Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a boy aged 13 years treated since 8 years irregularly with chemotherapeutic agents for Hodgkin's disease suddenly signs of increased intracranial pressure developed. In EEG changes were found on the temporo-occipital area with prevalence of the right area. In the cerebrospinal fluid the cell count was 33/3.0, Pandy Nonne-Apelt++, protein 78 mg %, sugar 84 m %. Skull radiography in a-p and lateral projections demonstrated normal cranial bones and sella. Despite intrathecal administration of methotrexate and decompressing drugs the condition deteriorated and consciousness disturbances, vomiting and dysarthria appeared. After 19 days of hospital treatment death occurred. Pathological and histological examinations demonstrated metastases to the pons. The necessity is stressed of considering possible cerebral metastases in Hodgkin's disease.
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PMID:[A rare form of Hodgkin's disease complicated by involvement of the central nervous system in a 13-year-old boy]. 181 Nov 89

A 65-year-old woman with known breast carcinoma developed headaches, followed shortly by disequilibrium, vertical diplopia and dysarthria. Cranial computerized tomography (CCT) demonstrated a dense, irregularly enhancing pontine lesion with associated mass effect. She received dexamethasone (Decadron) and radiotherapy and subsequently expired. Postmortem examination disclosed a ruptured brain stem arteriovenous malformation within a massive hemorrhage along with necrotic atypical cells suggestive of metastatic disease.
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PMID:Brain stem vascular malformation simulating a hemorrhagic metastasis: report of a case with pathologic correlation. 648 86

A 61-year-old Caucasian man presented with otalgia, dysarthria, and weight loss. Neurological examination revealed palatal hypomotility, and weakness of the facial and tongue muscles. Magnetic resonance imaging of the head demonstrated the presence of a soft tissue mass in the clivus. Histologic examination of resected tumor disclosed well-differentiated thyroid follicles that invaded the local osseous tissues. Physical examination and radioiodine images of the thyroid gland were normal. The serum thyroglobulin concentration was markedly elevated (1011 ng/mL). A 0.9-cm well-differentiated benign-appearing left thyroid lobe follicular neoplasm with a thick fibrous capsule was found following diagnostic thyroidectomy. This report illustrates that clinically significant distant metastases can arise from occult follicular thyroid neoplasms that, according to standard histologic criteria, are benign. The presence of a thick fibrous capsule, even in the absence of vascular or capsular invasion, may identify follicular neoplasms that have metastatic potential.
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PMID:Metastatic follicular thyroid carcinoma masquerading as a chordoma. 758 Feb 71

We report a 24-year-old man who presented unilateral multiple cranial nerve involvements followed by progressive paraplegia. The patient expired after developing DIC and pneumonia. Post-mortem examination revealed Ewing's sarcoma originated in the pubic bone with extensive metastases including the clivus which was responsible for his cranial nerve lesions. The patient was well until 24 years of age when he noted an onset of pain and a mass in the pubic region. The histology of the biopsy specimen of the tumor suggested Ewing's sarcoma. He was treated with chemotherapy and local radiation. A year after, he noted an onset of nuchal pain, difficulty in tongue movement, dysarthria, deafness in the left ear, and diplopia. On admission to our hospital in July 1990, neurological examination revealed an alert and intelligent Japanese male in no acute distress. The olfactory to the trigeminal nerves appeared intact. He showed complete abducens nerve palsy, facial weakness, mild deafness, and weakness of the soft palate, the sternocleidomastoid muscle and the tongue, all on the left side. The remainder of the neurological examination was unremarkable except for dysesthesia along the left C8 and Th1 dermatoms. Radiological examination revealed a 10 x 10 cm sclerotic mass in the public bone and a high signal mass lesion between the clivus and the pons in the T2-weighted MRI. His clinical course was complicated by acute paraplegia with anesthesia below the Th4 dermatom, DIC, and respiratory distress due to plural effusion. Post-mortem examination revealed a necrotic and hemorrhagic tumor in the pubic bone. The histology was consistent with Ewing's sarcoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 24-year-old man presenting Garcin syndrome and paraplegia]. 847 71

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

A case of Collet-Sicard Syndrome caused by skull base metastasis of prostate carcinoma is reported. A fifty-five years old man presenting multiple lymph node and bone metastases of prostate carcinoma was treated with LH-RH agonist and Flutamide, which induced transient decrease in serum PSA levels and size of lymph node metastases. After 8 months of the treatment, the patient started complaining headache, dysphagia and dysarthria. Brain CT and MRI demonstrated a soft tissue mass replacing left pyramidal bone and occipital bone around left jugular foramen. The tumor was diagnosed as skull base metastasis of the prostate carcinoma and was treated with 50Gy of radiation. The symptom improved after the radiation but died of the disease in 4 months. The autopsy revealed the skull base metastasis of the prostate carcinoma and the tumor was proved to be poorly differentiated adenocarcinoma, which was positively stained by anti-PSA antibody. The case showed cranial nerve palsy of IX to XII, which is usually called Collet-Sicard syndrome. This is the third case report of Collet-Sicard syndrome caused by the skull base metastasis of prostate carcinoma, and it is the first case in Japan.
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PMID:[A case of Collet-Sicard syndrome caused by skull base metastasis of prostate carcinoma]. 1089 82

