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)

A total of 4676 patients and 1759 patients were treated with lisinopril and nifedipine respectively in a post-marketing surveillance study conducted in general practice in the UK. Patients were followed up for 12 months. Most of the lisinopril patients had hypertension, but a small number (180) had heart failure. Most of the nifedipine patients had uncomplicated hypertension, but some (22.57%) had other cardiovascular disease with or without hypertension. Lisinopril and nifedipine were equally effective in reducing blood pressure. During the study, 1.5% of hypertensive patients assigned to lisinopril died compared with 1.8% of patients assigned to nifedipine, and 15.1% of lisinopril patients compared with 19.7% of patients in the nifedipine group withdrew because of adverse events. Cough, malaise and fatigue, nausea and vomiting were more frequent causes of withdrawal from lisinopril than nifedipine. Conversely, headaches, pallor and flushing, oedema and palpitations caused more frequent withdrawals from nifedipine. Anaemia was more often encountered on nifedipine treatment than on lisinopril. In hypertensive patients, the frequency of first-dose hypotension was similar on both treatments. Serious events occurred in 0.8% and 0.5% of patients given lisinopril and nifedipine respectively. Lisinopril was well tolerated by heart failure patients: 16 patients (8.88%) died and an incidence of 4.44% of serious adverse events was reported, a pattern to be anticipated in such patients; dizziness, giddiness, dyspnoea, cough, nausea and vomiting were the most frequent causes of withdrawal; the incidence of first-dose hypotension was low (2.22%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Post-marketing surveillance of lisinopril in general practice in the UK. 811 50

Protoporphyria is a genetic disorder characterized by a defect in the enzyme ferrochelatase, which catalyzes the chelation of iron to protoporphyrin. This causes excessive accumulation and excretion of protoporphyrin. The predominant clinical feature is photosensitivity. Progressive and fatal liver disease occurs in a small percentage of cases. We report our experience with eight patients with end-stage protoporphyric liver disease in whom a syndrome developed before transplantation that resembled the neurological crises of the acute porphyrias. This syndrome was characterized by abdominal pain, hypertension, tachycardia, extremity pain and weakness, constipation and nausea and vomiting. Erythrocyte and serum protoporphyrin levels were markedly increased in all patients. In one patient, profound hemolysis developed during the anhepatic phase of transplantation and continued over a period of 72 hr, causing an extreme increase in the serum protoporphyrin level. Progressive weakness deteriorated to paralysis in this patient. This phenomenon suggests that protoporphyrin may gain access to neural tissue when serum levels are markedly increased, causing neurotoxicity.
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PMID:Evidence for neurological dysfunction in end-stage protoporphyric liver disease. 798 71

The advantages of pediatric out-patient surgery are: 1) greater psychological ease; 2) lower rate of infection; 3) less impact on patient habits, and 4) lower cost. Surgery must not involve organs, must have a low rate of complications, and be short. The preanesthetic interview should include clinical history and complementary examinations, information on anesthetic technique, perioperative recommendations and psychological preparation of parents and child. Detailed information reassures parents and improves collaboration; their presence during induction may be useful. At this time complete fasting is not recommended; although solids are not permitted, clear liquids should be taken up to 2-3 hours before anesthesia. In this way the child is less irritable and hypoglycemia and hypotension during inhalational induction are prevented. Low doses of midazolam and ketamine have been used for premedication, which though possibly useful, is not recommended because recovery may be prolonged. Halogenated anesthetics are very useful, with nitrous oxide providing an excellent complement. The potentially toxic effect of halothane on the liver does not keep this agent from being the most popular. Recovery is fast with any of the usual hypnotics (etomidate, propofol, thiopentone). Although thiopentone continues to be the hypnotic drug of reference, propofol's versatility is causing it to gain wider acceptance. The use of atracurium or vecuronium is justified if the dose is adjusted in keeping with type of surgery and duration. Intraoperative analgesics include meperidine, fentanyl and alfentanyl; morphine is not recommended. Should tracheal intubation be necessary, laryngeal edema may be avoided by gentle, cautious laryngoscopy, the use of a tube without a balloon, and 3 h of postanesthetic observation. A laryngeal mask may serve as an alternative to tracheal intubation. Local-regional anesthesia, excepting epidural and spinal anesthesia, offers a number of advantages: blockade of nociceptive stimuli, avoidance of opioid drugs, rapid and pleasant awakening (excellent for postoperative analgesia), and less need for postoperative analgesics. The postoperative complications seen most often are related to respiration or hypertension, making routine postanesthetic pulse oximetry a recommendation. The most frequently used analgesics are paracetamol, magnesium dipyrone, diclofenac, ketorolac, or codeine compounds. Although the incidence of nausea and vomiting is low in children, they are frequently a cause of hospitalization. Inappropriate postoperative care can increase the rate of admissions and medico-legal problems.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Ambulatory pediatric anesthesia: preanesthetic evaluation, anesthetic techniques, and immediate postoperative care]. 837 62

