[net-gold] MEDICAL: DISEASES: CANCER : CHILDREN: HEALTH AND MEDICAL: Late Effects of Treatment for Childhood Cancer (PDQ)

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MEDICAL: DISEASES: CANCER :
CHILDREN: HEALTH AND MEDICAL:
Late Effects of Treatment for Childhood Cancer (PDQ)


Late Effects of Treatment for Childhood Cancer (PDQ)

National Cancer Institute <http://www.cancer.gov/cancertopics/pdq/treatment/lateeffects/patient>

Late effects are treatment-related health problems that appear months or years after treatment has ended.

The treatment of cancer may damage healthy cells at the same time it destroys cancer cells. Some cancer treatments, such as chemotherapy, radiation therapy, and bone marrow or stem cell transplant, stop the growth of rapidly dividing cells, such as cancer cells. Since bones, tissues, and organs that are growing with the child have cells that are also dividing rapidly, cancer treatment can prevent them from developing normally. Other cancer treatments include surgery to remove all or part of certain organs that have cancer in them. The damage from these cancer treatments can be mild or serious, and the effects may be seen during treatment or months to years later.

Side effects that continue or appear after cancer treatment has ended are called late effects. It is important for the parents and the patient to know that children treated for cancer (childhood cancer survivors) may develop late effects from their treatment.

Late effects of cancer treatment may affect the following in childhood cancer survivors:

Organs, bones, or body tissues.

Mood, feelings, and actions.

Thinking, learning, and memory.

The risk of developing late effects is related to the type of cancer or type of treatment.

The risk that a cancer treatment will cause late effects depends on many things, including the following:

The type of cancer and where it is in the body.

The childs age (when treated).

The type and amount of treatment.

The area treated.



Genetic factors or health problems the child had before the cancer.

Regular follow-up by health professionals who are expert in finding and treating late effects is important for the long-term health of childhood cancer survivors. Records about the cancer diagnosis and treatment, including all test results, should be kept by childhood cancer survivors (or their caregivers). This information may be used to help find and treat late effects.

Doctors are studying the late effects that cancer treatments cause in childhood cancer survivors. They are trying to find out if changing treatment can help prevent or lessen late effects in childhood cancer survivors.

Purpose of This PDQ Summary

<http://www.cancer.gov/cancertopics/pdq/treatment/ lateeffects/HealthProfessional>

A shorter URL for the above link:



<http://tinyurl.com/ybam6x5>

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the late effects of treatment for childhood cancers and is organized by organ system. This summary is reviewed regularly and updated as necessary by the PDQ Pediatric Treatment Editorial Board.

Information about the following is included in this summary:



Risk factors.

Late effects by body system.

Second malignant neoplasms.

Monitoring for late effects.

This summary is intended as a resource to inform and assist clinicians and other health professionals who care for pediatric cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

General Information

<http://www.cancer.gov/cancertopics/pdq/treatment/ lateeffects/HealthProfessional/page2>

A shorter URL for the above link:



<http://tinyurl.com/yjzm3ss>

During the past 3 decades, multimodality therapy for childhood cancer has resulted in markedly improved survival. For the period from 1985 to 1997, the 5-year survival rate for childhood cancer reported by the National Cancer Institutes Surveillance, Epidemiology, and End Results Program is 75%.[1] The therapy responsible for this survival can also produce adverse long-term health-related outcomes that manifest months to years after completion of cancer treatment, and are commonly referred to as late effects. It has been clearly demonstrated that long-term survivors of childhood cancer carry a high burden of morbidity with one-third of the survivors reporting severe or life threatening complications 30 years after diagnosis of their primary cancer.[2] Long-term survivors of childhood cancer are at an 8.4-fold increased risk of premature death when compared with an age-matched and gender-matched general population, with increases in cause-specific mortality seen for deaths due to second cancers, and cardiac and pulmonary causes.[3] Late effects include organ dysfunction, second malignant neoplasms, and adverse psychosocial sequelae. Unfortunately, the majority of childhood cancer survivors do not receive recommended risk-based care. The Childhood Cancer Survivor Study reported that 88.8% of survivors were receiving some form of medical care, but only 31.5% reported care that focused on their prior cancer (survivor-focused care) and 17.8% reported survivor-focused care that included advice about risk reduction and discussion or ordering of screening tests.[4]

Risk factors for late effects include:


Tumor-related factors

Direct tissue effects.

