Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0042963 (vomiting)
31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurrence of hemorrhage from pituitary adenoma (so-called "pituitary apoplexy") was investigated in a consecutive series of 560 cases operated on during the past 30 years. There were 93 cases (16.6%) in which hemorrhage from pituitary adenomas was confirmed either clinically or surgically. These patients were analyzed in terms of age, sex, symptoms and signs, size of tumor, hormonal function, and histological types of adenomas, and computerized tomography findings. In 90 cases (16.6%), hematoma or old bloody fluid was verified within the tumor tissue at surgery. Three other patients presented with subarachnoid hemorrhage, but there was no detectable intratumor hematoma in any of them. Among these 93 patients, 42 (7.5%) showed no evidence of clinical symptoms related to hemorrhage (asymptomatic hemorrhage). Fifty-one patients (9.1%) had definite histories of an acute episode that suggested sudden bleeding (symptomatic hemorrhage: pituitary apoplexy). Thirty-eight patients (6.8%) had a major attack manifested by disturbances of consciousness, hemiparesis, loss of vision, or ocular palsy. In two acromegalic patients, pituitary apoplexy developed during bromocriptine treatment. There was one case of sudden death due to massive hemorrhage from the tumor 14 months after the completion of postoperative radiation therapy. The other 13 symptomatic patients (2.3%) developed a minor attack which included headache, nausea, vomiting, and vertigo. Bleeding from pituitary adenomas was not statistically correlated with any of the following factors: sex, hormonal function of adenomas, and histological types, but it was correlated with age. The number of asymptomatic cases in the third decade was significantly greater than that of the whole group of pituitary adenoma patients in the same decade. The present investigation revealed that the incidence of pituitary apoplexy was unexpectedly high: a major attack in 6.8% of pituitary adenoma patients, a minor attack in 2.3%, and asymptomatic hemorrhage in 7.5% of the cases. This risk of pituitary apoplexy should be kept in mind in treating pituitary adenomas.
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PMID:Pituitary apoplexy: its incidence and clinical significance. 725 41

A case of arterio-venous malformation (AVM) at the right parietal area in association with agenesis of the left internal carotid artery (ICA) is described. A 27-year-old male complained of severe headache and vomiting on September 27th in 1980. He lost his consciousness and became stuporous within several minutes after the ictus. He was then transferred to Kurume University Hospital. On admission, he was semicomatose, anisocoria and left hemiparesis marked in the lower limbs, and bilateral Babinski reflex were noted. A emergency CT scan revealed a round high density area suggesting intracerebral hematoma at the right parieto-occipital area. Right retrograde brachial angiography was then performed which showed a small AVM at the right parietal lobe mainly fed by the right posterior parietal arterial branch, and drained into the superior sagittal sinus, via the subcortial veins. Left MCA bilateral PCA and SCA also were demonstrated on the angiogram. The angiogram suggested on abnormality of the Willis ring. Emergency operation fro the small AVM associated with intracerebral hematoma was then performed. The AVM was sufficiently removed and approximately 80 gr. of intracerebral clots were also evacuated completely. Histological examination indicated a typical small AVM. The postoperative course was uneventful. Left CAG performed by seldinger method from the femoral artery after the operation showed no demonstration of the left ICA. the left common carotid artery was terminated as the external carotid artery without carotid bifurcation at the neck. The left ophthalmic artery was fed by the meningeal artery of the internal maxillary artery. Left vertebrobasilar system was normal. From an angiogram, the agenesis of the left ICA was most suspected. An agenesis of ICA was uncommon among the literature in which there was no case with this anomaly associated with cerebral AVM. The embryological consideration about this case was mainly discussed.
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PMID:[A case of arterio-venous malformation associated with agenesis of unilateral internal carotid artery (author's transl)]. 734 82

Mitochondrial myopathy, encephalopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome is one of the mitochondrial encephalomyopathies that has distinct clinical features including stroke-like episodes with migraine-like headache, nausea, vomiting, encephalopathy and lactic acidosis. We report a 27-year-old woman who presented with partial seizure, stroke-like episodes including hemiparesis, hemianopia and hemihypethesia, sensorineural hearing loss, migraine-like headache, and lactic acidosis. Brain computed tomographic scan showed encephalomalacia in the right parieto-occipital area and recent hypodensity in the left temporoparieto-occipital area with cortical atrophy. Muscle biopsy revealed ragged-red fibers and paracrystaline inclusions in the mitochondria. Genetic study revealed an A to G point mutation at nucleotide position (np) 3243 of mitochondrial DNA. External ophthalmoplegia and ptosis were also found during two exaggerated episodes in this patient. Therefore, the overlapping syndrome of chronic progressive external ophthalmoplegia in the MELAS syndrome is considered in this case. Furthermore, we also found carnitine deficiency in this patient and she was responsive well to steroid therapy. Muscle biopsy also revealed excessive lipid droplets deposits. Therefore, the carnitine deficiency may occur in MELAS syndrome with the A to G point mutation at np 3243. We recommend the steroid or carnitine supplement therapy be applied to the MELAS syndrome with carnitine deficiency.
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PMID:CPEO and carnitine deficiency overlapping in MELAS syndrome. 748 81

