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W. Nemrok, M.B. B.CH. B.A.O., M.B.B.Ch., Ph.D.

Deputy Director, William Carey University College of Osteopathic Medicine

Radiographic findings include diffuse, fluffy infiltrates consistent with pulmonary edema. The activated leukocytes then migrate to the lungs where they bind to the pulmonary capillary bed via integrins and other cell adhesion molecules. Proteolytic enzymes are then released that destroy tissue, resulting in a capillary leak syndrome and pulmonary edema. These risks continue to drive government-mandated pretransfusion testing requirements. Serum alanine aminotransferase, measured in most European countries as a nonspecific surrogate marker of hepatitis, is no longer required by American Association of Blood Bank standards. Routine vaccination of infants and young children with hepatitis B vaccine should also decrease the risk of transfusion-transmitted hepatitis B as these children enter the blood donor pool. The chances of a health care worker contracting hepatitis B from a single contaminated needle stick is estimated to be between 2% and 40%. These differences may be at least in part related to the higher number of viral particles present in the blood of carriers of hepatitis B. The rate of transmitting hepatitis C through needle stick is probably on the order of 5%. Therefore, these patients must be offered counseling that addresses the complications of hepatitis C, as well as the risk to close contacts and family members. Hepatitis G virus has been transferred by blood transfusion, but its significance is unclear in that transfusion-acquired infection has not been associated with acute or chronic hepatitis. Due to the low risk of viral infection by transfusion and the fact that most patients who receive plasma also receive cellular blood components, the cost-effectiveness of virally inactivated plasma is low. This prevalence varies widely in different parts of the United States and other countries. A number of other infectious diseases are known or are suspected to be transmitted by blood transfusion. The risk of acquiring babesiosis by blood transfusion is unknown because it is endemic in many areas and often results in asymptomatic infection. The risk of new variant Creutzfeldt-Jakob disease, first described in 1996, is unknown. It is unclear whether new variant Creutzfeldt-Jakob disease is transmissible by blood transfusion, and this route of transmission has not been reported. Accordingly, they are prone to a wide variety of viral and bacterial infections and to harmful cellular-mediated immune responses. Thus, oncology patients should receive blood products that have been specially processed to prevent these and other complications. Leukocytes are effectively removed from red cell and platelet concentrates by leukocyte reduction filters. Currently used third-generation leukocyte reduction filters remove 3 to 4 log 10 of the total intact leukocytes found in red cell and platelet concentrates. Red cells are leukoreduced shortly after blood collection (pre-storage leukodepletion), following refrigerated storage (poststorage leukodepletion), or at the bedside during transfusion. Platelets collected by modern apheresis devices are designed to directly collect leukoreduced platelets. Many physicians believe that these products do not require further leukoreduction. White cell reduction by each of these techniques requires quality control measures (using cyclic good manufacturing practices) that verify adequate leukoreduction of cellular blood products. They are also indicated for patients with leukemia, lymphoma, and aplastic anemia. Patients with solid tumors who are not transplant patients but who have large anticipated cellular blood product needs should also receive leukoreduced products, as should any patient with chronic transfusion needs (thalassemia, sickle cell disease). Prestorage leukoreduced products are preferable because they are also devoid of cytokines and other biologic response modifiers that play a role in transfusion complications. Many of these proteins are not efficiently removed by leukocyte reduction filters.