A 59-year-old male visited us with a chief complaint of dysuria. The serum prostate specific antigen (PSA) level was within normal limits, and intravenous pyelography and urethrocystography showed no abnormal findings. Because of his urinary retention, transurethral resection of prostate was performed under a clinical diagnosis of benign prostatic hyperplasia. The pathological diagnosis was poorly differentiated adenocarcinoma of the prostate. Not only combination hormone therapy with goserelin acetate and flutamide, but also intermittent arterial infusion chemotherapy with cisplatin (CDDP) and pirarubicin (THP) using a reservoir system was administered. Additionally total pelvic irradiation was delivered. Magnetic resonance imaging (MRI) demonstrated that his prostate was reduced to less than 50% in size and he had no difficulty in voiding. He suddenly developed dysarthria and hemiplegia 3 months later. MRI and computed tomography (CT) revealed multiple brain metastases. After the gamma knife radiosurgery, neurological findings disappeared and MRI showed dramatic shrinkage of metastatic brain tumors. Metastasis to the pancreas was recognized on CT and he died of multiple organ failure 30 months after his first visit.
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PMID:[Complete remission of brain metastases from prostate cancer by gamma knife radiosurgery: a case report]. 1143 55

A 54-year-old female with small volume residual stage III ovarian cancer had received two courses of carboplatin chemotherapy with obvious response, when she developed rapidly progressive neurological symptoms. Over a period of 48 h, an incapacitating syndrome of ataxia, nystagmus and dysarthria evolved. Central nervous system metastases were excluded by computed tomography scanning and cerebrospinal fluid cytology. Anti-Purkinje cell antibodies ('anti-Yo') detected in the serum confirmed the diagnosis of paraneoplastic cerebellar degeneration. Isolated reports have suggested that the clinical course of this condition can be ameliorated with high dose steroids and plasmapheresis. However, in this case the very early introduction of both these did not bring about any improvement in the patient's symptoms. She remained severely incapacitated and unable to care for herself for the remaining 15 months of her life. The patient died of progressive ovarian cancer that had become clinically evident 10 months after the onset of neurological symptoms. This case illustrates many of the classical features of this rare condition, and the world literature is reviewed.
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PMID:Paraneoplastic cerebellar degeneration in a patient with chemotherapy-responsive ovarian cancer. 1157 11

Paraneoplastic neurologic syndromes are disorders of the nervous system function caused by cancer but not due to metastatic disease, vascular or metabolic deficits, infections, nutritive deficiency, nor side effects of antineoplastic drugs or irradiation. Immunologic factors probably play the crucial role in the pathogenesis of paraneoplastic neurologic syndromes, but nonimmunologic mechanisms that include metabolic abnormalities and competition for substrate are also involved. Paraneoplastic cerebellar degeneration most commonly occurs in the setting of gynecologic cancers, but it accompanies the small-cell lung cancer too. Other tumors are infrequently associated with cerebellar degeneration. Several paraneoplastic antibodies have been identified in patients with paraneoplastic cerebellar degeneration. Their association with particular cancers may help identify an occult lesion. Anti-Yo antibodies are directed against Purkinje cell antigens and occur in patients with cerebellar degeneration who have breast cancer or gynecologic tumors. A target antigen of anti-Yo antibody is CDR2 protein that is normally expressed only in the brain and testis. Patients with paraneoplastic cerebellar degeneration present with dizziness, nausea and vomiting followed by gait instability, diplopia, gait and appendicular ataxia, dysarthria and dysphagia. Therapeutic options include tumor excision, chemotherapy and/or irradiation, and adjuvant therapy with glucocorticoids, immunoglobulins and plasmapheresis. The role of plasmapheresis in the treatment of paraneoplastic cerebellar degeneration is still uncertain. Reports of its efficacy are anecdotal. We present patient with paraneoplastic cerebellar degeneration with positive anti-Yo antibodies and tumor of the ovaries whose neurologic status significantly improved after four daily plasmaphereses, which was accompanied by a fourfold decrease in the anti-Yo antibodies titer. Further investigations are needed to define a protocol for plasmapheresis in the treatment of patients with paraneoplastic syndromes.
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PMID:[Importance of plasmapheresis in the treatment of paraneoplastic cerebellar degeneration]. 1512 96

The clinical efficacy of gefitinib, a tyrosine kinase inhibitor of epidermal growth factor receptor (EGFR), on brain metastases (BMs) from non-small-cell lung cancer (NSCLC) was evaluated. Fifteen patients with recurrent NSCLC with metastasis to the brain were treated with gefitinib. The objective tumor response rate (60%; 9 of 15 patients) for BM was the same as for primary tumors. The median time to response of BM was 26 days. In 8 of 9 patients who exhibited partial response in the thoracic lesion, BM showed dramatic regression, including 1 complete response. One patient with stable primary tumor also exhibited partial response in BM with this monotherapy. Brain metastasis-related neurologic symptoms such as hemiparesis, dysarthria, dysphagia, and vertigo improved or disappeared with the objective response of BM as confirmed by magnetic resonance imaging. Central nervous system toxicities were not observed during the treatment. Four of the 9 BM responders are still under treatment with neither adverse events nor disease progression. Two discontinued the treatment because of severe hepatic toxicity and 3 died because of acquired resistance in pulmonary lesions, even though partial response was observed in the BMs. Finally, median duration of response of BM was 8.7 months and median overall survival was 8.3 months (range, 1.8 to > 15.7 months). Molecular targeted therapy against EGFR could be an option for the treatment of BM from NSCLC refractory to conventional chemotherapy plus radiation therapy because it has demonstrated a distinct therapeutic potential against BM compared with primary lung tumor and extracranial metastases.
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PMID:Gefitinib in patients with brain metastases from non-small-cell lung cancer: review of 15 clinical cases. 1547 98


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