Ornithine transcarbamylase deficiency is an X-linked recessive disorder of urea biosynthesis characterized by recurrent, often fatal, hyperammonemic encephalopathy in affected males; carrier females are usually asymptomatic. We report here the clinical and laboratory findings in five symptomatic heterozygous females with ornithine transcarbamylase deficiency. In each case, the onset of symptoms occurred in the 1st year of life, but diagnosis was delayed by up to 15 years. Symptoms included recurrent vomiting with lethargy (five patients), dietary protein intolerance (five), irritability (four), severe acute encephalopathy (three), ataxia (three), and acute hemiparesis (two). All eventually showed evidence of developmental delay or learning difficulties. Two of the three who experienced severe, acute, hyperammonemic encephalopathy suffered serious, permanent neurologic sequelae. Three of the patients showed decreased ornithine transcarbamylase activity in liver obtained by needle biopsy, and the other two had marked orotic aciduria associated with hyperammonemia. Neuroimaging studies demonstrated persistent abnormal lobar attenuation and abnormal signal on computed tomographic scan and magnetic resonance imaging. All patients showed marked symptomatic improvement on treatment with dietary protein restriction supplemented by pharmacologic measures to increase nonprotein nitrogen excretion. Ornithine transcarbamylase deficiency should be considered in the differential diagnosis of acute or chronic encephalopathy in females at any age.
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PMID:Ornithine transcarbamylase deficiency in females: an often overlooked cause of treatable encephalopathy. 749 56

We report two patients with solitary thalamic abscesses, occurring among 91 consecutive patients (2.2%) with computed tomography (CT)-diagnosed and surgically-verified brain abscess experienced in our college during 1975 to 1991. A 9-year-old girl with congenital heart disease experienced frequent vomiting followed by left hemiparesis and deterioration of consciousness. CT demonstrated a right thalamic ring-enhanced lesion. Purulent material was aspirated via a burr hole. She died of heart failure on the 5th postoperative day. Autopsy disclosed diffuse brain swelling and an encapsulated abscess in the right thalamus, which had ruptured into the third ventricle. A 30-year-old female experienced headache, nausea, and vomiting, which progressed to somnolence and right hemiparesis. CT demonstrated a left thalamic ring-enhanced lesion. Purulent material was aspirated by stereotactic procedures. All symptoms had resolved by the end of the 2nd postoperative week.
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PMID:Solitary pyogenic thalamic abscess--two case reports. 750 3

We report a case of triple intracranial tumors of different cell types without phacomatosis. The patient was a 77-year-old female who was hospitalized with left hemiparesis and vomiting. Computed tomography (CT) scans revealed a large tumor mass in the right frontal lobe and relatively small tumor masses in the medial right frontal and parietal lobes. Other tumors were also detected in the sella turcica, left sphenoidal wing, left anterior clinoidal process and left cerebellar convexity. This case was considered to be one of metastatic brain tumors, and surgery was performed for the right frontal tumor because of its mass effect. The tumor was so highly vascular that it could not be totally removed. Postoperatively, the mass effect showed a gradual increase on CT scans because of intratumoral hemorrhage and peritumoral edema. The patient's consciousness level gradually fell, and she died of pneumonia and cardiac insufficiency 1 month after the operation. The surgical specimen of the tumor was diagnosed as glioblastoma multiforme by histological examination. At autopsy, the small tumors in the medial frontal lobe and parietal lobe were found to be clearly separated from the large right frontal tumor and were diagnosed as multicentric glioblastoma multiforme. The sellar tumor revealed chromophobe pituitary adenoma and was diagnosed as a prolactinoma by immunohistochemical examination. The tumors in the left sphenoidal wing and left cerebellar convexity were diagnosed as transitional meningiomas. Multiple primary intracranial tumors of different cell types without phacomatosis are relatively rare, but almost 100 reported cases could be found in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Triple primary intracranial tumors of different cell types: a case report]. 760 38

