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)

Lisinopril, a long-acting angiotensin-converting enzyme inhibitor, is excreted unchanged by the kidney. To determine how reduced renal function affects the drug's antihypertensive efficacy and safety, we studied 26 patients with hypertension associated with impaired renal function, having glomerular filtration rates (GFRs) of 60 ml/minute or less. These patients were enrolled in an open trial of 12 weeks' duration. They were given single daily doses of lisinopril, starting with 2.5 mg in patients with a GFR of less than 30 ml/minute, and 5 mg in the other patients. The dose was titrated to a maximum of 40 mg daily according to the blood pressure response. A diuretic was then added if required. Mean sitting and standing blood pressures at four, eight, and 12 weeks of treatment were significantly reduced compared with pretreatment values. The median dose of lisinopril was 10 mg daily (range, 2.5 to 40 mg), and only four patients required the addition of a diuretic. The mean GFR was unchanged during the study (36 +/- 16.4 ml/minute at baseline, 39 +/- 20.8 ml/minute after 12 weeks of treatment). Twenty-five patients completed the study. The one patient withdrew because of nausea and vomiting due to reflux esophagitis, which was probably not drug-related. Another patient had transient angioneurotic edema and continued to receive lisinopril. No clinically significant hematologic or biochemical abnormalities were observed. Sixteen patients continued to receive lisinopril for one year. Blood pressure control and GFR were well maintained throughout. Thus, in a group of patients who are often difficult to treat, lisinopril provided highly effective blood pressure control and was generally well tolerated.
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PMID:Lisinopril in the treatment of hypertensive patients with renal impairment. 284 84

Benign intracranial hypertension with papilloedema developed in a 18-year-old woman following Minocycline administration. Tetracycline therapy was prescribed for acne vulgaris. One month after the beginning of the treatment, she presented with headache, nausea and vomiting; there were no visual symptoms. Visual acuity and visual field were normal, fundus examination showed bilateral papilloedema. After Minocycline was discontinued and steroid therapy was administrated, symptoms rapidly resolved and papilloedema disappeared. Minocycline is known to penetrate into the central nervous system more effectively and to have a greater lipoid solubility than the other antibiotics of the same group. However the pathogenesis of benign intracranial hypertension after Minocycline therapy remains unknown.
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PMID:[Papilledema caused by minocycline: apropos of a case]. 297 95

Eighty-one cases with vestibular neuronitis were examined. The diagnostic criteria were a sudden onset of vertigo without previous symptoms, spontaneous nystagmus towards the healthy side, totally extinguished caloric responses with 44 degrees C and 30 degrees C water irrigation and no involvement of hearing associated with the onset of the disease. The series was divided into a prospective and a retrospective group. The prospective group A was examined at the acute stage, about 1 month and 1 year afterwards. The retrospective group B fulfilled the same criteria as group A and was examined 1-8 years after the acute stage. The results of the acute stage in group B were analysed from the case history reports, electronystagmo- and audiograms. The preceding and predisposing factors and symptoms were inquired. The examination scheme included the clinical otoneurological examination, the nystagmographic, audiological and clinical neurophysiological measurements and the serological and hematological specimens were collected at the acute stage of group A to examine the role of virus infections in the etiology of vestibular neuronitis. The liquor specimens of 16 cases available in group A were analysed. A recent respiratory infection was reported by 9 cases (27.3 percent) in group A and by 18 cases (37.5 percent) in group B. The serological evidence (increase of IgM-antibodies) was observed in 1 case against influenza A and in 1 case against parainfluenza 3 and the hematological examinations revealed clues of virus infection in 6 cases (18.2 percent) of group A. Cell counts and protein analyses of the liquor specimens were within normal limits. Cases with arterial hypertension under medical control were observed in 15.2 percent of group A and 14.6 percent in group B. These figures do not exceed the age- and sex-correlated prevalence of arterial hypertension in Finnish population. The clinical symptoms included an acute chiefly rotatory vertigo associated with nausea and vomiting without subjective involvement of hearing. The prominent symptoms lessened gradually during the first week and most of the patients were able to their earlier work after one month. The prognosis of the disease was good. The clinical otoneurological findings of the acute stage included spontaneous nystagmus with Frenzel's glasses and disturbances of the vestibulospinal tests. These abnormalities improved markedly during the follow-up period. The results of electronystagmography were characteristic of a pure peripheral vestibular disorder. Nystagmic beats were observed almost regularly in the pendular eye-tracking test at the acute stage examination.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vestibular neuronitis. An otoneurological evaluation. 306 52

