapy as follows: (1) any CD4 count: oral and esophageal Candidiasis, Mycobacteria including tuberculosis, bacterial pneumonias, histoplasmosis, or coccidiomycosis, (2) CD4 <100: MAI, Toxoplasma, encephalitis, and (3) CD4 <50: CMV retinitis, pneumonitis, or colitis, or progressive multifocal leukoencephalopathy.
V. EVALUATION OF ANEMIA IN AN HIV-POSITIVE PATIENT WITH A MALIGNANCY should consider causes other than chemotherapy or antiretrovirals, and should also include other causes of decreased erythropoiesis including (1) drugs (e.g., trimethoprim-sulfamethoxazole, ganciclovir, and dapsone), (2) nutritional deficiency of iron, folate, or vitamin B12, (3) effects of uncontrolled HIV on bone marrow stromal cells, (4) OIs (e.g., parvovirus, atypical or typical mycobacteria, or histoplasmosis, and (5) preexisting conditions (e.g., sickle cell disease or thalassemia). Alternatively, causes of erythrocyte loss should also be considered, including (1) hemolysis due to thrombotic thrombocytopenic purpura, glucose-6-phosphate dehydrogenase deficiency, autoimmune hemolytic anemia, or drug-induced hemolysis, (2) GI bleeding that may complicate lymphoma, Kaposi sarcoma (KS), or enteric infections due to CMV, Candida, or parasites, or (3) hypersplenism associated with infection, lymphoma, or cirrhosis that may complicate hepatitis B or C virus infections.
VI. EVALUATION OF NEUTROPENIA IN AN HIV-POSITIVE PATIENT WITH A MALIGNANCY should consider causes other than chemotherapy or antiretrovirals. These include causes of decreased myelopoiesis from drugs (e.g., ganciclovir, trimethoprim-sulfamethoxazole, pentamidine, rifabutin, and dapsone), nutritional deficiencies (e.g., folate or vitamin B12 deficiency), infections (e.g., uncontrolled HIV, atypical or typical mycobacteria, histoplasma), or bone marrow involvement by the malignancy (e.g., lymphoma, multiple myeloma). Increased loss of neutrophils may occur with autoimmune neutropenia or hypersplenism. Granulocyte colony stimulating factor (G-CSF) has been shown to be safe and effective in HIV-infected patients, although there is controversy about the use of granulocyte–macrophage colony stimulating factor (GM-CSF), which can potentiate HIV replication in macrophages.
VII. EVALUATION OF THROMBOCYTOPENIA IN AN HIV-POSITIVE PATIENT WITH A MALIGNANCY should consider causes other than chemotherapy or antiretrovirals. Causes of decreased thrombopoiesis include (1) drugs (e.g., trimethoprim-sulfamethoxazole, pyrimethamine, ganciclovir, fluconazole, and clarithromycin), (2) nutritional deficiency (e.g., folate or vitamin B12), (3) infection (e.g., uncontrolled HIV, mycobacteria, histoplasma, or Bartonella henselae), or (4) bone marrow involvement by lymphoma. Causes of decreased platelet survival include (1) immune thrombocytopenic purpura from HIV infection or autoimmune conditions, (2) thrombotic thrombocytopenic purpura, or (3) hypersplenism.
ACQUIRED IMMUNODEFICIENCY SYNDROME-ASSOCIATED DIFFUSE LARGE B-CELL LYMPHOMAS (DLBCL)
I. CLINICAL PRESENTATION
A. Non-Hodgkin’s lymphomas (NHL) are 100- to 200-fold more frequent in HIV-positive individuals than the general population, and occur in 5% to 10% of HIV-infected individuals. HIV-DLBCL accounts for about 5% of all DLBCL cases in the United States. AIDS-associated lymphomas are generally aggressive B-cell malignancies that present at an advanced stage with extranodal involvement in more than two-thirds of individuals.
B. Pertinent history should include performance status, duration of HIV infection, treatment of OIs, and current antiretroviral regimen.
C. B symptoms, such as fever, night sweats, and weight loss in excess of 10% of the normal body weight, are very common, but should be attributed to AIDS-associated lymphoma only after the exclusion of OIs. Extreme fatigue from anemia caused by bone marrow involvement may be seen.