Mannitol is an osmotic diuretic used in acute oliguric renal failure, acute cerebral edema, and acute glaucoma. It is metabolically inert and is excreted through the kidneys. So once renal function is impaired, mannitol accumulates and the movement of water into the intravascular space with resultant cellular dehydration. Two patients suffered reversible acute oliguric renal failure following mannitol infusion given as treatment for intracranial hypertension. Both patients experienced nausea and vomiting and became increasingly lethargic with edema of general body. Congestive heart failure occurred. Laboratory data showed severe dilutional hyponatremia with hyperosmolality. We successfully treated them with extracorporeal ultrafiltration method (ECUM) and hemodialysis (HD). Some discussions were presented about acute renal failure following mannitol infusion.
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PMID:[Acute renal failure following mannitol infusion]. 837 73

Nineteen patients treated by continuous ambulatory peritoneal dialysis (CAPD) were studied according to clinical outcome parameters: insomnia, asthenia, pruritus, arterial hypertension, anorexia, nausea and/or vomiting, anemia, and rate of hospitalization. Using clinical scores, three groups were defined: poor clinical outcome (P), intermediate (I), and good (G). The quantity of treatment by PD was evaluated monthly with urea kinetic tests (weekly Kt/V, weekly urea clearance/1.73 m2 of body surface area (BSA), index of dialysis by Teehan), and with the weekly creatinine clearance/1.73 m2 of BSA. The metabolic index was analyzed: normalized protein catabolic rate (NPCR), serum albumin (Alb) and prealbumin, and reabsorption of glucose. There was good correlation between clinical scores and quantity of dialysis. The Alb was lower in group P. Group G was differentiated from group I and from group P by quantification tests and NPCR, with lower levels as follows: weekly Kt/V = 2.06, urea clearance 70 L/week/1.73 m2, index of dialysis = 0.87, and creatinine clearance = 60 L/week/1.73 m2. We conclude that the qualitative clinical approach is not sufficient to predict deleterious signs, and the quantitative approach is predictive of the good clinical outcome and good nutritional status. We think that levels proposed to now are insufficient, and we suggest the following: weekly urea clearance > 70 L, weekly Kt/V > 2, weekly creatinine clearance > 60 L, and index of dialysis > 0.85.
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PMID:Quantification of adequacy of peritoneal dialysis. 839 69

Sumatriptan is a potent and selective agonist at the vascular 5HT1 receptor which mediates constriction of certain large cranial blood vessels and/or inhibits the release of vasoactive neuropeptides from perivascular trigeminal axons in the dura mater following activation of the trigeminovascular system. The mode of action of this drug in migraine and cluster headache is discussed. On the basis of a detailed review of all published trials and available data from post-marketing studies, the efficacy, safety, tolerability and the place of oral and subcutaneous sumatriptan in the treatment of both conditions are assessed. A number of double-blind clinical trials have demonstrated that sumatriptan 100 mg administered orally is clearly superior to placebo in the acute treatment of migraine headache and achieves significantly greater response rates than ergotamine or aspirin. In other studies, 70 to 80% of patients receiving sumatriptan 6 mg sc experienced relief of migraine headaches by 1 or 2 h after administration, and patients consistently required less rescue medication for unresolved symptoms. Sumatriptan was also effective in relieving associated migraine symptoms like nausea and vomiting. Sumatriptan was equally effective regardless of migraine type or duration of migraine symptoms. Overall, approximately 40% of patients who initially responded to oral or subcutaneous sumatriptan experienced recurrence of their headache usually within 24 h, effectively treated by a further dose of this drug. In 75% of patients with cluster headache treated with sumatriptan 6 mg sc, relief was achieved within 15 min. Based on pooled study data, sumatriptan is generally well tolerated and most adverse events are transient. Adverse events following oral administration include nausea, vomiting, malaise, fatigue and dizziness. With the subcutaneous injection, injection site reactions occur in approximately 30%. Chest syumptoms are reported in 3 to 5% but have been associated with myocardial ischaemia only in rare isolated cases. The recommended dosage of sumatriptan at the onset of migraine symptoms is 100 mg orally or 6 mg subcutaneously. The recommended dosage for cluster headache is 6 mg sumatriptan sc. Sumatriptan must not be given together with vasoconstrictive substances, e.g., ergotamines, or with migraine prophylactics with similar properties, e.g., methysergide. Sumatriptan should not be given during the migraine aura. It is contraindicated in patients with ischaemic heart disease, previous myocardial infarction, Prinzmetal (variant) angina and uncontrolled hypertension.
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PMID:Migraine and cluster headache--their management with sumatriptan: a critical review of the current clinical experience. 853 93