Tumor-induced organ dysfunction.

Mechanical effects.

Treatment-related factors

Radiation therapy: Total dose and fraction size, organ or tissue volume, and machine energy are the most critical factors.

Chemotherapy: Agent type, single and cumulative dose and schedule may modify risk.

Surgery: Technique and site are relevant.

Host-related factors

Developmental status.

Genetic predisposition.

Inherent tissue sensitivities and capacity for normal tissue repair.

Function of organs not affected by radiation therapy or chemotherapy.
Premorbid state.

Several comprehensive reviews and books that address late effects of childhood cancer and its therapy have been published.[5-12] An example of specific recommendations for surveillance based on therapeutic exposure can be found in the Children's Oncology Group long-term follow-up guidelines.[Survivorship Guidelines]

[Table Omitted]

Information concerning late effects is summarized in tables throughout the summary. Tables in the Common Late Effects of Childhood Cancer by Body System section of the summary have been modified from another review, with author permission.[8]

References

Ries LA, Smith MA, Gurney JG, et al., eds.: Cancer incidence and survival among children and adolescents: United States SEER Program 1975-1995. Bethesda, Md: National Cancer Institute, SEER Program, 1999. NIH Pub.No. 99-4649. Also available online. Last accessed April 19, 2007.

Oeffinger KC, Mertens AC, Sklar CA, et al.: Chronic health conditions in adult survivors of childhood cancer. N Engl J Med 355 (15): 1572-82, 2006. [PUBMED Abstract]

Mertens AC, Liu Q, Neglia JP, et al.: Cause-specific late mortality among 5-year survivors of childhood cancer: the Childhood Cancer Survivor Study. J Natl Cancer Inst 100 (19): 1368-79, 2008. [PUBMED Abstract]

Nathan PC, Greenberg ML, Ness KK, et al.: Medical care in long-term survivors of childhood cancer: a report from the childhood cancer survivor study. J Clin Oncol 26 (27): 4401-9, 2008. [PUBMED Abstract]

Oeffinger KC, Hudson MM: Long-term complications following childhood and adolescent cancer: foundations for providing risk-based health care for survivors. CA Cancer J Clin 54 (4): 208-36, 2004 Jul-Aug. [PUBMED Abstract]

Meister LA, Meadows AT: Late effects of childhood cancer therapy. Curr Probl Pediatr 23 (3): 102-31, 1993. [PUBMED Abstract]

Schwartz CL: Long-term survivors of childhood cancer: the late effects of therapy. Oncologist 4 (1): 45-54, 1999. [PUBMED Abstract]

Schwartz C L, Hobbie WL, Constine LS, et al., eds.: Survivors of Childhood Cancer: Assessment and Management. St. Louis, Mo: Mosby, 1994.

Constine LS: Late effects of cancer treatment. In: Halperin EC, Constine LS, Tarbell NJ, et al.: Pediatric Radiation Oncology. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins, 1999, pp 457-537.

Green DM, D'Angio GJ, eds.: Late Effects of Treatment for Childhood Cancer. New York, NY: Wiley-Liss, Inc., 1992.

