How to Trip Rapid Review

Step 1: Select articles relevant to your search (remember the system is only optimised for single intervention studies)

Step 2: press

Step 3: review the result, and maybe amend the or if you know better! If we're unsure of the overall sentiment of the trial we will display the conclusion under the article title. We then require you to tell us what the correct sentiment is.

35,367 results for

Hypertension Causes

by
...
Latest & greatest
Alerts

Export results

Use check boxes to select individual results below

SmartSearch available

Trip's SmartSearch engine has discovered connected searches & results. Click to show

41. Nephron‐Specific Disruption of Nitric Oxide Synthase 3 Causes Hypertension and Impaired Salt Excretion (PubMed)

Nephron‐Specific Disruption of Nitric Oxide Synthase 3 Causes Hypertension and Impaired Salt Excretion In vitro studies suggest that nephron nitric oxide synthase 3 (NOS3) modulates tubule Na+ transport.To assess nephron NOS3 relevance in vivo, knockout (KO) mice with doxycycline-inducible nephron-wide deletion of NOS3 were generated. During 1 week of salt loading, KO mice, as compared with controls, had higher arterial pressure and Na+ retention, a tendency towards reduced plasma renin

Full Text available with Trip Pro

2018 Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

42. Esophageal Ulcers in Primary Biliary Cholangitis: A Rare Cause of Hematemesis in the Setting of Portal Hypertension and Esophageal Varices (PubMed)

Esophageal Ulcers in Primary Biliary Cholangitis: A Rare Cause of Hematemesis in the Setting of Portal Hypertension and Esophageal Varices Our patient with primary biliary cholangitis, previously termed as primary biliary cirrhosis, presented with an unexpected and unusual cause of hematemesis in the form of multiple esophageal ulcers in-between variceal columns. Given that upon endoscopic examination, the esophageal ulcers were found to bleeding instead of the varices; they should

Full Text available with Trip Pro

2018 Gastroenterology research

43. A Case of Recurrent Thrombotic Microangiopathy Caused by Hypertensive Urgency (PubMed)

A Case of Recurrent Thrombotic Microangiopathy Caused by Hypertensive Urgency A 26-year-old man presented to the emergency room with abdominal pain, nausea, and vomiting for four days. His medical history was significant for hypertension and end-stage renal disease managed with hemodialysis. He had been noncompliant with the antihypertensive regimen which included nifedipine, hydralazine, and spironolactone. At presentation, his blood pressure was 231/123 mmHg. Laboratory workup showed white (...) microangiopathy secondary to severe hypertension and was started on intravenous nicardipine. With appropriate blood pressure control, hematological parameters improved with normalization of the platelet count within 10 days. Notably, the patient had one similar episode of hypertension-induced thrombotic microangiopathy within a period of the last three months and ADAMTS-13 (a disintegrin and metalloprotease with thrombospondin type 1 motif 13) activity was normal on his previous admission.

Full Text available with Trip Pro

2018 Cureus

44. In-the-bag multifocal intraocular lens causing pigment dispersion and refractory secondary ocular hypertension (PubMed)

In-the-bag multifocal intraocular lens causing pigment dispersion and refractory secondary ocular hypertension Pigment dispersion and elevated intraocular pressure (IOP) with sulcus placed hydrophobic acrylic intraocular lenses (IOLs) are described and are rare with in-the-bag IOLs. We report a case of a young lady with elevated IOP and pigment dispersion in one eye following an uneventful phacoemulsification and multifocal IOL implantation. The eye had eccentric capsulorrhexis and localized

Full Text available with Trip Pro

2018 Indian journal of ophthalmology

45. Accessory Hepatic Lobe: A Rare Cause of Prehepatic Portal Hypertension in a Child (PubMed)

Accessory Hepatic Lobe: A Rare Cause of Prehepatic Portal Hypertension in a Child Accessory hepatic lobe is noted as and considered a rare disease in children. It can manifest with various symptoms and complications depending on the location, volume, type and position of the disease as presented on a child. The patient presented as a 14-month-old girl who was seen with a notable hepatosplenomegaly and portal hypertension. A diagnosis was made after taking an extensive medical history (...) , observation and radiological examinations. The formal diagnosis was a prehepatic portal hypertension associated with accessory hepatic lobe.