A 16-year-old female presented with clinical, morphologic and molecular features of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). Her early development was normal. Starting from the age of 14 years, she experienced recurrent episodes of headaches, with vomiting, seizures, transient right hemiparesis and decreased visual acuity. Computed tomographic brain scans revealed calcification in the bilateral basal ganglia. Biopsied specimens from her left biceps brachii and rectus femoris muscles revealed ragged-red fibers and strong succinate dehydrogenase-reactive blood vessels. Electron microscopy revealed paracrystalline inclusions in muscle mitochondria. Analysis of mitochondrial DNA (mtDNA) from blood, hair follicles and muscle specimens showed an A to G point mutation at nucleotide position 3,243 in the transfer RNA(Leu(UUR)). The proportion of mutant mtDNA in the patient's blood was 43%, in hair follicles 62% and in muscle 82%. The patient was followed up for 4 years and had progressive mental deterioration and died of an episode of status epilepticus. This patient and 5 other MELAS patients reported in Taiwan are compared.
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PMID:Heteroplasmic mitochondrial DNA mutation in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. 761 32

The clinical manifestations and mitochondrial DNA (mtDNA) mutations in a Taiwanese family with a female proband exhibiting mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes syndrome are reported. Clinically, the proband had a stroke-like episode with right hemiparesis, hemianopsia and mental dysfunction as well as short stature, hearing impairments, and elevated lactate levels. Brain magnetic resonance images showed multiple increased signal intensities over the left frontal, parietal and temporal areas. There were no ragged-red fibers, but paracrystalline inclusion bodies were shown in the muscle biopsies under electron microscopic examination. A deficiency of NADH-CoQ reductase was also found in biochemical studies of the muscles. The family survey revealed no abnormal findings except for headache and episodic vomiting in her mother. The molecular analysis of mtDNA disclosed a mutation from A to G at the nucleotide pair 3243 of the mitochondrial transfer RNA(Leu) gene in the blood, hair follicles and/or muscle of the maternal relatives. A characteristic finding of the MELAS family is variation of percentage of mutated mtDNA in various tissues and individuals. However, a higher proportion of mutated mtDNA was noted in the proband than that in the asymptomatic or oligosymptomatic family members. From the data, the variable clinical phenotypes in this MELAS family can be explained at least partly, by the different proportions of mutant mtDNA in the target tissues of the proband and maternal relatives.
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PMID:MELAS syndrome: correlation between clinical features and molecular genetic analysis. 788 36

We report a 78-year old woman with 30 years history of rheumatoid arthritis and nephrotic syndrome, who developed right hemiparesis and renal failure recently. The patient was diagnosed as having rheumatoid arthritis in 1965, and had been treated with gold -sol, steroid hormone, and non-steroidal anti-inflammatory drugs intermittently. Later on her clinical course was complicated by nephrotic syndrome, however, her renal function was well compensated. Otherwise, she was apparently doing well until October of 1988 when she had an onset of anomic aphasia; she was 73-year-old at that time. She was admitted to our hospital; a cranial CT scan at that time revealed a low density area in the left temporal region, and she was diagnosed as suffered from an atherothrombotic infarction involving the left middle cerebral artery territory. She recovered soon and was discharged for out patient follow up with ticlopidine 100 mg/day. She was doing well until December 15, 1990, when she had an acute onset of nausea, vomiting, and speech disturbance; she was admitted to our hospital for the second time. On admission, she was alert, but she had motor aphasia, right hemiparesis, and dysarthria. A cranial CT scan revealed a low density area in the left temporal region extending into adjacent frontal and parietal areas including the angular gyrus; in addition, leukoaraiosis, cortical atrophy, and ventricular dilatation were noted (Fig. 1A, B). She was treated supportively, and she showed improvement in her aphasia, however, moderate weakness remained in her right upper and lower extremities. She was discharged for out patient follow up. She was doing well until May 21, 1993, when she developed difficulty in swallowing and speech. She became unable to take foods orally and she was admitted again on May 31. On admission, she was afebrile and BP was 120/80 mmHg. General physical examination was unremarkable except for pitting edema and multiple contracture of her joints. On neurologic examination, she was alert but appeared to have aphasia and dementia; she could utter only a few simple words, and was able to understand only simple questions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 78-year-old woman with rheumatoid arthritis, right hemiparesis, and renal failure]. 789 38

Paranasal sinusitis complicated by subdural empyema (SDE) in a 14-year-old boy is described. He presented with fever, headache and vomiting. X-rays revealed left maxillary and bilateral frontal sinusitis. While in the emergency room he had seizures; CT-scan showed an air leak adjacent to the right frontal sinus. Despite intravenous antibiotics, left hemiparesis developed and repeat CT showed interhemispheric SDE. Frontal craniotomy was performed and a large amount of purulent material was drained. Recovery followed 4 weeks of intravenous antibiotic treatment without neurologic sequelae. SDE is a rare complication of paranasal sinusitis and constitutes approximately 20% of all localized intracranial infections. Clinical features include fever, headache, vomiting, convulsions and neurologic deficits. Modern imaging methods and combined surgical and antibiotic treatment have lowered mortality to 5-10%. A high index of suspicion is important for early diagnosis and successful treatment.
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PMID:[Subdural empyema complicating sinusitis]. 791 Nov 17


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