UMLS:C0020538 - FACTA Search

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170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 41-year old primigravida underwent caesarean section because of foetal distress following prostin induction of labour. Intraoperative coagulopathy, haemorrhage and hypotension necessitated a hysterectomy. Subsequently, she developed respiratory and renal failure, requiring mechanical ventilation and haemodialysis. She made a full recovery. The likely diagnosis was amniotic fluid embolism (AFE), a rare complication of pregnancy with a variable presentation, ranging from cardiac arrest and death through to mild degrees of organ system dysfunction with or without coagulopathy. The differential diagnosis includes pre-eclamptic toxaemia/pregnancy-induced hypertension, anaphylaxis and pulmonary embolism. There is no diagnostic test for AFE; the finding of foetal elements in the maternal circulation is non-specific. Historically, AFE was thought to induce cardiovascular collapse by mechanical obstruction of the pulmonary circulation. It is now thought that a combination of left ventricular dysfunction and acute lung injury occur, with activation of several of the clotting factors. An immunological basis for these effects is postulated. There is no specific therapy and treatment is supportive. The mortality of the condition remains high.
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PMID:Amniotic fluid embolism: a case report and review. 1069 74

Most solid malignancies display interstitial hypertension and a poor uptake of anticancer drugs. Platelet-derived growth factor (PDGF) and the cognate tyrosine kinase receptors are expressed in many tumors. Signaling through PDGFbeta receptors was shown recently to increase interstitial fluid pressure (IFP) in dermis after anaphylaxis-induced lowering of IFP. In this study, we show that treatment with the selective PDGF receptor kinase inhibitor, STI571, formerly known as CGP57148B, decreased the interstitial hypertension and increased capillary-to-interstitium transport of 51Cr-EDTA in s.c. growing rat PROb colonic carcinomas. Furthermore, treatment with an antagonistic PDGF-B oligonucleotide aptamer decreased interstitial hypertension in these tumors. PDGFbeta receptors were expressed in blood vessels and stromal cells but not in the tumor cells of PROb colonic carcinomas. Our study indicates a previously unrecognized role of PDGF receptors in tumor biology, although similar effects of PDGF on IFP have been demonstrated previously in the dermis. The data suggest interference with PDGF receptors, or their ligands, as a novel strategy to increase drug uptake and therapeutic effectiveness of cancer chemotherapy.
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PMID:Inhibition of platelet-derived growth factor receptors reduces interstitial hypertension and increases transcapillary transport in tumors. 1130 70

Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells. Catalysis along the cell surface requires zinc-dependent binding of factor XII and high-molecular-weight kininogen to proteins, such as the receptor for the globular heads of the C1q subcomponent of complement, cytokeratin 1, and urokinase plasminogen activator receptor. These 3 proteins complex together within the cell membrane, and initiation depends on autoactivation of factor XII on binding to gC1qR (the receptor for the globular heads of the C1q subcomponent of complement). There is also a factor XII-independent bypass mechanism requiring a cell-derived cofactor or protease that activates prekallikrein. Bradykinin is degraded by carboxypeptidase N and angiotensin-converting enzyme. Angioedema that is bradykinin dependent results from hereditary or acquired C1 inhibitor deficiencies or use of angiotensin-converting enzyme inhibitors to treat hypertension, heart failure, diabetes, or scleroderma. The role for bradykinin in allergic rhinitis, asthma, and anaphylaxis is to contribute to tissue hyperresponsiveness, local inflammation, and hypotension. Activation of the plasma cascade occurs as a result of heparin release and endothelial-cell activation and as a secondary event caused by other pathways of inflammation.
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PMID:Pathways for bradykinin formation and inflammatory disease. 1184 87

The purpose of this study was to describe the perceptions of nurse anesthesia students (NAS) who used a MedSim simulator (MedSim USA, Inc, Ft Lauderdale, Fla) as part of their educational training. A convenience sample of 12 NAS in their first year of clinical training was researched. The researcher analyzed data qualitatively from observations made during 4 different sessions. Session 1 introduced the students to the simulator. Session 2 involved each student performing an anesthetic induction. A minor incident such as hypotension, hypertension, bradycardia or tachycardia occurred in session 3, and a major incident such as cardiac ischemia, anaphylaxis, bronchospasm, or malignant hyperthermia occurred in session 4. Data collection involved observation by the primary investigator, journal entries by the anesthesia students, and focus group interviews with the students. Results of the study indicate that, although students experience feelings of apprehension, uneasiness, or fear during the sessions, they felt it was very educational. Disadvantages include the lack of reality, lack of knowledge on handling crisis events, possibility of fixation errors, and the presence of anxiety. Advantages include improved critical thinking and decision-making skills, increased confidence, and improved clinical preparation. Results can be used to assist instructors in improving the students' learning experiences and to teach more effectively.
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PMID:Nurse anesthesia students' perceptions of the anesthesia patient simulator: a qualitative study. 1207 70