Friedman DL, Meadows AT: Late effects of childhood cancer therapy. Pediatr Clin North Am 49 (5): 1083-106, x, 2002. [PUBMED Abstract]

Smith M, Hare ML: An overview of progress in childhood cancer survival. J Pediatr Oncol Nurs 21 (3): 160-4, 2004 May-Jun. [PUBMED Abstract]

Common Late Effects of Childhood Cancer by Body System

<http://www.cancer.gov/cancertopics/pdq/
treatment/lateeffects/HealthProfessional/page3>



A shorter URL for the above link:



<http://tinyurl.com/y8mojtg>



Central Nervous System
        Neurocognitive
        Psychosocial
Special Senses
        Hearing
        Optic and orbital
Digestive System
        Dental
        Hepatic
        Digestive tract
Immune System
        Spleen
Circulatory System
        Cardiovascular
Respiratory System
        Pulmonary
Urinary System
        Renal
Endocrine System
        Thyroid gland
Neuroendocrine System
Musculoskeletal System
        Bone and body composition
        Obesity
Reproductive System
        Gonadal function
        Reproduction




Central Nervous System


Neurocognitive

Neurocognitive late effects most commonly follow treatment of malignancies that require central nervous system (CNS)-directed therapies, such as cranial radiation or intraventricular/intrathecal (IT) chemotherapy; thus, children with CNS tumors, head and neck sarcomas, and acute lymphoblastic leukemia (ALL) are most commonly affected. Deficits occur in a variety of areas that include the following:[1-6]

General intelligence.

Age-appropriate developmental progress.

Academic achievement (especially in reading, language, and mathematics).

Visual and perceptual motor skills.

Nonverbal and verbal memory.

Receptive and expressive language and attention.

For both CNS tumors and ALL, younger age at time of treatment is associated with an increased neurocognitive deficit.[7-11]

Some studies of children treated with cranial or craniospinal radiation therapy for CNS tumors demonstrated a significant adverse neurocognitive effect of therapy.[4] Other studies using lower doses and more targeted volumes, however, have demonstrated improved results.[12-14] One study supports the hypothesis that medulloblastoma patients demonstrate a decline in intelligence quotient (IQ) values because of an inability to acquire new skills and information at a rate comparable to their healthy same-age peers, not because of a loss of previously acquired information and skills.[15] In a Danish study of 133 children treated for brain tumors, younger age at diagnosis, tumor site in the cerebral hemisphere, hydrocephalus treatment with shunt, and radiation therapy were predictors of lower cognitive functions.[16] Another study evaluated quantitative tissue volumes from magnetic resonance imaging scans, correlating these results with neurocognitive assessments for 40 long-term survivors of pediatric brain tumors treated with radiation therapy with or without chemotherapy 2.6 to 15.3 years earlier (median, 5.7 years) at an age of 1.7 to 14.8 years (median, 6.5 years). Analyses revealed significant impairments in patients neurocognitive test performance on all measures. After statistically controlling for age at time of radiation therapy and time from radiation therapy, significant associations were found between normal-appearing white matter volumes and both attentional abilities and IQ, and between attentional abilities and IQ. These associations were also correlated with deficiencies in academic skills such as reading, spelling, and math.[17]

For children with ALL, studies again show significant neurocognitive impairment [18,19] when cranial radiation is combined with IT chemotherapy. Reduction in the cranial radiation dose may result in less neurocognitive impairment.[11,20-23]

The effects of radiation on the brain are difficult to define, especially when cranial radiation is a part of multimodality therapy that may also include surgery, systemic chemotherapy, or IT chemotherapy. Moreover, tumor-related deficits because of direct invasion of the brain, seizures, and hydrocephalus must be recognized.[24] Studies on CNS prophylaxis for ALL comparing craniospinal radiation therapy with cranial radiation therapy combined with IT methotrexate showed that children who were younger than 5 years at time of treatment and had received radiation therapy and intrathecal chemotherapy had lower IQ scores than those who received craniospinal radiation therapy alone.[25] Similarly, another study found a significant IQ deficit in children treated with 24 Gy of cranial radiation combined with IT methotrexate, as compared with childhood cancer survivors who received no CNS-directed therapy, with the effect greatest among those younger than 5 years.[18] A similar effect on cognition with the addition of IT methotrexate has been found in children treated for medulloblastoma.[26]

