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)

The case report of a 27-year-old woman who had been normotensive before her 1st pregnancy 6 years earlier is presented. At 2 months postdelivery she began taking estro-progesterone. She was given Enidrel R (norethynodrel 4.925 mg, mestranol .075 mg) for 18 months and then Ovariostat (lynestrenol 2.5 mg, mestranol .075 mg). Her blood pressure was not recorded until 2 years later when it was 180 mm Hg systolic. Contraceptive therapy was then stopped. A month later pregnancy occurred. At that time her blood pressure was 120 mm Hg. The delivery was normal. 4 months later she began taking Ovariostat again. Headaches soon developed and her blood pressure was found to be 270/150 mm Hg. On admission to the hospital 3 weeks later her blood pressure was 250/100 mm Hg. Renal failure was present. Creatinine clearance was 12 ml/minute. No cause for this hypertension was found. 1 month later hypertension was 210/160 mm Ha. Retinal hemorrhaging had lessened but azotemia persisted. Heart failure and oliguria followed. Dialysis was done weekly. A bilateral nephrectomy was done. Microscopic study of renal tissue showed malignant nephroangiosclerosis. After 10 days her blood pressure was 150/100 mm Hg. Her general condition improved. A salt-free diet was prescribed. Blood pressure subsided to 140/80 mm Hg before dialysis. A renal graft was done and 10 months later blood pressure was normal. These hypertensions are usually benign and subside when the contraceptive therapy is discontinued. When estrogen-progesterones are prescribed, blood pressures should be recorded frequently and therapy stopped if hypertension arises.
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PMID:Malignant hypertension with irreversible renal failure due to oral contraceptives. 119 51

The demonstration that long-term administration of relatively low doses of clonidine decreased the responsiveness of blood vessels to vasodilator and vasoconstrictor drugs in animals led to its investigation in the prevention of migraine in man. Results of placebo-controlled and open therapeutic trials have shown that clonidine in low dosages (75 to 150 mug daily) is useful in preventing migraine headaches in about 30%-50% of patients. A 50% or greater reduction in headache frequency or headache indices has been reported in 40% of patients in controlled and open studies. Thus clonidine, like other drugs used in the interval therapy of migraine, can be expected to be effective in only a proportion of patients. Although clonidine has not been compared directly with other drugs used in the prophylactic treatment of migraine, the general clinical impression is that it is less effective then pizotifen or methysergide. Because it is relatively well tolerated at dosages of 75 to 150 mug daily it is worthy of a trial, particularly in patients considered to need prophylactic migraine therapy for the first time, and when migraine occurs in association with hypertension. At the dosages used in migraine prophylaxis, which are almost invariably lower than used in hypertension, clonidine does not cause hypotension and can be used in patients with cardiovascular disease. The principal side-effects are drowsiness and dry mouth which tend to diminish as treatment continues.
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PMID:Low-dose clonidine: a review of its therapeutic efficacy in migraine prophylaxis. 120 7

PR-G-138-C1, a new antihypertensive agent with vasodilating properties, was studied in ten patients with moderate to severe hypertension. The patients were admitted to a metabolic ward and followed on a 2 gm salt diet. Placebo was given daily until blood pressure and weight were stabilized. A dose titration was then started with increasing single daily doses of 3, 5, 8, and 10 mg of PR-G-138-C1 orally. The dose at which the mean arterial pressure was reduced by 15 mm Hg was continued for a total of seven days. PR-G-138-C1 lowered sitting mean arterial pressures significantly in all subjects (133.8+/-15.1 leads to 116.0+/-12.4 mm Hg, p less than 0.001). The antihypertensive effect was first noted 30 minutes following drug administration and persisted for as long as six hours with a peak effect at one hour. All patients had a significant increase in sitting pulse rate (80.4+/-9.11 leads to 90.0+/-6.91/min, p less than 0.002). Blood pressure reduction and increase in pulse rate were dose related. The most common side effects noted were headaches in eight out of ten patients and postural dizziness in seven out of ten patients. There were no signs of fluid retention (weight gain or edema). Electrocardiogram and other laboratory parameters remained essentially unchanged.
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PMID:Initial clinical experience with a new peripheral vasodilator, PR-G-138-Cl, in hypertensive patients. 123 41