This article reviews the clinical pharmacology, adverse events, and comparative tolerability of the drugs commonly available for treating ulcerative colitis. Synthetic glucocorticoids are the most commonly used conventional corticosteroids in the treatment of ulcerative colitis. Corticosteroids can be expected to impact on every organ system and most metabolic activities of the body. Suppression of the hypothalamic-pituitary-adrenal axis is common, but reversible, with conventional corticosteroids, but not with newer topically-acting corticosteroids. A serious complication of corticosteroids in children is growth retardation. The frequent adverse effects associated with the use of corticosteroids have prompted the development of a new group of rectal agents with equivalent efficacy and a more benign adverse event profile such as prednisolone metasulfobenzoate, fluticasone propionate, tixocortol pivalate, beclomethasone dipropionate and budesonide. The incidence of adverse effects related to the use of sulfasalazine (5-aminosalicylic acid plus sulfapyridine) is high and is dose related. The most frequently reported adverse effect is intolerance, not allergy, and relates to the sulfapyridine moiety correlating with the acetylator phenotype. Tolerance to 5-aminosalicylic acid by 80 to 90% of those patients allergic to, or intolerant of, sulfasalazine has given further evidence suggesting that the sulfa moiety is responsible for much of the toxicity of sulfasalazine. However, 10 to 20% of patients who are sulfasalazine intolerant have similar reactions to 5-aminosalicylic acid formulations, indicating that the 5-aminosalicylic acid moiety is responsible for adverse events in some patients taking sulfasalazine. Adverse effects resulting from treatment with azathioprine and mercaptopurine can be divided into two categories: allergic-type reactions that appear to be dose-independent and nonallergic-type reactions that are probably dose- and metabolism-dependent. It is well established now that genotype and thiopurine methyltransferase activity have an important impact on the rate of adverse effects during azathioprine or mercaptopurine therapy. Adverse effects resulting from high dose cyclosporin therapy for inflammatory bowel disease include: renal insufficiency, hypertension, opportunistic infections, seizures, paresthesias, tremor, headache, gingival hyperplasia, hypertrichosis, and anaphylaxis with intravenous cyclosporin. In contrast, the incidence of adverse events was relatively low when low-dose oral cyclosporin was used. The incidence of adverse events associated with any of the medications used in the treatment of ulcerative colitis is difficult to assess and it is therefore hard to make a comparative evaluation. The broadening of the drug regimen available to the clinician has advanced our knowledge about the disease, and further development of more effective, less toxic agents can be anticipated in the future.
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PMID:Comparative tolerability of therapies for ulcerative colitis. 1211 42

A 35-years old gravida IV and para II underwent caesarean section because of fetal distress following induction of labour. During operation the patient developed disseminated intravascular coagulation (DIC), severe haemorrhage and shock necessitating massive blood transfusion,hysterectomy with pelvic packing, and high-dose catecholamines. Ultimately, recombinant factor VIIa was given to control bleeding. During the first 24 hours after operation, both clinical and laboratory findings showed that the severe DIC was on the course to recovery.However, the patient subsequently developed multiple organ dysfunction syndrome with respiratory and renal failure requiring mechanical ventilation and haemodialysis.All therapeutical efforts could not help that the patient passed away due to an inevitable multiple organ failure on the 12th day after the operation. Given the constellation of diagnostic and clinical findings, the most likely diagnosis was amniotic fluid embolism (AFE), a rare complication of pregnancy. The following differential diagnoses were less likely or excluded in this reported patient: pre-eclampsia/pregnancy-induced hypertension,HELLP syndrome,anaphylaxis,uterine rupture, transfusion reactions,pulmonary embolism. AFE occurs rarely, and because studies in animal models cannot reproduce accurately the pathophysiological and clinical alterations seen in humans, its pathogenesis remains unclear. It has been proposed that the clinical syndrome of AFE occurs when fetal antigens pass the maternal immunological barrier in susceptible mothers. The recognition of fetal antigens by maternal immune system subsequently triggers the release of endogenous mediators that are responsible for dramatic pathophysiological disturbances.Furthermore, the components of amniotic fluid initiate the DIC. These events are more consistent with septic shock and anaphylactic shock than with an embolic process and it was proposed that the term "amniotic fluid embolism" be changed to "anaphylactoid syndrome of pregnancy". At present, no therapy has been found to consistently improve outcomes in women with AFE.Patients who survive the initial insult are at high risk for multiple organ failure. The mortality of AFE remains high.
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PMID:[Pathophysiological and therapeutic aspects of amniotic fluid embolism (anaphylactoid syndrome of pregnancy): case report with lethal outcome and overview]. 1275 Aug 26

