Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 74-year-old man developed progressive deafness and unsteady gait two years after gastrectomy for a gastric cancer. Neurological examination revealed an alert and intelligent Japanese male in no acute distress. The optic fundi were normal. The pupils and the extraocular muscles were normal, however, horizontal nystagmus was noted in right and left gaze. He showed marked bilateral deafness, and loss of caloric response bilaterally. No muscle atrophy nor weakness was noted. His gait was wide-based and ataxic. Tandem gait was impossible. Romberg sign was present. No cerebellar ataxia was noted in the finger-to-nose or the heel-to-knee test. No adiadochokinesis was noted. Hyperextensibility was noted in the lower extremities. Deep reflexes were normal in the upper limbs, and diminished in the lower extremities. Sensation was intact. He showed the jumbling phenomenon, and the disturbance of the righting reflex in the tilt-table examination. Neuroradiological as well as laboratory studies were unremarkable except for the high titer of CEA in the CSF. Four months after his admission, malignant tumor cells were found in the CSF. It seemed likely that he had completely lost bilateral vestibular and auditory functions caused by meningeal carcinomatosis. His disturbance of gait and station was apparently similar to cerebellar ataxic gait, however, he did not have limb ataxia. The cranial CT scans failed to show cerebellar atrophy. It was our impression that his motor disturbance was in all likelihood caused by the bilateral loss of vestibular functions, i.e., vestibular ataxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vestibular ataxia caused by meningeal carcinomatosis]. 236 34

We report a 91-year-old man who had a stroke and died of renal failure. He had been treated for hypertension since 20 years before the onset of the present illness. In addition, he was operated on a gastric cancer 17 years previously. Otherwise he was doing well until May 29, 1991 (when he was 87-year-old) when he had sudden onset of dysarthria and right facial weakness. He was admitted to our hospital. On admission, general physical examination was unremarkable, and neurologic examination revealed a mentally sound man with slight dysarthria, right facial weakness, orolingual dyskinesia, and dysequilibrium in which he showed difficulty in tandem gait; however, no cerebellar ataxia was noted. A cranial CT scan revealed leukoaraiosis with multiple low density areas in the cerebral white matter. His BUN was 37 mg/dl and Cr 2.2 mg/dl. His neurologic symptoms cleared within the next few weeks and he was discharged with ticlopidine 100 mg q.d.. He had been doing well after the discharge except for gradual worsening of his renal function; his BUN was 65 mg/dl and Cr 3.27 mg/dl in April of 1994. On March 10, 1995, he fell down and hit his back; he became unable to walk because of pain, and he was admitted again on March 16, 1995. On admission, his blood pressure was 170/80 mmHg. There was an 1 + pitting pretibial edema; otherwise general physical examination was unremarkable. Neurologic examination revealed an alert and oriented man, however, Hasegawa's dementia scale was 23/30. Higher cerebral functions as well as cranial nerves were intact. He showed some unsteadiness of gait, however, no motor weakness or ataxia was noted. Deep tendon reflexes were diminished, but Chaddock sign was positive bilaterally. Vibration was diminished in the feet, however, pain and touch sensations were intact. Laboratory examination revealed a compression fracture of the twelfth thoracic vertebra. Blood count and chemistries were as follows; Hb 7.6 g/dl, Hct 23.3%, TP 6.0 g/dl, Alb 3.6 g/dl, BUN 87 mg/dl, Cr 4.53 mg/dl, T-Chol 174 mg/dl, HDL-Chol 49 mg/dl, Glu 156 mg/dl, Na 142 mEq/L, K 5.4 mEq/L, Cl 115 mEq/L. A urine specimen contained 1 + protein and 1 + glucose, and the sediments contained hyaline casts. A cranial CT scan was essentially same as that taken four years ago. His hospital course was complicated with pneumonia, congestive heart failure, and progressive renal failure. He was treated with intravenous fluid, chemotherapy, and other supportive measures, however, he expired from respiratory failure on April 30, 1995. He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were divided regarding the question as to whether or not this patient had Binswanger's disease. Although his cranial CT scan revealed leukoaraiosis, his dementia and gait disturbance was only mild until his fall on March, 1995. Clinical features did not conform to those of Binswanger's disease. Postmortem examination of the right hemisphere revealed wide spread atherosclerosis and arteriolosclerosis. The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries and the left middle cerebral artery with 70% stenosis. Myelin stain showed diffuse myelin pallor of the cerebral white matters with scattered small infarcts. Arterioles in the white matter showed arteriolosclerosis. Small infarcts were also seen in the putamen and in the thalamus. This patient appeared to have had circulatory disturbance of the white matter which is the basic abnormality causing Binswanger's disease. However, white matter changes in this patient were not quite severe enough to make a pathologic diagnosis of Binswanger's disease.
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PMID:[A 91-year-old man with a stroke, hypertension, and renal failure]. 899 Apr 84

