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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Breast cancer is the most common cause of metastatic epidural spinal cord compression (SCC) in women, and this condition results in significant neurologic dysfunction and morbidity. Prior studies of patients with suspected SCC did not employ multivariate analysis techniques, often included persons with a wide variety of malignancies, and generally focused on identifying associated neurologic and radiologic features. We therefore conducted a study examining a more comprehensive set of potential clinical risk factors in breast cancer patients with suspected SCC. We retrospectively analysed 123 episodes of suspected SCC among 93 breast cancer patients evaluated by spine computed tomography (CT) scanning. Multiple logistic regression analysis was employed to identify independent predictors of SCC. Clinically significant metastatic epidural cancer was defined as thecal sac compression (TSC), which occurred in 33 episodes (27%). Four independent predictors of TSC were identified and included oncologic features (known bone metastases > or = 2 years, metastatic disease at initial diagnosis) in addition to neurologic and radiologic features (objective weakness, vertebral compression fracture on spine radiograph). These four predictors stratified episodes into subgroups with widely varying risks of TSC, ranging from 12% (0 risk factors) to 85% (> or = 3 risk factors). These results suggest that the evaluation of breast cancer patients with suspected SCC should include clinical information about their disease course in addition to neurologic examination and prior imaging studies. If confirmed, these predictors may help clinicians assess risk in this patient population.
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PMID:Suspected spinal cord compression in breast cancer patients: a multidisciplinary risk assessment. 987 74

Neurologic complications occur frequently in patients with cancer. After routine chemotherapy, these complications are the most common reason for hospitalization of these patients. Brain metastases are the most prevalent complication, affecting 20 to 40 percent of cancer patients and typically presenting as headache, altered mental status or focal weakness. Other common metastatic complications are epidural spinal cord compression and leptomeningeal metastases. Cord compression can be a medical emergency, and the rapid institution of high-dose corticosteroid therapy, radiation therapy or surgical decompression is often necessary to preserve neurologic function. Leptomeningeal metastases should be suspected when a patient presents with neurologic dysfunction in more than one site. Metabolic encephalopathy is the common nonmetastatic cause of altered mental status in cancer patients. Cerebrovascular complications such as stroke or hemorrhage can occur in a variety of tumor-related conditions, including direct invasion, coagulation disorders, chemotherapy side effects and nonbacterial thrombotic endocarditis. Radiation therapy is the most commonly employed palliative measure for metastases. Chemotherapy or surgical removal of tumors is used in selected patients.
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PMID:Neurologic complications of systemic cancer. 1006 11

Neuroblastoma is the second most common malignant solid tumor in the pediatric population. Recent advances in treatment options and identification of prognostic subsets have made early detection important. Early classification into a favorable stage and subset may carry a 10-year survival of about 90% (1). With newer treatment regimens, the probability of long-term survival in patients with metastatic disease has also increased about fourfold since 1979 (2). Emergency physicians can contribute to improved morbidity and mortality with appropriate evaluation and disposition of the patient presenting with neuroblastoma. Two patients, a 6-month-old and a 2-week-old, presented to the Emergency Department with weakness. Both had a presumptive diagnosis of neuroblastoma made by the emergency physician. A brief discussion of the incidence, presentation, and diagnosis of neuroblastoma follows.
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PMID:Two cases of neuroblastoma presenting to the emergency department. 1019 84