Angiotensin II converting enzyme inhibitors (ACE) and angiotensin II receptor blockers (ARB) are frequently avoided as treatment for hypertension in the early posttransplant period (0 to 90 days) for fear of nephrotoxicity. The following retrospective study was designed to explore the safety of these drugs in the early posttransplant period and determine appropriate clinical criteria for starting these medications. The records of all adult renal transplants performed between January 1997 and December 2000 (N = 290) were reviewed. All patients started on ACE or ARB for treatment of hypertension within 90 days of their transplant were included in the analysis (n = 17). Controls (n = 19) were patients who were treated with a calcium channel blocker (CCB) for hypertension. Cases and controls were matched for gender and type of transplant, living or cadaver. Patients were considered to be enrolled whey they met the following criteria: hypertension, serum creatinine < or =3.0 mg/dL, or falling 1 mg/dL/d and serum potassium < or =5.5 mEq/L. Exclusion criteria were coexistent pancreas transplant, anaphylaxis to ACE, and use of ACE or ARB for treatment of posttransplant erythrocytosis. There were no differences between cases and controls in hemoglobin or serum potassium concentrations or calculated glomerular filtration rate at 3, 6, and 9 months. In renal transplant patients with reasonable allograft function, administration of ACE and ARB to treat hypertension in the early posttransplant period appears to be well tolerated and not associated with excess hyperkalemia, anemia, or acute renal dysfunction.
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PMID:Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers used for the treatment of hypertension appear to be safe in the early posttransplant period. 1562 Nov 21

Dermatologists use a variety of systemic drugs, some of which can cause severe adverse reactions and even fatalities. Ivermectin, a well-tolerated drug, can cause severe neurological side effects, whereas metronidazole, in high cumulative doses, has been associated with convulsions and rarely with hepatotoxicity. Dapsone is associated with frequent hematologic side effects, such as methemoglobinemia, hemolysis, and anemia. Although hepatotoxicity is rare and usually mild and reversible with the new antifungal agents, severe cutaneous reactions (such as toxic epidermal necrolysis, Stevens-Johnson syndrome, and anaphylaxis) have been reported. Even a relatively safe drug such as acyclovir has been reported to be the cause of renal failure and neurotoxicity. Retinoids can cause not so benign "benign" intracranial hypertension. Methotrexate can cause not only liver toxicity, but also myelosuppression and pancytopenia, which may be acute and life threatening. Nephrotoxicity is a well-recognized side effect of cyclosporine, whereas thrombotic thrombocytopenic purpura, which is associated with high morbidity and mortality, is less well known. Dermatologists should be familiar with these and other severe adverse reactions of the most popular and most used systemic medications of our trade.
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PMID:The life-threatening complications of dermatologic therapies. 1580 12

We describe a case of intraoperative gelatine-induced anaphylaxis whose diagnosis was delayed as the use of gelatine during surgical procedures was omitted for two times in patient's medical records. The subject is a 66-year old woman, with a negative medical history of atopy, food and drug allergy, with arterial hypertension on a course of beta-blockers and with bladder carcinoma requiring surgery. The patient had tolerated both general and local anaesthesia on several previous occasions. On the first occasion she experienced arterial fibrillation secondary to a severe episode of hypotension following local anaesthesia, while on a course of beta-blockers. On the second occasion she developed a very severe episode of hypotension followed by the outbreak of a generalised rash during general anaesthesia. The tryptase sera level was 109 mg/L one hour after the reaction had subsided, while the basal values were normal. On the third occasion the patient redeveloped severe hypotension and a generalised rash during general anaesthesia. The allergological work-up was negative, except for intradermal test with gelatine. A study of the intra-cellular cytokines in blood lymphocytes showed a production of IL4 from CD4+ lymphocytes after stimulation by gelatine. The patient underwent a successive surgical procedure without any adverse event.
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PMID:Intraoperative anaphylaxis: verba volant, scripta manent! 1645 64

We report the case of an atopic male, 76 years old, with post-myocardial infarction ischaemic cardiopathy, arterial hypertension and a history of insect-sting induced large local reactions who died because of a biphasic anaphylaxis subsequent to multiple Vespid stings (about 15). Within approximately ten minutes after the stings he developed urticaria, extended erythema and hypotension (90/60 mmHg), measured by a family member. The objective physical examination by the emergency doctor at the patient's home revealed an orticarioid reaction and erythema of the back and neck, an unaffected respiratory apparatus and CNS, normal pupils, a pulse rate of 74, normal blood pressure ranging from 120/70 to 130/60 mmHg. The patient was administered antihistamine and corticosteroid through parenteral route. During the 45' observation period at the patient's home the urticaria subsided but not to completion. Approximately 40 minutes after the emergency doctor left, the urticaria reoccurred, angioedema of the neck and worsening asthenia developed. The patient died, despite attempts to resuscitate him by the emergency doctor that had been called out again. A post-mortem examination revealed generalised eodema of the lungs, brain, glottis, and bowels due to the severe characteristic systemic compromise of anaphylaxis. The Authors discuss whether an early use of adrenalin and/or a longer observation time could have saved the patient.
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PMID:A case of fatal biphasic anaphylaxis secondary to multiple stings: adrenalin and/or a longer observation time could have saved the patient? 1645 66

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