D. Lymph node enlargement may be asymptomatic or associated with pain or obstructive symptoms. This should be differentiated from persistent generalized lymphadenopathy (PGL) due to HIV replication or other AIDS-related OIs. Splenomegaly is commonly present, and may be related to the cause of lymphadenopathy.
E. GI involvement causing anorexia, nausea, vomiting, hemorrhage, change in bowel habits, or obstruction occurs in 10% to 25% of patients. Jaundice and abdominal discomfort may be due to lymphomatous hepatic or pancreatic involvement.
F. CNS or meningeal involvement resulting in seizures, altered mental status, and neurological defects occurs in 10% to 30% of patients. Other causes of neurological defects in this patient population should also be considered, such as HIV-associated encephalopathy.
G. Pleural or pericardial effusions may cause dyspnea and chest discomfort.
H. The physical examination should include careful examination and measurements of enlarged lymph nodes, spleen, and liver. Pulmonary and cardiac examinations may reveal pleural or pericardial effusions. A thorough neurological examination should be done to determine the presence of meningismus or focal neurological defects.
II. DIAGNOSTIC WORKUP AND STAGING
A. Pathology. Definitive diagnosis of AIDS-associated NHL is made with the identification of lymphoma in lymph node biopsies or other tissues (bone marrow, cerebrospinal fluid (CSF), pleural fluid, and liver), in an HIV-infected individual. DLBCL is characterized by large noncleaved cells that usually express cell surface pan-B-cell marker, CD20, and lymphocyte common antigen, CD45, but not CD3. The transcription factor Bcl-6 is expressed in the centroblastic subtype but not the immunoblastic subtype. In contrast, the immunoblastic subtype is typically characterized by CD138 expression as well as EBV latent membrane protein-1 (LMP-1). Centroblastic DLBCL is thought to arise in the germinal center (GC), whereas immunoblastic DLBCL is a post-GC lymphoma. GC B-cell-like type DLBCL is considered when CD10 is expressed in >30% of the malignant tumor cells, or if cells are CD10−, BCL6+, and IRF4/MUM1−. All others are considered to be activated B-cell-like type or non-GC types. Cytogenetics or FISH should be performed for MYC translocations, since these variants have a poor outcome with CHOP therapy.
B. Laboratory tests. Complete blood counts may reveal anemia, leukopenia, or thrombocytopenia, even if there is no marrow involvement. Serum chemistries may show abnormalities in liver function tests, elevated lactate dehydrogenase (LDH), calcium, or uric acid. Electrolytes and creatinine should also be monitored during therapy.
C. Radiology/procedures
1. Computed tomography (CT) scan of the chest, abdomen, and pelvis with a CT or an MRI scan of the brain is necessary for the staging of AIDS-related NHL. Special attention should be given to mesenteric adenopathy, a site not usually affected in PGL.
2. PET scans are helpful in distinguishing adenopathy due to lymphoma that generally shows significant uptake of fluorodeoxyglucose (FDG) from that associated with PGL or OIs, which show less intense FDG uptake. Alternatively, gallium scanning may be useful for this purpose. PET or gallium scans are useful to detect residual disease after therapy, and to distinguish fibrosis from refractory tumor.
3. Bone marrow aspiration and biopsies reveal bone marrow involvement in approximately 20% of patients, and may be associated with increased risk of CSF involvement.
4. Lumbar puncture should be performed and CSF sent for cytological examination. Cell count and protein may be normal or elevated, whereas glucose may be low. Analysis of CSF by flow cytometry or for EBV DNA by polymerase chain reaction (PCR) may predict lymphomatous meningitis.
D. The Ann Arbor staging for NHL also is used for AIDS-related NHL. Prognostic factors correlating with poor survival in patients with AIDS-related NHL include stage IV disease, Karnofsky performance status less than 70%, CD4 count less than 100/mm3, elevated LDH, and history of OIs before lymphoma diagnosis.