Ataxia-Telangiectasia (A-T) is a rare autosomal recessive disease characterised by cutaneous telangiectasia, cerebellar ataxia, immunodeficiency, high sensitivity to ionising radiation, chromosomal instability and an increased risk of cancer. The gene mutated in A-T patients, ATM, is located on chromosome 11q22-23. ATM heterozygotes are thought to have a high tendency to develop malignancies, such as breast cancer. In order to determine the contribution of heterozygous ATM mutation to cancer, studies of cancer-affected patients have been undertaken in non site-specific cancer families and sporadic breast cancer cases. No evidence of an important role of ATM heterozygous mutations has been shown. In order to give another contribution to these results, we tried to define a specific family phenotype according to the most common cancers observed in ATM heterozygotes. Breast and gastric cancers appear to be the most frequent malignancies in A-T carriers and one ATM germ-line mutation has been described in a breast/gastric cancer family. Therefore we further investigated the role of ATM mutation in additional breast/gastric cancer families. In eighteen families associating these two malignancies, we used the protein transcription/translation test to detect ATM mutations in the index case from each family. We found one case of ATM mutation which did not cosegregate with the gastric cancer in the family.
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PMID:No evidence for constitutional ATM mutation in breast/gastric cancer families. 959 4

We report a case of a 63-year-old man suffering from anti-Ri-associated paraneoplastic cerebellar degeneration (PCD) with gastric cancer. The neurologic presentation was limited to severe cerebellar ataxia without opsoclonus. The gastric cancer was composed of both poorly differentiated adenocarcinoma and neuro-endocrine carcinoma. The patient's serum reacted with recombinant Ri antigen and the neuroendocrine tumor component. It is thus considered that PCD without opsoclonus in the present case was related to the gastric neuroendocrine tumor and anti-Ri antibody.
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PMID:Anti-Ri-associated paraneoplastic cerebellar degeneration without opsoclonus in a patient with a neuroendocrine carcinoma of the stomach. 1082 24

Antibodies against a glutamate receptor in the central nervous system are reported to be an important autoimmune factor in infantile or childhood refractory epilepsy and in adult-onset paraneoplasstic cerebellar ataxia. We here reported a patient with glutamate receptor antibodies-positive elderly-onset intractable epilepsy and advanced-stage stomach cancer. A 77-year-old man with a history of resected bladder cancer suddenly developed an attack of epilepsia partialis continua in the right arm, followed by a generalized epileptic status. The ictal EEG showed spikes in the left parietal region with diffuse slow wave backgrounds. The brain MRI demonstrated a focal high signal intensity in the left postcentral gyrus on the T2-weighted and FLAIR images. The SPECT showed a high uptake in the focal area corresponding to the MRI lesion, suggesting a seizure focus. The routine analysis in the CSF was normal, but the glutamate receptor antibodies (IgG, IgM and C-terminal) were all positive. The status epilepticus was refractory to anticonvalsants, and the barbiturate anesthesia was introduced. Subsequently, the epilepsy has been fairly controlled by valproic acid and phenobarbital. The post ictal MRI demonstrated a focal atrophy in the left postcentral gyrus. The systemic evaluations revealed an advanced-stage stomach cancer. The glutamate receptor antibodies may play a role in late-onset refractory epilepsy, and may be an autoimmune factor in paraneoplstic neurologic syndrome presenting with epilepsy.
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PMID:[Intrathecal glutamate receptor antibodies in a patient with elderly-onset refractory epilepsy]. 1450 54