Since Fincher reported a case with arteriovenous fistula between the external carotid artery and dural sinus, many type of cases have been reported. On the other hand, so called the external carotid avernous fistula has been recognized less 20 cases in literature. We have observed three additional cases of dural arteriovenous shunts in the region of the cavernous sinus. Case 1. A 52 year old woman had suffered from left side sever headache. There was weakness of the left extraocular muscles and left ptosis. A bruit was heard over the left orbit. She was treated for hypertension since 38 year old. And she has no history of recent trauma. Selective internal and external carotid angiographies showed the bilateral external carotid cavernous sinus fistula. No operative treatment was performed in this case and the symptomes disappeared with decrease of blood pressure. Case 2. A 50 year old man came to this clinic with chief complaints of right ptosis, diplopia and headache. He was treated for diabetes mellitus and hypertension for six month...
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PMID:[Three cases of spontaneous bilateral external carotid-cavernous sinus fistula (dural arteriovenous shunts in the region of the cavernous sinus) (author's transl)]. 123 13

The hematomas occupied between the inner surface of skull and brain surface are well known and the majority of these intracranial hematomas are elicited by head injury. On the other hand, the intracerebral hematomas formed in the brain tissue are produced by the various causative diseases and the majority of these cause are cerebrovascular disease. The causative diseases of intracerebral hematomas were cerebrovascular diseases like hypertension, intracranial aneurysm and cerebral arteriovenous malformation in 65.7% and head injury in 32.4%. The cause of two cases were bleeding from asymptomatic brain tumors and formation of intracerebral hematoma produced initial clinical symptom of these cases. Age distribution of intracerebral hematoma has peculiarity in each causative disease. Hypertensive intracerebral hematomas occurred in patients over 30 years old and intracerebral hematoma due to bleeding from cerebral arteriovenous malformation was not observed in patient over 50 years old. The frequency of consciousness change as initial symptom of traumatic intracerebral hematome, hypertensive intracerebral hematome, intracerebral hematoma caused by bleeding from cerebral arteriovenous malformation and bleeding from intracranial aneurysm and spontane intracerebral hematome are 79.4%, 57.1%, 57.1%, 40.0% and 25.0% respectively. Headache as initial symptom are conspicuous in patients of intracerebral hematoma caused by bleeding from intracranial aneurysm and arteriovenous malformation, and each frequency were 86.7% and 71.4%. The frequency of motor disturbance as initial symptom was highest in patients of hypertensive intracerebral hematoma and its frequency was 50.0%. Clinical symptoms observed at admission were as follows: Consciousness change in patients of hypertensive intracerebral hematoma and traumatic intracerebral hematoma were 100% but in patients of cerebral arteriovenous malformation and intracranial aneurysm were 64.3% and 60.0%. Consciousness change in patients of spontane intracerebral hematoma were only 50.0%. Motor disturbance as clinical symptom were 85.0% in hypertensive intracerebral hematoma and this frequency was highest in all causative diseases. The frequency of coincidence between the side of dilated pupil under anisocoria and the side of hematoma was less than 50.0% in average and this frequency was marked lower by compared with the frequency in patients of hematome formed between the skull and brain surface.
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PMID:[On the intracerebral hematoma --clinical analysis of 105 operated cases-- (author's transl)]. 124 Aug 45

The side effects of using estrogen treatments to relieve menopausal symptoms in women are presented. Estrogens are effective in relieving headaches, vertigo, palpitations, and nervous symptoms such as depression, as well as degeneration and atrophy of the genital organs. In Norway, 2.5% of women over 45 as compared with 50% in the U.S. use estrogens to relieve menopausal symptoms. The incidence of endometrial cancer has risen from 9.2/100,000 in 1955 to 15.4 in 1974. Increased susceptibility to endometrial cancer has been linked to long-term use of estrogens, obesity, hypertension, diabetes, and nulliparity. In American studies, Premarin has been associated with increased risk of cancer related to the chemical equilinine, which has a long half-life. After menopause, the need for estrogen is met by the conversion of androstenedione, which is produced by the adrenal gland. When estrogens are taken, it may result in an overstimulation of the endometrium, which could cause cancer. Estrogens have bene found useful and safe for short-term relief of menopausal symptoms, and any patient using estrogens should be under routine observation to prevent development of cancer.
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PMID:[From the Adverse Drug Reaction Committee. Can long-term estrogen treatment induce uterine neoplasms in post-climacteric women?]. 125 36