Systemic methotrexate in high doses and combined with radiation therapy can lead to a well-described leukoencephalopathy, in which severe neurocognitive deficits are obvious.[2,27,28] Because of its penetrance into the CNS, systemic methotrexate has been used in a variety of low-dose and high-dose regimens for leukemia CNS prophylaxis. The deleterious effects of systemic methotrexate, especially at doses above 1 g/m2 may be no different or worse than those of 18 Gy of cranial radiation therapy.[29,30] At lower methotrexate doses, there does not appear to be a consistent pattern of neurocognitive deficits.[31] One long-term study of infants who received high-dose systemic methotrexate combined with intrathecal cytarabine and methotrexate for CNS leukemia prophylaxis and who were tested 3 to 9 years posttreatment showed that cognitive function was in the average range.[32]

Chemotherapy alone for ALL may result in cognitive dysfunction. One study examined 48 children treated for leukemia without cranial radiation therapy and found impairment in tasks of higher-order cognitive functioning and learning disabilities in the area of mathematics.[29] Another study showed that children, particularly females, treated with systemic and IT methotrexate for CNS leukemia prophylaxis showed impairment of verbal memory and coding.[22] One other study reported mild visual and verbal short-term memory deficits in leukemia survivors treated with IT chemotherapy.[33] Another study examined 20 patients treated for leukemia without cranial radiation therapy and found no significant neurocognitive deficits, even when patients were exposed to either IT or high-dose intravenous (IV) methotrexate.[21] In general, patients who receive IT chemotherapy without cranial radiation as CNS therapy appear to have a low incidence of neurocognitive sequelae, and the deficits that develop represent relatively modest declines in a limited number of domains of neuropsychological functioning.[34-36] This modest decline is especially seen in young children and girls.[37] Controversy exists about whether patients who receive dexamethasone are at higher risk for neurocognitive disturbances,[38] although long-term neurocognitive testing in 92 children with a history of standard-risk ALL who had received either dexamethasone or prednisone during treatment did not demonstrate any meaningful differences in cognitive functioning based on corticosteroid randomization.[39] Treatment intensity and duration can also adversely affect cognitive performance, because of absences from school and interruption of studies.[40]

Cognitive and academic consequences of stem cell transplantation in children has also been evaluated. In a report from the St. Jude Childrens Research Hospital in which 268 patients were treated with stem cell transplant, minimal risk of late cognitive and academic sequelae was seen. Subgroups of patients were at relatively higher risk, including those undergoing unrelated donor transplantation, receiving total-body irradiation, and those with graft-versus-host disease. However, these differences were small relative to differences in premorbid functioning, particularly those associated with socioeconomic status.[41]

[Table Omitted]




Psychosocial

Many childhood cancer survivors have adverse quality of life or other adverse psychologic outcomes. Incorporation of psychological screening into clinical visits for childhood cancer survivors may be valuable; however, limiting such evaluations to those returning to long-term follow-up clinics may result in a biased subsample of those with more difficulties, and precise prevalence rates may be difficult to establish. A review of behavioral, emotional, and social adjustment among survivors of childhood brain tumors illustrates this point, in whom rates of psychological maladjustment range from 25% to 93%.[43]

Studies in the early 1990s described childhood cancer survivors as generally well adjusted, though a subset had psychological difficulties that resulted in functional impairment.[44-46] Further in-depth analyses have led to the description of posttraumatic stress disorder (PTSD) in some childhood cancer survivors and their mothers. The core features of PTSD include the following:[47]

Experiencing an event perceived as life threatening, with an accompanying reaction of intense fear, horror, or helplessness.

Persistent re-experiencing of the event.

Avoiding things, events, or people surrounding the event or decreased responsiveness to same.

Experiencing persistent symptoms of increased sleep disturbance, irritability, hypervigilance, and difficulty concentrating. Because avoidance of places and persons associated with the cancer is part of PTSD, the syndrome may interfere with obtaining appropriate health care. Those with PTSD perceived greater current threats to their lives or the lives of their children. Other risk factors include poor family functioning, decreased social support, and noncancer stressors.[48-53] One study of 78 young adult survivors of childhood cancer found 20.5% met the criteria for PTSD. In contrast, only 4.5% of younger children met the criteria for the syndrome.[48] In several studies performed by the same group of investigators, 9% to 10% of parents of childhood cancer survivors met the criteria for PTSD.[52,54] For more information about PTSD in cancer patients, please see the PDQ summary on Post-traumatic Stress Disorder.

