Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lacunar syndrome can be an initial manifestation of the metastatic brain tumor in young adults. Two patients were encountered with previously undiagnosed lung cancer, one with anaplastic carcinoma and the other with adenocarcinoma. A neurologic syndrome occurred in the morning with unusual headache and stroke-like episodes, presenting an acute ataxic hemiparesis and a pure motor hemiparesis, respectively. Papilloedema was a universal finding. The headache and neurologic deficits responded rapidly to glucocorticoid. A preexisting intracranial mass with an outburst of brain edema is thought to be the mechanism in this situation.
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PMID:Metastatic brain tumor manifesting as lacunar syndrome in adults. 834 Sep 54

Patients with nonmetastatic lung cancer may rarely experience facial pain as a presenting symptom, during the course of the disease or upon recurrence of the disease. This study reviews a 10-year experience at Mayo Clinic. The aim of this study was to (1) further characterize the clinical features of facial pain as a symptom of nonmetastatic lung cancer, and (2) assist clinicians in recognizing this association. Ten cases were identified. All patients complained of severe, aching, facial pain typically aural-temporal in location, ipsilateral to the lung cancer. Six of the 10 cases involved the left side. Recent weight loss was present in 7 of 10 patients, with an elevated sedimentation rate in 6. Digital clubbing was documented in three. Neurologic examinations and neuroimaging were normal in all patients. Lumbar puncture, when performed, was normal. Facial pain preceded the diagnosis of lung cancer by 1 to 24 months. In three patients, facial pain was the initial symptom of tumor recurrence. Four of the 10 tumors were adenocarcinoma; radiation with or without chemotherapy appears to be the treatment of choice for the facial pain. The presumed mechanism is local invasion of the vagus nerve. In suspected cases, a chest x-ray and chest CT are indicated.
Headache
PMID:Facial pain as a symptom of nonmetastatic lung cancer. 855 Mar 57

Pituitary metastasis are rare but represent an important differential diagnosis of intrasellar tumorous syndromes. We report one case of intrasellar metastasis of a bronchial adenocarcinoma in a 50 year old woman. Clinical syndrome associated a tumorous syndrome (cephalalgia, bitemporal hemianopsia) and an anterior and posterior hypopituitarism biologically proven. A large intra and suprasellar mass which compressed the optic chiasma and highly enhanced after gadolinium injection was found by nuclear magnetic resonance imaging. The surgical biopsy displayed a pituitary metastasis of a right inferior lobar bronchial adenocarcinoma with bone secondary localizations. Cerebral radiotherapy and corticotherapy allowed recovery of visual loss but did not prevent rapid death. The clinical and radiological features which may evoke an intrasellar metastasis were: the tumorous syndrome associated with or revealed by diabetes insipidus, loss of spontaneous hypersignal of the neurohypophysis in nuclear magnetic resonance imaging, bulking pituitary stalk, bilobar character of the mass which is in favour of rapid cell proliferation, postero-superior extension, lowering of the V3 floor and very strong and homogeneous signal after gadolinium injection.
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PMID:[Diabetes insipidus revealing pituitary metastasis of bronchial carcinoma]. 899 Nov 5

We reported a case of long survival brain metastasis and meningeal carcinomatosis from lung cancer without radiochemotherapy. A 59-year-old female admitted to our hospital suffered from headache, anorexia and nausea. Papilledema was noticed, and examinations showed a brain tumor in the left parietal lobe and cancer cells in cerebrospinal fluid. Removal of the tumor and ventriculoperitoneal shunt were performed. Pathology showed adenocarcinoma. No neurological deficit was found during the postoperative course and the patient asked for home treatment. She survived for 25 months and spent a useful life in the 15 months after the onset in spite of no radiochemotherapy for meningeal carcinomatosis. In this case, because of the slow progression of the clinical symptoms, it is considered that cancer cells in the cerebrospinal fluid space grow slowly. The first CT and MRI findings of metastatic tumor of this case showed atypical for brain metastasis. Calcifications were found in plain CT and a high intensive tumor in both T1 and T2 weighted images of MRI. Enhancement due to contrast media was very slight in both CT and MRI. We considered that these findings were related to the slow growing of cancer cells.
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PMID:[A slowly progressed case of brain metastasis and meningeal carcinomatosis from lung cancer]. 943 Jan 51