In a series of 27 patients with proved pheochromocytoma, differential analysis of catecholamines in blood, urine, and tumor specimens of 19 patients enabled grouping of subjects into those whose tumors produced predominantly norepinephrine (NE) (11 patients), predominantly epinephrine (E [Two patients]) and approximately equal amounts of both (six patients). Sustained hypertension was more common in the first group and pallor and tremor in the latter two groups, but no distinctive syndrome could be recognized as signifying the secretion of NE or E. Headache was a symptom in 20 of 27 patients and was related to sudden, transient elevation of the blood pressure, rather than sustained hypertension. The variable duration and intensity of the headache in different patients can be explained by the pressor and cranial vasoconstrictor effects of the secreted amines, which respectively enhance and diminish vascular headache.
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PMID:Symptoms of pheochromocytoma, with particular reference to headache, correlated with catecholamine production. 125 42

At their first visit to a hospital clinic 178 patients referred with a diagnosis of hypertension were given a self-administered questionnaire. They received a similar questionnaire 12 months later. Of the 178 patients 99 were not initially on treatment. Similarly 78 normotensive subjects were drawn randomly from the local population and sent a second questionnaire 10 months later. The symptoms at the first visit of the normotensive controls, the untreated hypertensive patients, and 477 patients on long-term treatment in the hypertension clinic were compared. Treated and untreated hypertensive patients complained more of nocturia and also of unsteadiness either on standing or in the morning. Treated hypertensives complained more of sleepiness, dry mouth, diarrhoea, and, in men, impotence and failure of ejaculation. Similarly, untreated hypertensives complained of excessive depression, blurred vision, and waking headache. Fifty-five of the normotensive subjects and 110 of the newly referred hypertensive patients responded to the second questionnaire. The proportions losing and gaining symptoms were calculated together with the proportions always complaining and never complaining of a symptom. Hypertensive patients tended to lose the complaints of unsteadiness and headache but to gain the symptoms of vivid dreams, a slow walking pace, and diarrhoea. The net improvement for a symptom was defined as the excess of patients who lost a symptom over those who gained the symptom, expressed as a percentage. Over the follow-up period the control subjects had a net improvement averaged over 14 symptoms of +2-4 per cent. A similar result was obtained for the hypertensive patients of +2-0 per cent, the symptoms lost being balanced by those gained. The changes in symptoms with time were related to the changes in blood pressure and it is suggested that only headache, 'unsteadiness, lightheadedness, or faintness' and nocturia can actually result from raised blood pressure and then only in a proportion of patients complaining of these symptoms.
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PMID:Change in symptoms of hypertensive patients after referral to hospital clinic. 125 26

An analysis of 100 observations permitted the authors to conclude that the basis of the clinical picture of acute epidural hematoma was the syndrome of intercranial hypertension manifesting itself in growing disturbances of consciousness, headaches, vomiting, bradycardia. The appearance of local neurological symptoms gives a possibility for a physician to orientate quickly in the pathological process localization. "A lucid period" and the initial syndrome of the acute brain dislocation often revealed in the manifestation of mydriase are typical of the clinical picture of epidural hematoma.
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PMID:[The clinical picture of acute epidural hematoma of traumatic origin]. 126 98

In a 31-year old woman with a six year history of headache and hypertension a diagnosis of primary aldosteronism was made on the basis of urine samples containing 45 mug/day of aldosterone. The preoperative systemic blood pressure was 240 mm Hg systolic and 120 mm Hg diastolic. The serum potassium level was 2.6 mEq/L and other laboratory findings were within normal limits. The patient was to undergo operation. Pre-medication consisted of oral pentobarbitone, intramuscular pethidine and atropine. For induction of anaesthesia, enflurane 2.0-2.5% maximum was given with O2 (21/min) and N2O (61/min); no intravenous agents were used. Suxamethonium chloride 40 mg was administered to facilitate endotracheal intubation. Anaesthesia was maintained with enflurane 1.5-2.0% with 50% N2O and O2. Tubocurarine 27 mg was given for muscle relaxation. When the tumour was manipulated, systemic arterial blood pressure was elevated again to 190 mm Hg systolic and 120 mm Hg diastolic. After removal of the tumour, the arterial pressure and heart rate were stable and recovery from anaesthesia was without circulatory or respiratory complications. Plasma aldosterone levels reached a maximum when the tumour was manipulated and fell to normal levels on the second post-operative day. Cortisol levels were not altered markedly even when the tumour was handled. These data imply that adrenocortical response to enflurane anaesthesia as jadged by plasma aldosterone levels would be different from that as estimated by plasma cortisol levels.
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PMID:Enflurane anaesthesia for removal of aldosterone producing adenoma. 126 18


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