The early detection of HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) is the basic condition for immediate therapeutic management, which mainly leads to prompt delivery. The classical symptoms despite the typical laboratory evaluation (hemolysis, elevated liver enzymes, low platelets) are epigastric or right upper quadrant pain and nausea and vomiting; the classical signs of preeclampsia (proteinuria and hypertension) may be absent in 20%. The differential diagnostic problems of HELLP syndrome arise in relation to the mimicry-symptomatic: upper abdomen pain can imitate gastroenterologic diseases (e.g. cholelithiasis, appendicitis), the elevated liver enzymes combined with hyperbilirubinemia liver diseases (e.g. viral hepatitis) and thrombocytopenia in combination with hemolytic anemia, neurological symptoms and renal failure other similar pathogenetic disorders due to the category of thrombotic microangiopathies. Regarding the common symptoms thrombocytopenia, hemolysis as well as signs of preeclampsia with or without renal failure the differentiation from various autoimmune diseases also can be difficult in special cases. Rare first manifestations and serious simultaneous diseases which can overlay the typical signs of HELLP syndrome show the variety of HELLP syndrome. Interdisciplinary detours and delay are the consequences of this differential diagnostic problems, which could imply deleterious effects on the mother and the fetus, until the final diagnosis is clear. Therefore all pregnant women with upper abdomen pain irrespective of symptoms of preeclampsia should be considered to have HELLP syndrome and immediate laboratory evaluation has to be done. If there is any doubt a interdisciplinary consultation is required!
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PMID:[Differential HELLP syndrome diagnosis]. 896 90

One hundred and two cases of HELLP Syndrome admitted at the Adults Intensive Care Unit since January 1992, to June 1994; 63 with severe preeclampsia, 26 eclamptics and 13 with chronic hypertension more preeclampsia-eclampsia were analysed. The mean age was 24 year (range, 15 to 42). All 102 of the patients had one or more symptoms, those more often were: headache (85), right upper-quadrant tenderness (61), nausea and/or vomiting (31). The diastolic blood pressure maximum before the admission was 100 mm Hg or less in patients and 46 had more than 110 mm Hg. The mean platelets count was 58000 (range, 17000 to 100000). The median of laboratory test were: lactic dehydrogenase (830 u/l), glutamic oxaloacetic transaminase (278 u/l), glutamic pyruvic transaminase (263 u/l), total bilirubin (3.3 mg/dl). There were complications in 37 patients; acute renal failure 20, disseminated intravascular coagulopathy in 11, cerebral hemorrhage in 10 and abruption placentae in 6 patients. During the study period there were 20 death due to preeclampsia-eclampsia and 14 were in patients with HELLP syndrome, cerebral hemorrhage was the main cause (70%). In the group study 11 intrauterine deaths were diagnosed.
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PMID:[HELLP syndrome. Analysis of 102 cases]. 901 34