Full Text available with Trip Pro

2018 Pediatric gastroenterology, hepatology & nutrition

46. Idiopathic pulmonary arterial hypertension - a unrecognized cause of high-shear high-flow haemostatic defects (otherwise referred to as acquired von Willebrand syndrome) in children. (PubMed)

Idiopathic pulmonary arterial hypertension - a unrecognized cause of high-shear high-flow haemostatic defects (otherwise referred to as acquired von Willebrand syndrome) in children. Acquired von Willebrand syndrome (AVWS) is reported in high-flow high-shear congenital cardiac disorders. We hypothesized that the narrowed pulmonary vasculature in idiopathic pulmonary arterial hypertension (IPAH) may induce AVWS. We conducted a cross-sectional evaluation of children with IPAH. Patients

2018 British journal of haematology

47. Argininosuccinate Lyase Deficiency Causes an Endothelial-Dependent Form of Hypertension. (PubMed)

Argininosuccinate Lyase Deficiency Causes an Endothelial-Dependent Form of Hypertension. Primary hypertension is a major risk factor for ischemic heart disease, stroke, and chronic kidney disease. Insights obtained from the study of rare Mendelian forms of hypertension have been invaluable in elucidating the mechanisms causing primary hypertension and development of antihypertensive therapies. Endothelial cells play a key role in the regulation of blood pressure; however, a Mendelian form (...) of hypertension that is primarily due to endothelial dysfunction has not yet been described. Here, we show that the urea cycle disorder, argininosuccinate lyase deficiency (ASLD), can manifest as a Mendelian form of endothelial-dependent hypertension. Using data from a human clinical study, a mouse model with endothelial-specific deletion of argininosuccinate lyase (Asl), and in vitro studies in human aortic endothelial cells and induced pluripotent stem cell-derived endothelial cells from individuals

2018 American Journal of Human Genetics

48. A one-year risk score to predict all-cause mortality in hypertensive inpatients. (PubMed)

A one-year risk score to predict all-cause mortality in hypertensive inpatients. The aim of this study was to construct and internally validate a scoring system to estimate the probability of death in hypertensive inpatients. Existing predictive models do not meet all the indications for clinical application because they were constructed in patients enrolled in clinical trials and did not use the recommended statistical methodology. This cohort study comprised 302 hypertensive patients (...) hospitalized between 2015 and 2017 in Spain. The main variable was time-to-death (all-cause mortality). Secondary variables (potential predictors of the model) were: age, gender, smoking, blood pressure, Charlson Comorbidity Index (CCI), physical activity, diet and quality of life. A Cox model was constructed and adapted to a points system to predict mortality one year from admission. The model was internally validated by bootstrapping, assessing both discrimination and calibration. The system

2018 European journal of internal medicine

49. Consequences of SPAK inactivation on Hyperkalemic Hypertension caused by WNK1 mutations: evidence for differential roles of WNK1 and WNK4 (PubMed)

Consequences of SPAK inactivation on Hyperkalemic Hypertension caused by WNK1 mutations: evidence for differential roles of WNK1 and WNK4 Mutations of the gene encoding WNK1 [With No lysine (K) kinase 1] or WNK4 cause Familial Hyperkalemic Hypertension (FHHt). Previous studies have shown that the activation of SPAK (Ste20-related Proline/Alanine-rich Kinase) plays a dominant role in the development of FHHt caused by WNK4 mutations. The implication of SPAK in FHHt caused by WNK1 mutation has (...) but remain higher than in SPAK 243A/243A mice. This is different from what was observed in WNK4-FHHt mice in which SPAK inactivation completely restored the phenotype and NCC expression to wild-type levels. Although these results confirm that FHHt caused by WNK1 mutations is dependent on the activation of SPAK, they suggest that WNK1 and WNK4 play different roles in the distal nephron.

Full Text available with Trip Pro

2018 Scientific reports

50. Nocturnal Hypertension in Multiple System Atrophy May Cause Posterior Reversible Encephalopathy Syndrome (PubMed)

Nocturnal Hypertension in Multiple System Atrophy May Cause Posterior Reversible Encephalopathy Syndrome Nocturnal hypertension (NH) is a symptom of cardiovascular dysautonomia in multiple system atrophy (MSA); however, care and medication are often insufficient. We herein report a patient with MSA who showed posterior reversible encephalopathy syndrome (PRES) caused by hypertension during sleep. He presented clinically with total blindness; T2-weighted magnetic resonance imaging showed high

Full Text available with Trip Pro

2018 Internal Medicine

51. Lipocalin-Like Prostaglandin D Synthase but Not Hemopoietic Prostaglandin D Synthase Deletion Causes Hypertension and Accelerates Thrombogenesis in Mice (PubMed)