In a study of 101 adult cancer survivors of childhood cancer, psychologic screening was performed during a routine annual evaluation at the survivorship clinic at the Dana Farber Cancer Institute. On the Symptom Checklist 90 Revised, 32 subjects had a positive screen (indicating psychological distress), and 14 subjects reported at least one suicidal symptom. Risk factors for psychological distress included subjects dissatisfaction with physical appearance, poor physical health, and treatment with cranial radiation. In this study, the instrument was shown to be feasible in the setting of a clinic visit because the psychological screening was completed in less than 30 minutes. In addition, completion of the instrument itself did not appear to result in distress on the part on the survivors in 80% of cases.[55] For more information about psychological distress and cancer patients, please see the PDQ summary on Adjustment to Cancer: Anxiety and Distress.

Special Senses

Hearing

Hearing loss is a common late effect of survivors of CNS cancers and cancers of the head and neck who received high doses of radiation therapy and platinum chemotherapy. Hearing loss in the speech range (0.5 kHz to 3 kHz), which may compromise language reception and expression, is reported with cumulative doses of cisplatin greater than 360 mg/m2, and 25% prevalence of hearing loss is reported with doses greater than 720 mg/m2. Fifty percent of children treated with cisplatin doses greater than 450 mg/m2 have sensorineural hearing loss (SNHL) in the high frequencies (6 kHz to 8 kHz). Younger age at time of administration increases risk.[56-60] Carboplatin may be less ototoxic, but further follow-up of patients treated with high cumulative doses is necessary before a clear dose-threshold can be established.[56] A German study of children treated for neuroblastoma demonstrated the influence of both cisplatin and carboplatin on hearing. For cisplatin, there was 12% hearing impairment at doses of 1 mg/m2 to 200 mg/m2, 13% at doses of 201 mg/m2 to 400 mg/m2, 26% at doses of 401 mg/m2 to 600 mg/m2, and 22% at 601 mg/m2 to 800 mg/m2. There was an additional effect of carboplatin when given in high-dose therapy with autologous stem cell infusion, in which 40% of patients developed hearing loss following a dose of 1,500 mg/m2.[61] Radiation therapy can result in cochlear damage, with SNHL occurring in about 25% of patients treated with doses approaching 60 Gy, but SNHL is less frequent with lower doses of radiation therapy if cisplatin is not included in the chemotherapy regimen. Data suggest that cochlear doses of 30 Gy to 50 Gy can cause intermediate-frequency SNHL, and that cerebrospinal fluid (CSF) shunting procedures increase the risk.[59,62-65] Cisplatin, at doses as low as 270 mg/m2, can result in hearing loss when combined with cranial radiation therapy doses of 40 Gy to 50 Gy.[59,60] The sequence of chemoradiotherapy appears to influence risk. Risk and severity of ototoxicity are greater when cisplatin is administered after cranial radiation.[57]

[Table Omitted]



Optic and orbital

Orbital complications are common following radiation therapy for childhood head and neck sarcomas, CNS tumors, and retinoblastoma and as part of total-body irradiation (TBI).

For survivors of retinoblastoma, a small orbital volume may result from either enucleation or radiation therapy. Age younger than 1 year may increase risk, but this is not consistent across studies.[66,67] Better management of prosthetic implants and newer methods of delivering radiation therapy are likely to reduce risk.[66,68] Newer strategies for treatment of retinoblastoma use chemotherapy to reduce tumor size, combined with local ophthalmic therapies that include thermotherapy, cryotherapy, and plaque radiation. Such an approach may be associated with local complications that can affect vision. Because these therapies are relatively recent, further follow-up is required to determine long-term effects. Treatment for tumors located near the macula and fovea increase risk of complications leading to visual loss.[68-73]