III. THERAPY
A. m-BACOD (methotrexate, bleomycin, doxorubicin, vincristne, and dexamethasone) was used in AIDS-DLBCL patients in the pre-HAART era. Given in a low-dose regimen, this resulted in 41% complete remissions and median survival of 35 weeks, whereas standard dose m-BACOD with GM-CSF resulted in 52% complete remissions with a median survival of 31 weeks and more grade 3 toxicity (70% vs. 51%). Since the demonstration in the HIV-negative population that m-BACOD was similar in efficacy to CHOP, the m-BACOD regimen has not been routinely utilized in AIDS-DLBCL.
B. CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone) given at the same doses as in the HIV-negative patient population together with HAART and G-CSF is feasible and effective (J Clin Oncol 2001;19:2171). In a nonrandomized study, this therapy resulted in a complete response (CR) rate of 30% when given in low doses, and 48% when full doses were provided. The chemotherapy had no adverse effect on HAART activity. Moreover, HAART with a PI, indinavir, had no effect on doxorubicin clearance and only a 1.5-fold reduction in cyclophosphamide clearance, which did not translate into excessive neutropenia.
C. R-CHOP was not significantly more effective than CHOP in AIDS-NHL (CR rates of 58% and 47%, respectively) in one study, but was significantly more toxic (14% and 2% serious treatment-related toxicities). The increase in mortality with R-CHOP compared with CHOP, in this randomized study, was primarily due to infectious deaths, particularly in individuals with CD4 lymphocyte counts <50/mm3. However, subsequent trials using prophylactic quinolone antibiotics for individuals with <100 CD4 cells/mm3 obviated this complication. Moreover, a meta-analysis of trials using various different forms of chemotherapy with or without rituximab found a reduced risk of lymphoma recurrence and death from any cause with the addition of rituximab to combination chemotherapy (Blood 2013;122:3251).
D. CDOP (cyclophosphamide, liposomal doxorubicin, vincristine, and prednisone) in combination with rituximab resulted in a 47% CR rate in a study of 40 patients.
E. The infusional dose-adjusted (DA) EPOCH regimen (etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin) with growth factor support resulted in complete remission in 74% of 39 patients, with 60% disease-free survival at 53 months. In this trial, antiretrovirals were withheld during chemotherapy, and after reinstitution of HAART, CD4 cells recovered by 12 months and viral load decreased below baseline by 3 months. Important features of this regimen are that it utilizes 5 days of oral prednisone (60 mg/m2/day), a 4-day infusion of etoposide (50 mg/m2/day), vincristine (0.4 mg/m2/day up to 2 mg total), and doxorubicin (10 mg/m2/day), and day 5 cyclophosphamide, followed by G-CSF or Neulasta. Cycle 1 cyclophosphamide dose is 375 mg/m2 for patients with CD4 <100 and 750 mg/m2 for patients with CD4 ≥100. In subsequent cycles, the cyclophosphamide dose is increased by 187 mg/m2 each cycle up to a maximum of 750 mg/m2 if grade 3 or 4 neutropenia or thrombocytopenia has not occurred, and decreased by 187 mg/m2 each cycle if one of these complications has occurred. Thus, monitoring of the CBC at days 8, 10, and 12 of each cycle is necessary for guiding subsequent therapy. Concurrent use of rituximab plus EPOCH resulted in a 73% CR in one study, and 5-year progression-free (PFS) and overall survivals (OS) of 84% and 68%, respectively, in another study.
F. Short-course EPOCH-RR regimen includes rituximab given on days 1 and 5 of each cycle. To determine the number of cycles of therapy, all patients undergo restaging with CT and FDG-PET after the second treatment cycle, and each cycle until achieving CR or no further tumor shrinkage. The criteria for stopping therapy after a minimum of 3 cycles of therapy is that there is less than 25% reduction in bidimensional tumor products compared with the previous interim CT scan and the standardized uptake values on FDG-PET have decreased at least 50% compared with the pretreatment FDG-PET. With 5 years of follow-up, PFS and OS were 84% and 68%, respectively, and 79% of patients only required 3 treatment cycles.
G. CDE (cyclophosphamide, doxorubicin, and etoposide) is an alternative infusional regimen that has resulted in CR rates of 46% to 86%, but grade 3 or 4 neutropenia and thrombocytopenia in 75% and 55% of participants, respectively.
H. ACVBP (doxorubicin, cyclophosphamide, vindesine, bleomycin, and prednisolone) is an alternative intensive regimen used primarily in Europe. In one study, the 5-year OS was 51% for good-risk patients.