Dear Colleague: I remember, but just barely, what it was like to practice medicine in the first half of this century. My Dad was a general practitioner in a very small farming community in central Illinois, with a hospital of six beds and a trusting clientele. His patients thought he knew how to do everything: deliver babies, set broken bones and take out an appendix. He was an advocate for his patients, not for an HMO or an insurance company. He derived great satisfaction from his practice and was comfortable in this role, up to a point, but knew that he frequently needed the help of specialists from Decatur, St. Louis, and the Mayo Clinic. As his experience and practice evolved, and as medicine itself changed, referrals became a sign of good practice and not an indication of weakness or inadequacy. Some doctors in our town continued to do more than they should have and resisted the trend, and their patients, many with blind faith in their doctor, suffered for it. Clearly, there were economic as well as emotional factors that contributed to this reluctance to ask for help. Clinical oncology is facing much the same situation today. Scientific and economic forces are revolutionizing medicine, but not always in compatible directions. Practice and research have evolved to the point where old patterns of practice are no longer optimal. Few cancer patients can be managed without the input, advice, and even direct involvement of specialists from sister disciplines. Thus, multimodality management of cancer patients is now the norm rather than the exception. At the same time, strong economic forces are dictating a movement in the opposite direction, undermining the strength of traditional academic centers and limiting choices, streamlining patient evaluation, and creating "pathways" to standardize patient management. Who should be setting the course for the cancer patient? We agree that it should not be a clerk at the other end of the phone at the HMO, a computerized practice manual, or even the gatekeeper, who watches his or her capitated bottom line with great nervousness. It should be the physician(s) best able to evaluate the alternatives and communicate these choices to the patient and family. Often it is not possible for a solo physician to make these choices in isolation, particularly when the decisions involve multiple specialties and multimodality therapies. At presentation, many primary cancers now require an integration of the opinion of more than one specialist, and increasingly this integration occurs before surgery. Breast, lung, and prostate cancer, three of our most common diseases, illustrate this point with growing clarity. While less convenient for the doctor, and perhaps less efficient than the "old style" of practice, multimodatity disease center clinics offer significant advantages both to the patient and to the research effort, and are here to stay. Certainly for the payer it is faster and cheaper to have one doctor do it all, but I doubt that the results will be as good. Obviously not all patients need this cooperative approach. It would waste good physicians' time to require that all patients be seen by a radiotherapist, surgeon, and medical oncologist or pediatric oncologist. The specific circumstances may clearly dictate a simple approach and an uncomplicated decision, particularly in dealing with metastatic solid tumors, or at the other extreme, in managing easily resectable, low-risk tumors. However, even here, optimal management of local disease or of potentially resectable metastases may require consideration of an expanded series of options. Thus, all cancer specialists need to be aware of the potential of their colleagues to contribute to disease management. ellipsisWhich brings us to the reason for this journal. The editorial board members of The Oncologist hold the belief that the various subspecialists in oncology should share the same information base and read from the same journal. We believe that cancer specialists should resist the trend to capitulate our responsibilities in disease management to payers, gatekeepers, and hospital administrators. It is up to us to defend the patient's turf and to assure that the patient has an advocate. In order to do so, we will have to be united and fully informed. In this journal, we hope to put the best and latest information on cancer management before our readership, to prepare them for the future, and to do their best as a team for every patient. To this end, we hope to challenge the reader to understand what is new and better, and to let you glimpse the future, not only in terms of research, but also in terms of new team approaches to disease management. We hope to explore how cancer medicine could be and will be practiced as we pass through the economic revolution and return to the future.
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PMID:Back to the Future for Clinical Oncology. 1038 77

Parathyroid carcinoma is a rare cause of primary hyperparathyroidism (1-2%). In this paper a case of parathyroid cancer of the right inferior parathyroid gland cyst (5 cm in diameter) localised mostly retrosternally is presented in a patient suffering from severe hypercalcaemia (Ca--3.7 mmol/l, Ca(++)--1.8 mmol/l), severe bone pains and weakness, huge osteoporosis with following L5 compression fracture and recurrent nephrolithiasis. PTH blood level before surgical treatment was 1243 pg/ml (Norm: 10-60 pg/ml). In the preoperative ultrasonography of the neck, a lesion was found, but it was considered to be a cyst in the inferior pole of the right thyroid lobe. In a fine-needle biopsy from the lesion-colloid mass without any cells was found. In a 99mTc-MIBI scintigraphy of the neck a suspicion of focus lesion in the right superior parathyroid gland was made, which was not confirmed intra-operatively. Parathyroid carcinoma was diagnosed intraoperatively in histological examination. 'En block' resection of the retrosternal parathyroid tumor and right thyroid lobe was performed from the jugular incision. Any enlarged jugular lymph nodes were not found. In a postoperative period a transient hypocalcaemia was present, which disappeared after pharmacological treatment. During 32 months of follow-up neither no features of local recurrence nor distant metastases were found. Calcium level in blood was normal, PTH 216.0 pg/ml, severity of bone pains and weakness lessened, osteoporosis in a course of pharmacological treatment--with no further progress.
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PMID:[Retrosternal parathyroid gland cystic neoplasm as a cause of primary hyperparathyroidism]. 1069 86