15 patients aged between 24 and 66 years with 10 different malignant tumor diseases were treated with a recombinant human tumor necrosis factor preparation PAC-4D in a phase-I trial. The starting dose was 10(5) U PAC-4D as an intravenous short infusion. The maximally tolerable dose is around 18 X 10(5) U/m2. As the main clinical side effects were observed: fever, chills, hypertension with subsequent hypotension, lethargy, transient somnolence, headache, neurological deficiency symptoms, nausea and vomiting. Important laboratory-chemical parameters were the increase in transaminases and, in higher dose levels, leukocytosis with the left shift and lymphopenia in the differential blood picture. As dose-limiting toxicity are estimated hypotension, and neurological side effects and hepatotoxicity. In one female patient who received 27 X 10(5) U PAC-4D there appeared pronounced, histologically verified necroses in the metastases of a malignant fibrous histiocytoma.
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PMID:Human pharmacological investigation of a human recombinant tumor necrosis factor preparation (PAC-4D) a phase-I trial. 337 52

The clinical response and pharmacokinetics of intravenous urapidil were studied in patients with uncontrolled severe hypertension. Six of nine patients achieved a diastolic blood pressure (DBP) of 100 mm Hg after initial administration of serial bolus doses and were then placed on maintenance infusions. Three of these six patients maintained a DBP 100 mm Hg or lower at infusion rates of 10 to 20 mg/hr, whereas the remaining three patients experienced a loss of DBP control despite rates of 40 mg/hr. Mean DBP was significantly reduced from 126 +/- 6 mm Hg (N = 9) to 105 +/- 15 mm Hg after the bolus phase (N = 9, P less than .05) and 99 +/- 18 mm Hg after the infusion phase (N = 6, P less than .05). Significant reductions in systolic blood pressure were also achieved after bolus and infusion phases. Adverse reactions included drowsiness, tachycardia, nausea and vomiting but were considered mild. Estimated pharmacokinetic parameters included Vz (0.80 +/- 0.20 L/kg), CL (2.53 +/- 0.99 mL/min/kg) and t1/2 (4.0 +/- 1.5 hr). Urapidil safely reduces blood pressure in patients with severe hypertension. An alternative dosing regimen is suggested.
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PMID:Pharmacokinetics and pharmacodynamics of urapidil in severe hypertension. 339 39

Crisnatol is a novel lipophilic arylmethylaminopropanediol with significant antineoplastic activity in a variety of murine and human tumor models which functions as a DNA intercalator. In this Phase I trial, a 6-h infusion of the drug was administered i.v. in 700 to 1500 ml of 5% dextrose in water every 28 days. Eighty-five courses at doses of 7.5 to 516 mg/m2 were administered to 43 patients with refractory solid tumors. Reversible neurological toxicity was dose limiting at 516 mg/m2 and was manifested as somnolence, dizziness, blurred vision, unsteady gait, and alpha-slowing on electroencephalogram at the end of infusion. All neurological signs and symptoms were reversible. No hematological toxicity was observed. Other toxicities included phlebitis, mild to moderate nausea and vomiting, reversible sinus node arrest in one patient, and hypertension. Crisnatol plasma concentrations were determined by high-pressure liquid chromatography. After infusion, plasma concentrations declined biexponentially with a terminal t1/2 of 2.9 h. Using a two-compartment model, the mean apparent volume of distribution at steady state and total-body clearance were 58.8 liters/m2 and 18.3 liters/h/m2, respectively, indicative of extensive tissue distribution and rapid hepatic clearance. Peak plasma levels occurred at the end of infusion and correlated with the onset of neurological toxicity. The recommended Phase II dose for this schedule is 388 mg/m2.
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PMID:Phase I and clinical pharmacology trial of crisnatol (BWA770U mesylate) using a monthly single-dose schedule. 339 16