Survivors of orbital rhabdomyosarcoma are at risk of dry eye, cataract, orbital hypoplasia, ptosis, retinopathy, keratoconjunctivitis, optic neuropathy, lid epithelioma, and impairment of vision following radiation therapy doses of 30 Gy to 65 Gy. The higher dose ranges (>50 Gy) are associated with lid epitheliomas, keratoconjunctivitis, lacrimal duct atrophy, and severe dry eye. Retinitis and optic neuropathy may also result from doses of 50 Gy to 65 Gy and even at lower total doses if the individual fraction size is greater than 2 Gy.[74] Cataracts are reported following lower doses of 10 Gy to 18 Gy.[59,64,75-78]

Patients treated with TBI are also at increased risk of cataracts. Risk ranges from approximately 10% to 60% at 10 years posttreatment, depending on the total dose and fractionation, with a shorter latency period and more severe cataracts noted after single fraction and higher dose or dose-rate TBI. Corticosteroids and graft-versus-host disease (GVHD) may further increase risk. Young children may actually be at a lower risk than adolescents and adults.[79-84]

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References



References

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Duffner PK, Cohen ME: The long-term effects of central nervous system therapy on children with brain tumors. Neurol Clin 9 (2): 479-95, 1991. [PUBMED Abstract]

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Donnez J, Godin PA, Qu J, et al.: Gonadal cryopreservation in the young patient with gynaecological malignancy. Curr Opin Obstet Gynecol 12 (1): 1-9, 2000. [PUBMED Abstract]

Newton H: The cryopreservation of ovarian tissue as a strategy for preserving the fertility of cancer patients. Hum Reprod Update 4 (3): 237-47, 1998 May-Jun. [PUBMED Abstract]

Winther JF, Boice JD Jr, Mulvihill JJ, et al.: Chromosomal abnormalities among offspring of childhood-cancer survivors in Denmark: a population-based study. Am J Hum Genet 74 (6): 1282-5, 2004. [PUBMED Abstract]

Byrne J, Rasmussen SA, Steinhorn SC, et al.: Genetic disease in offspring of long-term survivors of childhood and adolescent cancer. Am J Hum Genet 62 (1): 45-52, 1998. [PUBMED Abstract]

Green DM, Fiorello A, Zevon MA, et al.: Birth defects and childhood cancer in offspring of survivors of childhood cancer. Arch Pediatr Adolesc Med 151 (4): 379-83, 1997. [PUBMED Abstract]

Hansen M, Kurinczuk JJ, Bower C, et al.: The risk of major birth defects after intracytoplasmic sperm injection and in vitro fertilization. N Engl J Med 346 (10): 725-30, 2002. [PUBMED Abstract]

Bonduelle M, Liebaers I, Deketelaere V, et al.: Neonatal data on a cohort of 2889 infants born after ICSI (1991-1999) and of 2995 infants born after IVF (1983-1999). Hum Reprod 17 (3): 671-94, 2002. [PUBMED Abstract]

Simpson JL, Lamb DJ: Genetic effects of intracytoplasmic sperm injection. Semin Reprod Med 19 (3): 239-49, 2001. [PUBMED Abstract]

Serafini P: Outcome and follow-up of children born after IVF-surrogacy. Hum Reprod Update 7 (1): 23-7, 2001 Jan-Feb. [PUBMED Abstract]

Ericson A, Kl B: Congenital malformations in infants born after IVF: a population-based study. Hum Reprod 16 (3): 504-9, 2001. [PUBMED Abstract]

Sankila R, Olsen JH, Anderson H, et al.: Risk of cancer among offspring of childhood-cancer survivors. Association of the Nordic Cancer Registries and the Nordic Society of Paediatric Haematology and Oncology. N Engl J Med 338 (19): 1339-44, 1998. [PUBMED Abstract]

Friedman DL, Kadan-Lottick N, Liu Y, et al.: History of cancer among first-degree relatives of childhood cancer survivors: a report from the Childhood Cancer Survivor Study. [Abstract] Proceedings of the American Society of Clinical Oncology 20: A-1728, 433a, 2001.

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