Treatment of recurrent primary intracranial childhood tumors with cis-diamine-dichloroplatinum. Clinical experience with vincristine in tumors of the central nervous system and other malignant diseases. The efficacy of vincristine and cyclophosphamide in the therapy of recurrent medulloblastoma. Eight drugs in 1 day chemotherapy for brain tumors: experience in 107 children and rationale for preirradiation chemotherapy. Results of treatment of children with recurrent medulloblastoma/primitive neuroectodermal tumors with lomustine, cisplatin, and vincristine. Improved survival with the use of adjuvant chemotherapy in the treatment of medulloblastoma. Nitrogen mustard, vincristine, procarbazine, and prednisone as adjuvant chemotherapy in the treatment of medulloblastoma: a Pediatric Oncology Group Study. Chemotherapeutic response in metastatic: report of two cases and review of the literature. Radiotherapy of primary intracranial germinomas: the case against routine craniospinal irradiation. The role of cerebrospinal fluid cytology in radiotherapy planning for intracranial germinoma. Radiation therapy of pineal region tumors: 25 new cases and a review of 208 previously reported cases. Neoadjuvant chemotherapy for newly diagnosed germ-cell tumors of the central nervous system. Five cases of primary intracranial germ cell tumors treated by combination chemotherapy with cisplatin. Combination chemotherapy with cisplatin and etoposide for intracranial germ cell tumors. Exceptional sensitivity of testicular germ cell tumour cell lines to the new anti-cancer agent, temozolomide. Radiotherapy for nonfuctional pituitary adenomas: analysis of long-term tumor control. Pituitary irradiation is ineffective in normalizing plasma insulin-like growth factor I in patients with acromegaly. The effect of extenal pituitary irradiation on elevated serum prolactin levels in patients with pituitary microadenomas. Cabergoline: a first choice treatment in patients with previously untreated prolactin-secreting pituitary adenoma. Risk of second brain tumor after conservative surgery and radiotherapy for pituitary adenoma. Phosphorus-32 intracavitary irradiation of cystic craniopharyngiomas: current technique and long-term results. A comparison of the roles of surgery and radiation therapy in the management of craniopharyngiomas. Endocrine and neurologic outcome in childhood craniopharyngioma: review of effect of treatment in 42 patients. Neurological and psychophysiological sequelae following different treatments of craniopharyngiomas in children. Gamma knife radiosurgery for acoustic tumors: multivariate analysis of 4-year results. Cranial nerve length predicts the risk of delayed facial and trigeminal neuropathies after acoustiv tumor stereotactic radiosurgery. Dose reduction improves hearing preservation rates after intercanalicular acoustic tumor radiosurgery. Radiation or surgery for chemodectoma of the temporal bone: a review of local control and complications. Skull base chordomas: treatment outcome and prognostic factors in adult patients following conformal treatment with 3D planning and high dose fractionated combined proton and photon radiation therapy. Chondrosarcoma of the base of the skull: a clinicopathologic study of 200 cases with emphasis on its distinction from chordoma. Charged particle irradiation of chordoma and chondrosarcoma of the base of the skull and cervical spine: the Lawrence Berkeley Laboratory Experience.

Effect on Fat Metabolism Altered fat metabolism is apparent clinically in catabolic patients from the observation that fat stores are diminished in association with weight loss. Further study of this factor is needed to elucidate its full effects in cancer cachexia. Regulation of Protein and Amino Acid Metabolism Marked changes in protein and amino acid metabolism are characteristic of cancer patients, and a number of published studies have evaluated the effects of cytokines on muscle protein metabolism with conflicting results. In studies evaluating the effects of corticosterone on muscle protein breakdown, this glucocorticoid was noted to accelerate protein degradation and diminish protein synthesis. There is a diminished risk of such events when the nutritional deficiency is corrected. Although it seems apparent that the provision of nutritional support to the malnourished patient with cancer is essential and would be beneficial, evidence indicating that currently available nutritional formulae alone can maintain or reverse malnutrition in the patient with advanced malignant disease is lacking. This observation suggests that many patients with cancer exhibit ongoing catabolism of body cell mass that persists and is refractory to nutritional repletion. Despite diminished food intake, the tumor-bearing host does not adapt to partial starvation by conserving lean body mass. Instead, the host continues to deplete its own muscle mass to provide amino acids taken up by the tumor to support growth and by the liver to support gluconeogenesis and biosynthesis of important defense proteins. The rationale behind the provision of specialized nutritional support, whether it be enteral or parenteral, is the belief that such support will preferentially benefit the patient rather than stimulate tumor growth. From a more practical standpoint, nutritional support would not be indicated if it clearly demonstrated no favorable effect on the response to antineoplastic therapies, no lengthening of the disease-free survival, or no improvement in the quality of life. Interestingly, a consensus of opinion regarding the role and efficacy of nutritional support in patients with cancer is lacking. Nonetheless, several well-designed clinical studies have allowed us to generate guidelines for the use of enteral and parenteral nutrition in patients with cancer, and most physicians and surgeons who care for patients with cancer continue to use nutritional support aggressively under specific circumstances. Several studies have suggested additional therapies can be used along with nutritional support to alleviate the tumor cachexia. These agents have been able to improve appetite, well-being, and quality of life as well as decreasing nausea and vomiting. Tisdale reported eicosapentaenoic acid, a component of fish oil, attenuated the action of cachectic factors and stabilized the weight loss and energy expenditure in patients with pancreatic cancer. They also suggested b-adrenergic agonists might help as well because of their effect on muscle metabolism. This is done by a careful history and physical examination followed by additional tests to confirm the clinical impression. The history should include inquiries about appetite, preferred foods, and weight loss. The physical examination can establish the diagnosis of muscle wasting and specific nutrient deficiencies. Anthropometric measurements should be done including measurement of body weight and height, skinfold thickness, and a 24-hour urine collection for the measurement of nitrogen. Peripheral blood lymphocyte count and skin testing to common antigens for assessment of delayed hypersensitivity have been used as indicators of immunocompetence in the cancer patient. Altered immunologic responses are not specific for nutritional deficiencies and are often observed even in patients with advanced malignant disease who are well nourished. Other laboratory studies useful in nutritional assessment include red blood cell indices to determine iron and micronutrient deficiencies, plasma glucose to assess insulin resistance, blood urea nitrogen to determine renal status, and liver function tests to evaluate hepatic function. However, concerns over the stimulation of tumor growth have existed for many years. While animal studies indicate that tumor growth can be enhanced with a high-protein diet and diminished by protein-depleted diets, studies in cancer patients are less clear. Baron and coworkers studied 14 malnourished patients with untreated head and neck squamous cell carcinoma who underwent biopsies of both normal and malignant tissues. It is likely that species differences exist and that different tumors respond dissimilarly to nutrient manipulation. If tumor growth is stimulated by nutritional or metabolic support, this could potentially be exploited with cycle-specific chemotherapeutic agents.