Malignant diffuse mesothelioma is a tumour related to asbestos exposure, more common in males and located primarily in the chest cavity. Its diagnosis requires ruling out other tumours with pleural or peritoneal metastases, a biopsy showing a morphological pattern consistent with mesothelioma and in many cases to perform immunohistochemical markers to rule out an adenocarcinoma. We report here 20 cases of diffuse pleural mesothelioma and three cases of peritoneal mesothelioma in 20 males and three cases of peritoneal mesothelioma in 20 males and three females. Asbestos exposure was observed for 31% of cases. The most common clinical manifestations included headache and dyspnea; interestingly, three cases had hydropneumothorax with poor response to drainage. The diagnostic confirmation was obtained mainly with thoracotomy or laparoscopy biopsies and to rule out an adenocarcinoma immunohistochemical stainings were performed.
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PMID:[Malignant diffuse mesothelioma: contribution of 23 cases]. 984 55

The main form of chemotherapy for non small cell lung cancer is a multiple combination therapy centered on cisplatin (CDDP). We herein report a case in which a favorable course was obtained for a patient with extremely rare AFP-producing lung cancer by single oral administrations of UFT, following extirpation of brain metastasis. The patient was an 80-year-old male whose main complaints were headache and aphasia. Following close examination, a diagnosis was made of moderately differentiated adenocarcinoma with the primary lesion in S6 of the right lung. A metastatic lesion was found in the left occipital lobe. Blood AFP was an abnormally high 17,000 ng/ml. No tumorous lesions were found in the liver. The brain metastasis were extirpated to alleviate cranial nerve symptoms, and the tissue was found to be the same as that of the primary lesion. AFP staining of the tumor tissue revealed positive cells. Because there was proliferation in the primary tumor following surgery, administration of UFT (300 mg/day Tegafur) was begun. Four weeks later the tumor had begun to shrink, and at 15 weeks was judged to be a partial response. A reduction in AFP was also seen. The patient showed absolutely no side effects from UFT, thus enabling outpatient treatment. Good results were obtained both in reducing the tumor and in maintaining the patient's quality of life.
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PMID:[Effective treatment of AFP-producing lung cancer with UFT]. 1006 6

Murine anti-CD3 (OKT3, Muromonab-CD3) is a potent human T-lymphocyte mitogen. A previous clinical Phase I trial examined OKT3 as an immunomodulator for the treatment of cancer. However, the murine monoclonal antibody triggered a potent humoral response that neutralized the antibody activity during subsequent administration. Thus, a "humanized" form of OKT3 (hOKT3gamma4) was developed to minimize immunogenicity. The genetically engineered human anti-CD3 retained its binding activity and effectively activated T cells in vitro. Therefore, we evaluated the safety and activity of hOKT3gamma4 in a Phase I clinical trial. hOKT3gamma4 was administered as a 10-min i.v. infusion every 2 weeks for three injections (one course of therapy). Six dose levels ranging from 50 to 1600 microg/injection were evaluated. Headache and fever were common, transient toxicities but were not dose limiting. The dose-limiting toxicities were rigors and dyspnea at the 1600-microg dose level, which defined 800 microg as the maximally tolerated dose in this trial. A dose-dependent in vivo T-lymphocyte activation was produced by this treatment, and the most significant T-lymphocyte activation occurred in patients treated at the two highest dose levels (800 and 1600 microg). Persistent CD3 modulation occurred after administration of 1600 microg of hOKT3gamma4. Anti-idiotypic antibodies were detected in only 6 of 24 patients after multiple injections and were not associated with attenuation of T-lymphocyte activation. Malignant ascites resolved in three patients, one each with peritoneal mesothelioma, pancreatic adenocarcinoma, and ovarian adenocarcinoma. hOKT3gamma4 can induce T-lymphocyte activation in patients with cancer, and the immunogenicity of the "humanized" antibody is sufficiently reduced relative to its murine "parent" to permit immunostimulation by repetitive i.v. administration. The therapeutic potential of biweekly i.v. hOKT3gamma4 at a dose of 800 microg should be further evaluated.
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PMID:Phase I evaluation of humanized OKT3: toxicity and immunomodulatory effects of hOKT3gamma4. 1023 94