I. Indications for CNS prophylaxis in AIDS-DLBCL are not well defined. Bone marrow involvement has been suggested as increasing the likelihood of CNS relapse, as well as paraspinal, paranasal, epidural, testicular, or widespread systemic involvement. When CNS prophylaxis is provided, the usual recommendation is 4 weekly treatments of either intrathecal cytarabine (50 mg) or methotrexate (12 mg).
J. Lymphomatous meningitis should be treated with intrathecal cytarabine or methotrexate 2 to 3 times weekly via Omaya reservoir until the CSF is clear of malignant cells, then weekly for 4 weeks, and then monthly. The duration of therapy remains poorly defined, but is often given for 6 to 12 months. Alternatively, liposomal cytarabine (Depocyt) can be given with a 5-day course of decadron 4 mg bid with each treatment, on weeks 1 and 3 for induction, on weeks 5, 7, 9, and 13 for consolidation, and weeks 17, 21, 25, and 29 for maintenance. In patients failing to respond to intraventricular chemotherapy, CSF flow studies can be performed after instilling radioisotope to identify possible blockade.
K. Radiotherapy may be given as palliation to bulky, rapidly enlarging, organ compressing, or CNS lesions or as consolidation to patients with localized lymphoma after chemotherapy.
L. Duration of first-line therapy for AIDS-DLBCL should be 3 to 8 cycles, unless there is severe toxicity or lymphoma progression. This should include 1 to 2 cycles after obtaining a CR. For patients with stage I disease and good prognostic characteristics, 3 cycles of therapy followed by involved field radiation is appropriate therapy.
M. Salvage chemotherapy regimens for AIDS-associated lymphomas are not highly effective (response rates of 10% to 25%) with most patients relapsing within months, as in the HIV-negative population. This includes the use of rituximab with etoposide and high-dose cytosine arabinoside and cisplatin (ESHAP), mitoguazone, or a combination of etoposide, mitoxantrone, and prednimustine. The use of rituximab with ifosfamide, carboplatin, and etoposide (R-ICE) is a reasonable choice for a salvage regimen, but trials in AIDS patients have not yet been reported. There is little reported experience with dexamethasone, cisplatin, cytarabine (DHAP), mesna, ifosfamide, mitoxantrone, etoposide (MINE), or carmustine, etoposide, cytarabine, melphalan (miniBEAM) regimens in this patient population.
N. Autologous stem cell transplantation has also been utilized for refractory or relapsed AIDS-associated lymphomas, particularly in the HAART era. In individuals with a good performance status, lacking severe immune compromise, stem cell collections were successful in 80% to 100% of cases, and graft failure was rare. Long-term survivors have been reported from such studies, but the number of patients in each series remains low. In one study of 68 patients from 20 institutions, including 16 patients in first CR and 44 patients in CR more than 1, partial remission, or chemotherapy-sensitive relapse, and 8 patients with chemotherapy-resistant disease, nonrelapse mortality was 30% at 24 months. Only anecdotal reports have appeared thus far for the use of allogeneic transplants in HIV-infected individuals.
IV. COMPLICATIONS
A. Complications of disease. Rapidly enlarging tumors may compromise airways and other vital organs. Significant hepatic dysfunction, hypercalcemia, and CNS relapse may occur. OIs and other AIDS-related illnesses are causes for morbidity and mortality in patients with AIDS-NHL; thus, PCP and mycobacterial prophyalxis should be continued during active lymphoma therapy, if indicated.
B. Complications of therapy
1. Lymphocytotoxic chemotherapy may cause depletion of CD4 and total lymphocyte counts, increasing the risk of severe myelosuppression and infections. Potential interactions with chemotherapy and HAART may produce substantial and unexpected toxicity that may require dose delay or reduction, possibly compromising optimal antilymphoma therapy.
2. Intrathecal chemotherapy may cause chemical arachnoiditis that is relatively acute, subacute neurological deficits occurring within days to weeks, or chronic encephalopathy occurring over weeks to months.
3. Cardiomyopathy may occur after the use of doxorubicin, particularly in individuals receiving cumulative doses of more than 550 mg/m2
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