Syndromes

• Drinking lots of water (drink small amounts often throughout the day).
• Very early stage cervical cancer (stage 0 or IA1)
• Insomnia (sleeping difficulty)
• Tongue biopsy
• Symptoms of low blood sugar (weakness or tiredness, trembling, sweating, feeling irritable, unclear thinking, fast heartbeat, double or blurry vision, feeling uneasy)
• Turkey or chicken with the skin removed, or bison (also called buffalo meat)
• You have a fever, red streaks running from the sore, a lot of swelling around the carbuncle, or pain that gets worse

Until these influences and their interrelationships are better understood, empiric end points, such as the development of acute hematopoietic toxicity after chemotherapy, might be explored for their value as possible surrogate markers of secondary leukemia risk. Many chemotherapeutic agents are known mutagens and animal carcinogens, 88 and the induction period of solid tumors may be longer than the observation period available in published research. Thus, the question of whether the increased risks of leukemia after chemotherapy might be later followed by excess solid tumors is important. The contribution of chemotherapy to radiation-induced solid tumors 50,55,104,111,122 should also be investigated. Moderately increased risks (two- to fivefold) are observed for a number of solid tumors, such as cancers of the lung, stomach, colon, breast, mouth, and pharynx, as well as melanoma. Solid tumors account for the majority of excess cancers (38 per 10,000 patients per year), with lung cancer contributing 13 excess cases per 10,000 person-years. In the majority of studies, increased leukemia risk is observed as early as 2 to 4 years after initiation of chemotherapy, with peak occurrence between 5 and 9 years and decreasing risks thereafter. In some studies, the risk remains rather constant over time, 48,55 whereas others report that risk increases with time since treatment. In the few studies that include data on 20-year survivors, the relative risk of solid tumors continued to increase through the 15- to 20-year follow-up period. In females, breast cancer accounts for most of the absolute excess risk in 10-year survivors (58 per 10,000 per year). Several studies have compared the leukemogenicity of different chemotherapy regimens. When examining the combined effects of radiation dose to the active bone marrow and number of mechlorethamine-procarbazine containing cycles, it was found that, for each category of radiation dose (less than 10, 10 to 20, and more than 20 Gy to the marrow), leukemia risk clearly increased with the number of chemotherapy cycles. In contrast, among patients with a given number of chemotherapy cycles, risk of leukemia did not consistently increase with higher radiation dose. Taken together, the preponderance of available data does not support the hypothesis that the combination of chemotherapy and radiotherapy confers a higher risk of leukemia than chemotherapy alone. In other reports, however, splenectomy was either not linked or was only weakly related to leukemia risk. After adjustment for type and amount of chemotherapy, patients who showed a decrease of 70% or more in platelet counts after initial treatment had an approximately fivefold higher risk of developing leukemia than patients who showed a decrease of 50% or less. Severe acute thrombocytopenia may indicate greater bioavailability of cytotoxic drugs, which would likely contribute to the development of leukemia. This view is supported by several studies in which risk did not vary appreciably between treatments. A few studies have raised concern about a possible long-term effect of chemotherapy on lung cancer risk. A similar excess risk of lung cancer in patients given chemotherapy, but no radiotherapy, was found in a more recent expansion and update of this study. If chemotherapy indeed affects solid tumor risk, one would expect that patients receiving combined modality treatment would have a greater relative risk than patients treated solely with radiotherapy. Only one study to date has reported a significantly greater risk for solid cancers overall after chemotherapy and radiotherapy compared with irradiation alone, 55 whereas no such difference has been found in the majority of investigations. The inconsistent results reported with regard to the influence of chemotherapy on solid tumor risk may be partly related to the fact that most studies considered all solid tumors combined, whereas chemotherapy may differentially affect the risk of tumors at disparate sites. The risk of developing breast cancer increased dramatically with younger age at first irradiation. A similar trend, with even larger relative risks, has been reported from Stanford University. Generally, surveys with more complete follow-up have found lower relative risks of breast cancer 50,63,142,143 than those in which completeness of follow-up was less satisfactory or not addressed. Data from Stanford University and the United Kingdom show that the highest relative risks for gastrointestinal cancers (approximately eightfold) 63,122 and thyroid cancer 63 occur among patients treated before age 25, with no excesses observed for those treated after 45 years of age. This might point to a prolonged induction period, but it may also be due to this young patient group reaching an age at which solid tumor incidence begins to rise in the general population.