One of the complications of steroid therapy is the hypothalamic-pituitary-adrenal (HPA) axis' suppression, particularly in children where this can lead to growth suppression and other well known complications. Although there are a large number of studies on suppression of the HPA axis with the use of topical steroids, the subject is still controversial. We measured the HPA axis function in 3 groups of allergic children treated with: 1) intranasal beclomethasone dipropionate (BDP) 400 micrograms/day for 4 weeks or 2) BDP 800 micrograms/day for 4 weeks and 3) oral prednisone, 1 mg/kg/day for 2 weeks. The HPA response was obtained after lysine-vasopressin (LVP) stimulation. LVP acts on the pituitary or hypothalamus level, stimulating the whole axis. Peripheral blood samples through an intravenous line were obtained for serum cortisol measurement at zero, 30, 60, and 90 minutes after the intravenous injection of LVP, before and after the treatment period. Our results showed no suppression of the HPA axis in children medicated with BDP at either 400 micrograms/day or 800 micrograms/day. On the other hand, there was a suppression of the HPA axis after prednisone treatment (p < 0.05). During the LVP test some side effects, possibly due to systemic vasoconstriction, were noted such as abdominal pain, nausea and vomiting, and transient hypertension. In conclusion, intranasal BDP at the dose of 400 or 800 micrograms/day during 4 weeks did not induce HPA axis suppression. The LVP test is efficient to demonstrate HPA hypofunction or suppression and it produced only mild to moderate transient side effects. However, due to the side effects observed, a safer test such as urinary free cortisol (24 hours), should be used in the investigation of the HPA axis.
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PMID:Lysine-vasopressin in the evaluation of the hypothalamic-pituitary-adrenal axis in children with allergic rhinitis treated with intranasal beclomethasone dipropionate or oral prednisone. 909 35

Nitrates, which have been used for more than a century, are the second oldest drug (after digitalis alkaloids) in the cardiological pharmacological arsenal. However, several facets of their mode of use still remain controversial. Their vasodilator and arteriolodilator action (especially in coronary vessels) and their platelet aggregation inhibitory effect make them useful drugs, particularly in all clinical forms of ischaemic heart disease (unstable or stable angina and acute myocardial infarction), for the prevention or treatment of ischaemic episodes (silent or not) and also in heart failure where nitrates are useful not only as symptomatic treatment (alone or associated with diuretics), but also in view of their positive effect on survival (associated with hydralazine: V-Heft I trial). At the present time, nitrates can be administered via the sublingual, oral, intravenous of transdermal routes in the form of nitroglycerin and isosorbide dinitrate or mononitrate (short-acting and sustained-effect forms). Their rare contraindications concern patients suffering from severe hypotension (< 70 mmHg), severe anaemia, glaucoma or intracranial hypertension. The most serious adverse effects are pulsatile headache (which usually disappear after several days), postural hypotension (possibly causing fainting), facial erythema, vertigo, palpitations or nausea and vomiting. Most of these adverse effects can be controlled by dosage adaptation and it is rarely necessary to stop treatment. However, the major problem raised by the use of nitrates concerns the development of a tolerance. The pathophysiology of this multifactorial phenomenon is still unclear. The protagonist role played by loss of SH groups or activation of humoral feedback mechanisms, with an increase of circulating catecholamine levels, activation of the R-A-A system and increased plasma volume, has been postulated. This complication can be avoided by prescribing intermittent treatment, with a drug-free interval of 10-12 hours per day. A single dose of a sustained-release preparation (60 mg of isosorbide dinitrate or 40 to 60 mg of isosorbide mononitrate), or 2 or 3 doses of a short-acting preparation (20-40 mg of isosorbide mononitrate) can be prescribed via the oral route. When the transdermal route is used, the patch should be left in place for 12 hours. Treatment should be started at low doses, which are then gradually increased. The free period is usually at night, which can be covered, when necessary, by other antiischaemic drugs (for example, beta-blockers and/or calcium channel blockers), already usually used in combination with nitrates. This interruption is not accompanied by a rebound phenomenon. It must be remembered that nitrates potentiate the action of other vasodilators and calcium channel blockers and that, in some patients, intravenous nitroglycerin reduces the anticoagulant effect of heparin, while indomethacin can inhibit their vasodilator effect. Nitrates are therefore in very good health despite their advanced age and, when used correctly, they continue to be very useful in the pharmacological treatment of cardiovascular diseases.
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PMID:[Principles and rules of the use of nitrates]. 945 73


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