Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a 35-year-old woman with benign intracranial hypertension (BIH) secondary to systemic lupus erythematosus (SLE). She had low grade fever and skin eruptions, but neurological examination revealed no abnormal findings. Antinuclear and anti ds-DNA antibodies were positive, and complements were decreased. MRI demonstrated diffuse hyperintense white matter lesions on T2-weighted imaging. Mild bilateral papilledemas developed in the fundi, when her headache was exacerbated. The cerebrospinal fluid (CSF) pressure was 550 mmH2O. Cerebral angiography showed no cerebral sinus thrombosis. She was diagnosed as BIH secondary to SLE. Since RI cisternography revealed remarkably delayed absorption of the CSF, it was speculated that the CSF absorption by arachnoid villi would be probably disturbed in association with some autoimmune mechanisms by SLE. The subsequent rise of intraventricular pressure may result in retrograde transependymal flow of the CSF and the diffuse hyperintense white matter lesions on MRI.
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PMID:[A case of benign intracranial hypertension associated with systemic lupus erythematosus (SLE) showing diffuse white matter lesions on MRI]. 795 16

We report a rare case of primary hyperaldosteronism in an 11-year-old female patient due to a unilateral adrenal cortical adenoma. The patient presented with hypertension, hypokalaemia and metabolic alkalosis associated with inappropriate kaliuresis. The diagnosis was supported by the following laboratory findings: elevated plasma aldosterone, suppressed plasma renin activity, nonsuppressible aldosterone secretion following saline infusion and absent plasma aldosterone response to ambulation. MRI revealed a 1 cm diameter adrenal tumour on the left side. Even though the NP-59 scintigraphy gave a negative result, laparotomy with left adrenalectomy was performed. Pathological examination confirmed an adenoma in the adrenal cortex. The patient's blood pressure and biochemical laboratory data normalized postoperatively within 2 days. We recommended that in hypertensive children with hypokalaemia and metabolic alkalosis, primary aldosteronism should be considered.
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PMID:Aldosterone-secreting adrenal cortical adenoma in an 11-year-old child and collective review of the literature. 775 31

Spinal epidural haematomas (SEH) are rare; most are caused by trauma, anticoagulant therapy, vascular anomalies, hypertension, blood dyscrasias, epidural anaesthesia or, rarely, spinal surgery. We report 11 cases and review the literature (16 cases). The clinical picture is that of acute spinal cord compression. MRI characteristics are quite specific. On sagittal sections, the SEH appears as a biconvex mass, dorsal to the thecal sac, clearly outlined and with tapering superior and inferior margins. The dura mater is seen as curvilinear low signal separating the haematoma from the cord. Within 24 h of onset, the haematoma is isointense with the cord on T1-weighted images and heterogeneous on T2-weighted images. Later, it gives high signal on both T1- and T2-weighted images. Differential diagnosis must include subdural haematoma, epidural neoplasm and abscess. Complete neurological recovery rapidly follows laminectomy and removal of the clot. In three of our cases, the haematoma resolved spontaneously. MRI is the best examination for diagnostic and follow-up.
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PMID:Spinal epidural haematoma: report of 11 cases and review of the literature. 799 Oct 91

A 60-year-old lady with previous hypertension was studied with PET in the acute (early recovery) phase of an otherwise typical episode of transient global amnesia (TGA). Follow-up over > 1 year was uneventful, and delayed CT scans and MRI showed no brain damage. No medical cause was disclosed despite extensive work-up. The PET study revealed a matched reduction in cerebral blood flow and oxygen consumption over the entire lateral frontal cortex on the right side, with an associated, less significant reduction in ipsilateral thalamic and lentiform nucleus metabolism, but sparing the hippocampal area. These changes, which had resolved at a repeat PET study 3 months later, suggest right prefrontal metabolic depression, possibly secondary to thalamic dysfunction, as the underlying mechanism for TGA in this case, consistent with the emerging involvement of the prefrontal cortex in strategies or control of memory traces retrieval. Thus, in analogy with permanent amnesia, TGA may be a core syndrome with several possible foci of dysfunction along the neuronal networks that subserve explicit memory. In the future, combined PET neuropsychological assessment in the acute stage of TGA may prove useful in defining distinct neuropsychological-topographical subtypes of this intriguing clinical entity.
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PMID:Right frontal cortex hypometabolism in transient global amnesia. A PET study. 803 64