A 70-year-old patient with a history of hypertension and hypercholesterolemia was referred for evaluation of necrotic toes. The patient had a history of several cerebrovascular accidents during the previous month. Initially, she developed sudden-onset left upper extremity weakness which, over the ensuing 4 days, progressed to complete left-sided weakness. This was followed by the development of acute dysarthria. A transesophageal echocardiogram revealed moderate left ventricular hypertrophy, several vegetations on her tri-leaflet aortic valve associated with moderate aortic regurgitation, and a large right atrial thrombus with a mobile component. Bubble studies failed to reveal any septal defects. The patient's electrocardiogram was nonspecific. As serial blood cultures were negative despite fevers of up to 39.8 degrees C, the patient was treated with a 6-week course of intravenous ceftriaxone, ampicillin, gentamicin, and ciprofloxacin for a presumed diagnosis of culture-negative endocarditis. Fungal cultures of the blood were negative. The patient, however, progressed and developed several necrotic toes. Physical examination was significant for ischemic changes of the left first, second, third, and fifth toes, as well as the right first and second toes. Diffuse subungual splinter hemorrhages in the toenails, numerous 2-4-mm palpable purpuric papules on the lower extremities, and nontender hemorrhagic lesions of the soles were also noted. Peripheral and carotid pulses were intact and no carotid bruits were heard. Cardiopulmonary and abdominal examinations were unremarkable. Neurologic examination revealed a disoriented, dysarthric patient with left central facial nerve paralysis, as well as spasticity, hyperactive reflexes, and diminished strength and sensation in the left upper and lower extremities. A left visual field defect and left hemineglect were also present. The patient's last brain computerized tomogram revealed areas of low attenuation consistent with cerebral infarctions in three distinct areas of the brain. These included the left occipitotemporal area, the right parieto-occipital area, and the right posterior frontal region. The regions affected were in the distribution of both the anterior and posterior circulation. No evidence of hemorrhage was noted. The patient subsequently complained of abdominal discomfort. A computerized tomogram of the abdomen with oral and intravenous contrast revealed a 4-cm x 3-cm irregular mass in the tail of the pancreas with several low-attenuation lesions throughout the liver which were consistent with infarctions or metastases. Several splenic infarctions were also present. A biopsy of the tumor revealed pancreatic adenocarcinoma. The patient's carcinoembryonic antigen level was 18. 4 ng/mL (0-3) and the CA 19-9 antigen level was 207,000 U/mL (0-36). The alpha-fetoprotein level was normal. Other significant laboratory findings included a prothrombin time of 16.7 (international normalized ratio, 1.4), an activated partial thromboplastin time of 32 (ratio, 1.3), and a platelet count of 85,000/mm3. The Russell viper venom time, sedimentation rate, and C3 levels were normal, and the patient was negative for antinuclear antibodies, anticardiolipin antibodies, and antibodies to extractable nuclear antigens. Of note, the patient was not receiving any anticoagulation. Blood cultures for mycobacteria and fungi, human immunodeficiency virus serology, and urinalysis and culture were negative. The patient subsequently developed an inferior wall myocardial infarction and was transferred to the coronary care unit. In line with the family's request, aggressive care was ceased and the patient expired. The patient's family refused an autopsy.
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PMID:Cutaneous manifestations of marantic endocarditis. 1080 80

Advances in surgery, anesthesiology and in critical care remarkably elevated safety of surgical therapy of cancer. However, prognosis of most cancer types as esophageal and gastric carcinoma--as discussed in this part of the survey--did not improve, even not after adjuvant therapy. To enhance curative resection rate chemotherapy and radiation or a combination of both have been performed preoperatively. The weakness of radiotherapy is control of distant metastases, chemotherapy failed in local tumor control. Multimodal preoperative strategies offered enhanced survival in responders, but overall there was no significant survival advantage. Until now neither in esophageal nor in gastric cancer randomised studies could demonstrate a substantial overall survival benefit after extended lymphadenectomy.
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PMID:[Status of surgical studies in oncology. I]. 1094 31