A phase I and pharmacokinetic study of recombinant tumor necrosis factor (rH-TNF Asahi) was carried out in 29 patients, who received a total of 72 courses with doses ranging from 1 to 48 X 10(4) units/m2. Drug was given as 1-h i.v. infusions. Acute toxicities, taking the form of fever, chills, tachycardia, hypertension, peripheral cyanosis, nausea and vomiting, headache, chest tightness, low back pain, diarrhea and shortness of breath were seen, but were not dose-limiting or dose-related. Some early rise in SGOT, without any change in serum bilirubin, was noted at the highest doses. Eosinophilia, monocytosis, mild hypocalcemia and an increase in fibrin degradation products were seen in a few patients. The dose-limiting toxicity was hypotension, which occurred after the end of the drug infusion and was seen in all 5 patients treated at the highest dose. There was no mortality or long-term morbidity. There were no responses. Pharmacokinetic studies indicated a rapid plasma clearance and a short plasma half-life, generally less than 0.5 h.
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PMID:Phase I clinical trial of recombinant human tumor necrosis factor. 366 33

It is well known that the case of multiple myeloma shows punched-out lesions of the cranium without intracranial hypertension. In this paper a case of multiple myeloma is reported showing intracranial hypertension due to a large tumor that developed in the left parietal bone. There are only 13 case reports about cranial mass lesion of multiple myeloma since 1928. A 52 year-old female was admitted to Iwate Prefectural Isawa Hospital suffering from headache, nausea and vomiting. She had been already diagnosed as multiple myeloma and treated with chemotherapy using Cyclophosphamide, Melphalan and Prednisolone for 2 years. On admission, a large subcutaneous mass was presented on the left parietal region. Craniogram revealed large osteolytic lesion of the left parietal bone and 3 punched-out lesions of the frontal bone. CT scan revealed a large mass lesion in the left epidural space, diploe and subcutaneous space. Angiography showed avascular area. Brain scintigram showed diffuse hot area. Other skeletal bones showed no abnormality. Laboratory examination revealed high concentration of gamma-globulin and high erythrocyte sedimentation rate. Electrophoresis showed high value of immunoglobulin G; immunoglobulin assay was as follows: IgG-6000 mg/dl, IgA-150 mg/dl, IgM-410 mg/dl, IgE-0 mg/dl. Serum electrolytes were within normal limits. Urine didn't include Bence-Jones protein. The patient was diagnosed as multiple myeloma suffering from intracranial hypertension caused by large tumor which developed in the left parietal bone. On the operation, large tumor was existed in the epidural and subcutaneous space invading into the diploe but without infiltration into the dura mater or cerebral cortex.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of multiple myeloma showing intracranial hypertension due to large cranial mass lesions]. 375 28

Five cases of spontaneous intracerebellar hemorrhage are reported. Three had a vascular malformation and two had mild hypertension. The presenting symptom was sudden headache followed by nausea and vomiting. Signs of brain stem dysfunction without prominent cerebellar deficit were the commonest feature. Meningeal involvement was present in the majority of cases. Unsuspected sudden death can occur. It is suggested that patients below the age of 30 who present with sudden headache followed by brain stem dysfunction with or without a subarachnoid hemorrhage, and patients over the age of 45 who present this picture along with subarachnoid hemorrhage should be investigated urgently with contrast studies for possible cerebellar hemorrhage.
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PMID:Observations in five cases of spontaneous cerebellar hemorrhage. 500 36

We evaluated electrocardiographically the acute effect of captopril in the initial treatment of malignant or severe hypertension and the findings were compared with the data obtained with diazoxide. The captopril group included seven patients treated with captopril or with a combination of diuretics. The diazoxide group included seven patients initially treated with diazoxide. A significant and similar degree of reduction in blood pressure was observed the second day after treatment in both groups. From 15 to 60 minutes after treatment, however, the reduction in mean blood pressure was more pronounced in the diazoxide group and was followed by a reflex tachycardia. In the diazoxide group, two patients went into shock and another three had nausea and vomiting, whereas in the captopril group there were no complications in any of the patients. In the captopril group ECG ST-T findings in leads V5 and V6 did not deteriorate, while in the diazoxide group there was a significant deterioration (p = 0.01). Thus captopril may be an effective and safe compound for the initial treatment of malignant or severe hypertension.
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PMID:Acute electrocardiographic effects of captopril in the initial treatment of malignant or severe hypertension. 634 20


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