A case with brain metastasis involving bilateral middle cerebellar peduncles (bMCP) was reported. A 71-year-old male with gastric cancer was treated for multiple brain metastasis by gamma knife radiosurgery (GKR) in September, 2004. Two months after the initial GKR, MRI showed asymmetrical enhanced lesions involving bMCP. A few months later, MRI revealed an expansional infiltration of bMCP lesions. The patient had presented with headache loss of appetite, cerebellar ataxia, diplopia and slight dysmetria. PET showed 2-deoxy-2- [18F] fluoro-D-glucose (FDG) uptake of the bMCP lesions. The lesions were diagnosed as brain metastasis of gastric cancer. The patient underwent his second GKR (marginal dose : 19Gy, maximum dose 38Gy) MRI revealed the disappearance of the tumors 3 months after the second GKR. One year later, the patient showed no evidence of recurrence. For the last time, our case was diagnosed as brain metastasis from gastric cancer without meningeal carcinomatosis. It was suggested that FDG-PET can provide additional information about the lesion of bMCP. GKR may be useful to treat the tumor in bMCP.
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PMID:[A case of brain metastasis from gastric cancer involving bilateral middle cerebellar peduncles]. 1698 31

Acute cerebellar ataxia is a rare initial presenting feature of neoplastic meningitis (NM), particularly in gastric cancer. The authors report a 61-year-old woman with acute cerebellar ataxia secondary to NM from gastric cancer, which was not accompanied by other symptoms commonly associated with NM at initial presentation. It is suggested that NM should be considered in the differential diagnosis of cancer patients with acute cerebellar ataxia.
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PMID:Neoplastic meningitis presenting with acute cerebellar ataxia. 2123 73

We report a 61-year-old man with slowly progressive gait disturbance and paresthesia in the lower extremities following a total gastrectomy for gastric cancer 23 years previously. The patient presented with hyperreflexia, peripheral sensory neuropathy, and cerebellar ataxia. Magnetic resonance imaging showed atrophy of the cerebellum, and electrophysiological findings suggested the presence of disorder in both sides of the pyramidal tract, dorsal column, peripheral nerves, and optic nerve. Laboratory findings revealed anemia, neutropenia, and a remarkably low serum copper level (10 microg/dl; normal: 68-128). His serum vitamin E was slightly low and his serum vitamin B12 was within the normal limits. After administering an oral copper supplement, his symptoms improved with normalization of the serum copper level. We need to pay attention to myeloneuropathy caused by copper deficiency if the patient has a past history of total gastrectomy.
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PMID:[Peripheral neuropathy, myelopathy, cerebellar ataxia, and subclinical optic neuropathy associated with copper deficiency occurring 23 years after total gastrectomy]. 2173 33

Ataxia-telangiectasia (A-T) is an autosomal recessive primary immunodeficiency disease characterized by progressive cerebellar ataxia, telangiectasia, sinopulmoner recurrent infections, and cancer susceptibility. Individuals with A-T are known to be at increased risk of certain malignancies including leukemia, lymphoma, and breast and gastric cancer. We present an 18-year-old case of A-T with Hashimoto thyroiditis who admitted with complaints of nausea, vomiting, anorexia, and weight loss. An upper endoscopic biopsy revealed gastric signet ring cell carcinoma. To the best of our knowledge, we report the first case of signet ring cell carcinoma in the patient with A-T. Our experience with occurrence of Hashimoto thyroiditis and gastric signet ring cell carcinoma in the same case of A-T underlines that the clinicians handling A-T must be vigilant about both malignancy and autoimmune disorders.
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PMID:Gastric signet ring carcinoma in a patient with ataxia-telangiectasia: a case report and review of the literature. 2321 92

Opsoclonus-myoclonus syndrome (OMS) is an involuntary multidirectional eye movement accompanied by myoclonic jerks and a subtype of paraneoplastic neurological syndromes. Clinical features of OMS include opsoclonus with myoclonic jerks and cerebellar ataxia. Although there have been a few studies on brain FDG PET in paraneoplastic neurological syndrome associated with some kinds of malignancies such as lung and gastric cancer, brain FDG PET of patients with OMS caused by a mature cystic teratoma has not been reported. Here, we described a case of brain FDG PET/CT studies performed in a woman with OMS provoked from a mature cystic teratoma.
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PMID:18F-FDG PET/CT Brain Imaging on a Patient With Paraneoplastic Opsoclonus-Myoclonus Syndrome Arising out of a Mature Cystic Teratoma. 2654 25


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