A 77-year-old man with stage IIB squamous cell carcinoma of the lung underwent right upper lobectomy. One month later he was examined for right chest pain, dyspnea, cough, and weakness. A roentgenogram showed nondiagnostic diffuse opacification of his right lung cavity. An F-18 FDG positron emission tomographic (PET) study revealed extensive uptake in the right pleural area, left adrenal gland, right axilla, and soft tissues consistent with extensive local recurrence and metastatic disease. Biopsy of a right chest soft tissue lesion showed spindle cell carcinoma, a rare variant of squamous cell carcinoma.
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PMID:Extensive F-18 FDG uptake in metastatic spindle cell carcinoma of the lung. 1113 69

In breast cancer there is often overexpression of the breast cancer antigen CA15-3, the carcinoembryonic antigen (CEA) and the ovarian cancer antigen CA125, which makes them potential target antigens for immunotherapy. In this study, we used a multi-antigen vaccine, which included the following antigens: autologous breast cancer cells (AUTOC), allogeneic breast cancer MCF-7 cells (ALLOC), and the tumor associated antigens CA15-3, CEA and CA125, plus low doses of granulocyte/macrophage-colony-stimulating factor (GM-CSF) and interleukin 2 (IL-2). Forty-two breast cancer patients received weekly subcutaneous vaccination at the 1st, 2nd, 3rd, 7th, 11th and 15th weeks. Their lymphocyte proliferative responses to AUTOC, ALLOC, CA15-3, CEA and CA125 were tested in lymphocyte blastogenesis assays (LBA) before and after vaccination. The disease stage and serum CA15-3, CEA and CA125 concentrations were also determined pre- and post-vaccination. We found that the vaccine was safe, and the only major side effects were swelling at the site of injection, muscle pain, and weakness or fatigue. The vaccine induced a significant increase in post-vaccination lymphocyte proliferative responses to AUTOC, CA15-3, CEA and CA125 but not ALLOC, compared to pre-vaccination (p < 0.05, p < 0.01, p < 0.05, p < 0.01 and p > 0.05, respectively, a paired t Test). Computed tomography (CT), ultrasound or bone scan showed evidence of disease improvement in 2 (12%) patients after vaccination. Hepatic metastases were reduced in size and number and some actually disappeared one patient. Metastatic disease in the L5 vertebra and the skull decreased in size and some osteolytic sites completely healed in a second patient. In addition, 7 patients (44%) had stable disease and 7 patients (44%) had disease progression. We did not find vaccination significantly reduced serum tumor markers CA15-3, CEA and CA125 of these breast cancer patients. These results suggest that the vaccine mixture of autologous and allogeneic breast cancer cells and tumor associated antigens plus GM-CSF and IL-2 can be administered safely to breast cancer patients and there is evidence for improved immunity and clinical efficacy.
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PMID:Vaccination with a mixed vaccine of autogenous and allogeneic breast cancer cells and tumor associated antigens CA15-3, CEA and CA125--results in immune and clinical responses in breast cancer patients. 1115 21

We report a 78-year-old woman who had multiple leukemic cell tumors in the brain in the course of chronic myelocytic leukemia (CML). As far as we could survey, such brain tumors were extremely rare. She had been followed because of chronic phase of CML until October, 1998, when she noticed muscle weakness in her left upper and lower extremity. A head MRI revealed multiple masses in the brain, a biopsy of which revealed a tumor of CML cells. Although 40 Gy gamma-knife therapy had reduced the size and numbers of brain tumors, we found recurrence of left hemiparesis and tumors three months after the gamma-knife therapy. Whole brain irradiation therapy (total 30 Gy) was somewhat effective to the tumor and hemiparesis transiently subsided. Thereafter her general condition worsened again, and she died in June, 1999, eight months after the diagnosis of the brain tumors of leukemic cells. We had not seen any other clinical evidence of generalized blastic crisis in this patient. In our case, MRI of the brain showed two patterns of metastases, tumor forming and cortical invasive type. We thought that these two patterns of brain involvement might show different responses to the radiation therapy, and it was characteristic in this patient.
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PMID:[A case report of chronic myelocytic leukemia with multiple brain metastases, which responded to the gamma-knife therapy]. 1119 43


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