A 68-year-old man with metastatic brain tumors from adenoendocrine carcinoma of the common bile duct is reported. A common bile duct tumor and a metastatic liver tumor had been resected 6 years and 3 years prior to admission, respectively. Microscopically they showed two components; moderately differentiated tubular adenocarcinoma and neuroendocrine carcinoma. He presented with headache and vomiting and MRI revealed two metastatic brain tumors. They were successfully resected and radiotherapy was carried out. Histological diagnosis of the metastatic brain tumors was neuroendocrine carcinoma, but carbohydrate antigen (CA)-19-9 and carcinoembryonic antigen (CEA)-immunoreactive cells were observed without glandular pattern. Immunohistochemically serotonin and pancreatic polypeptide were detected, but somatostatin was not. As the endocrine cells demonstrated in the normal extrahepatic bile ducts are only somatostatin-containing D cells, these cells are considered to originate as part of a metaplastic process. To our knowledge, this represents the second case of adenoendocrine carcinoma of the common bile duct.
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PMID:Brain metastases from adenoendocrine carcinoma of the common bile duct: a case report. 1037 37

We present an occult metastatic signet-ring cell gallbladder carcinoma in a 78-year-old woman, who complained of recurrent headaches, dysarthria, and paresis of the tongue. Cranial imaging showed contrast enhancement of the basal leptomeninges, and the cerebrospinal fluid displayed clusters of adenocarcinoma cells proposed as leptomeningeal carcinomatosis of the breast, lung or gut. However, postmortem examination revealed the gallbladder as the site of the primary carcinoma with focal signet-ring cell differentiation. In patients with progressive neurologic deterioration due to leptomeningeal carcinomatosis, adenocarcinomas from the gastrointestinal and hepatic systems should be considered. It is likely that signet-ring cell carcinomas display an increased affinity to leptomeningeal spread.
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PMID:Leptomeningeal carcinomatosis and cranial nerve palsy as presenting symptoms of a clinically inapparent gallbladder carcinoma. 1044 66

A 42-year-old house wife presented with worsening headaches over 6 months in the absence of visual symptoms or symptoms suggestive of focal neurology. She was a life-long smoker. Systems review was unremarkable apart from secondary amenorrhoea and galactorrhoea of 6 months duration. Her serum prolactin was found to be 620 mU/l (60-400), FT4 12.6 nmol/l (9.8-23.1), TSH 1.38 mU/l (0.35-5.5), oestradiol < 73 pmol/l, LH and FSH of 4.4 and 12.6 mIU/l, respectively. She was on bromocriptine. A presumptive diagnosis of pneumonia, based on pyrexia and CXR findings, was made and she was started on IV antibiotics. Two days later she developed meningism and deterioration of conscious level. (Lumbar puncture results: no organisms, 312 neutrophils and 164 lymphocytes). CT scan revealed a 2.5-cm pituitary adenoma, with suprasellar extension. A repeat hormonal profile revealed FSH 1.4, LH < 0.3 mU/l, oestradiol < 73 pmol/l, prolactin 488 mU/l (60-400), and low random cortisol at 29 nmol/l. T1-weighted MRI revealed a large pituitary mass with evidence of haemorrhage. The patient subsequently underwent a transsphenoidal exploration with resection of the pituitary lesion. Whilst awaiting the histopathology results, CT of chest revealed a 1. 5-cm diameter rounded well defined density in the right lower lobe associated with hilar, pre- and right para-tracheal lymphadenopathy. The histopathology of the pituitary lesion, obtained piecemeal, revealed fragments of fibrous tissue infiltrated by sheets of acidophilic prolactin-positive cells, in keeping with a prolactinoma. In addition, other fragments with blood clot included highly atypical epithelial cells with mitotic figures. These were negative for prolactin but showed HMFG-and CEA-positivity, excluding them from a pituitary lineage. Transbronchial biopsy revealed moderately differentiated adenocarcinoma, with evidence of lymphatic spread. The overall conclusion was of bronchogenic adenocarcinoma, metastasizing to a prolactinoma and complicated by apoplexy.
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PMID:Pituitary apoplexy following metastasis of bronchogenic adenocarcinoma to a prolactinoma. 1046 19


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