Cerebral white matter lesions are a common finding on MRI in elderly persons. We studied the prevalence of white matter lesions and their relation with classic cardiovascular risk factors, thrombogenic factors, and cognitive function in an age- and gender-stratified random sample from the general population that consisted of 111 subjects 65 to 84 years of age. Overall, 27% of subjects had white matter lesions. The prevalence and severity of lesions increased with age. A history of stroke or myocardial infarction, factor VIIc activity, and fibrinogen level were each significantly and independently associated with the presence of white matter lesions. Significant relations with blood pressure level, hypertension, and plasma cholesterol were present only for subjects aged 65 to 74 years. White matter lesions tended to be associated with lower scores on tests of cognitive function and were significantly associated with subjective mental decline. This study suggests that classic cardiovascular risk factors, as well as thrombogenic factors, are associated with white matter lesions in subjects over 65 years of age in the general population, and that these lesions may be related to cognitive function.
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PMID:Cerebral white matter lesions, vascular risk factors, and cognitive function in a population-based study: the Rotterdam Study. 803 24

A 38 year old woman and her first cousin, a 41 year old man, presented both with hypertension, hypokalemia, hyperaldosteronism, and low plasma renin activity in our Hospital. In both patients, plasma and urine aldosterone were constantly above the normal range, even on a high NaCl diet (250 mEq/day), while the plasma aldosterone response to postural changes was normal. In the female patient abdominal ultrasonic scan, CT scan, MRI, and adrenal gland phlebography were normal, but blood from the left adrenal vein contained 1002 pg/ml of aldosterone, versus 91 pg/ml in the contralateral one. Interestingly, the secretion of cortisol was also lateralized (plasma cortisol levels being of 28.8 mcg% in the left, 2.3 mcg% in the right adrenal gland), although neither clinical nor laboratory signs of hypercortisolism were present. Spironolactone treatment (100 mg/daily) completely reversed the syndrome of mineralocorticoid excess. After 2 years, patient has normal blood pressure and serum K+ levels.
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PMID:Unilateral adrenal hypersecretion of both aldosterone and cortisol in two first cousins with a syndrome of mineralocorticoid excess but without signs of hypercortisolism. 805 32

We describe a 23-year-old girl with an extremely uncommon form of cerebral venous drainage and cerebellar leptomeningeal angiomatosis as a possible variant of the Sturge-Weber syndrome. Extensive congenital port-wine stains all over the body, hypoplastic left renal and subclavian and iliac veins, cardiomegaly and ptosis and hypoplasia of the left kidney had been recognised in early childhood. She rapidly developed signs of intracranial hypertension. CT and MRI showed a right medial temporal lesion. Angiography revealed cerebellar pial angiomatosis with enlarged medullary veins and no functioning sigmoid sinuses or jugular veins. Cerebral venous drainage was via enlarged ophthalmic veins. Although the intracranial venous abnormalities were characteristic of the Sturge-Weber syndrome anomalies beyond the encephalofacial territory suggested a more complex developmental abnormality.
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PMID:Cerebral venous drainage via the ophthalmic veins in the Sturge-Weber syndrome. 806 81

Cerebral vein thromboses constitute a major part of cerebral venous disease. They can occur at any age, generally in young subjects, and are due to a variety of causes, although no aetiology can be detected in one quarter of cases. They generally occur in the superior sagittal sinus and transverse sinuses, while involvement of the deep veins and posterior fossa veins is much less common. The symptoms consist of varying degrees of signs of intracranial hypertension (ICH) and focal and/or epileptic signs. The onset may be sudden, subacute or chronic, simulating a cerebral vascular accident, an abscess, encephalitis, a tumour or benign ICH. Radiological investigations, especially MRI and angiography, are the key to the diagnosis. A fatal outcome is observed in 10% of non-infectious forms. The benefit of heparin therapy, although controversial for a long time, has now been clearly established.
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PMID:[Cerebral venous thromboses. Clinical diagnosis]. 817 75

Left pure motor hemiparesis occurred in a 42-year-old woman with a history of hypertension and diabetes mellitus. The left hemiparesis affected the arm and leg equally. The face was almost spared, with only a very slight facial asymmetry. Brain CT and MRI showed a small infarction located in the external 2/3 of the right cerebral peduncle. Cerebral angiography did not reveal significant abnormalities.
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PMID:[A case of cerebral pedunclar infarction presenting with pure motor hemiparesis]. 819 75

A 45 year-old patient presented with an epidermoid carcinoma of the tongue and cranial hypertension. MRI showed dural venous sinus occlusion, without infiltration or compression by a metastatic tumor. Anticoagulation led to recanalization of the occluded sinuses, as shown by the follow-up MRI, three months later. The pathophysiology of these rare paraneoplastic cerebral venous thrombosis is discussed.
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PMID:[Paraneoplastic cerebral venous thrombosis]. 823 31


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