Lipocalin-Like Prostaglandin D Synthase but Not Hemopoietic Prostaglandin D Synthase Deletion Causes Hypertension and Accelerates Thrombogenesis in Mice Prostaglandin (PG) D2 is formed by two distinct PGD synthases (PGDS): lipocalin-type PGDS (L-PGDS), which acts as a PGD2-producing enzyme and as extracellular lipophilic transporter, and hematopoietic PGDS (H-PGDS), a σ glutathione-S-transferase. PGD2 plays an important role in the maintenance of vascular function; however, the relative

Full Text available with Trip Pro

2018 The Journal of pharmacology and experimental therapeutics

52. Cases of visual impairment caused by cerebral venous sinus occlusion-induced intracranial hypertension in the absence of headache. (PubMed)

Cases of visual impairment caused by cerebral venous sinus occlusion-induced intracranial hypertension in the absence of headache. Cerebral venous sinus thrombosis or stenosis (here collectively referred to as cerebral venous sinus occlusion, CVSO) can cause chronically-elevated intracranial pressure (ICP). Patients may have no neurological symptoms other than visual impairment, secondary to bilateral papilledema. Correctly recognizing these conditions, through proper ophthalmological (...) peak time of P2 wave, and pattern VEPs in one patient displayed decreased P100 amplitude in one eye, while a normal P100 wave in the other eye. In all patients, lumbar puncture (LP) revealed significantly elevated ICP. And magnetic resonance venography (MRV) demonstrated cerebral venous sinus abnormalities in every patient: one right sigmoid sinus thrombosis, one superior sagittal sinus thrombosis, and one right transverse sinus stenosis.CVSO can cause chronically-elevated ICP, leading to bilateral

Full Text available with Trip Pro

2018 BMC Neurology

53. Novel Pathogenesis of Hypertension and Diastolic Dysfunction Caused by M3R (Muscarinic Cholinergic 3 Receptor) Signaling. (PubMed)

Novel Pathogenesis of Hypertension and Diastolic Dysfunction Caused by M3R (Muscarinic Cholinergic 3 Receptor) Signaling. Multiple quantitative trait loci for blood pressure (BP) are localized in humans and rodent models. Model studies have not only produced human quantitative trait loci homologues but also provided unforeseen mechanistic insights into the function modality of quantitative trait loci actions. Presently, congenic knockins, gene-specific knockout, and in vitro and in vivo (...) function studies were used in a rat model of polygenic hypertension, DSS (Dahl salt sensitive) rats. One gene previously unknown in regulating BP was detected with 1 structural mutation(s) for each of 2 quantitative trait loci classified into 2 separate epistatic modules 1 and 3. C17QTL1 in epistatic module 2 was identified to be the gene Chrm3 encoding the M3R (muscarinic cholinergic 3 receptor), since a single function-enhancing M3RT556M conversion correlated with elevated BP. To definitively prove

Full Text available with Trip Pro

2018 Hypertension

54. Exposure to Maternal Diabetes Mellitus Causes Renal Dopamine D<sub>1</sub> Receptor Dysfunction and Hypertension in Adult Rat Offspring. (PubMed)

Exposure to Maternal Diabetes Mellitus Causes Renal Dopamine D1 Receptor Dysfunction and Hypertension in Adult Rat Offspring. Epidemiological and experimental studies suggest that maternal diabetes mellitus programs hypertension that is associated with impaired sodium excretion in the adult offspring. However, the underlying mechanisms are not clear. Because dopamine receptor function is involved in the pathogenesis of hypertension, we hypothesized that impaired renal dopamine D1 (...) , had increased oxidative stress, indicated by decreased renal glutathione and increased renal malondialdehyde and urine 8-isoprostane. Normalization of oxidative stress with tempol also normalized the renal D1 receptor phosphorylation, D1 receptor-mediated diuresis and natriuresis, and blood pressure in DMO. Our present study indicates that maternal diabetes mellitus-programed hypertension in the offspring is caused by impaired renal D1 receptor function because of oxidative stress that is mediated

2018 Hypertension

55. Pheochromocytoma as a rare cause of hypertension in a 46 X, i(X)(q10) turner syndrome: a case report and literature review. (PubMed)

Pheochromocytoma as a rare cause of hypertension in a 46 X, i(X)(q10) turner syndrome: a case report and literature review. Cardiovascular disease (CVD) presents the most serious health problems and contributes to the increased mortality in young women with Turner syndrome. Arterial hypertension in Turner syndrome patients is significantly more prevalent than that in a general age-matched control group. The aetiology of hypertension in Turner syndrome varies, even in the absence of cardiac (...) anomalies and obvious structural renal abnormalities. Pheochromocytoma is an extremely rare cause among various etiologies for hypertension in patients with Turner syndrome. Here, we reported a pheochromocytoma as a rare cause of hypertension in Turner syndrome patient.A 21-year-old woman who has diagnosed with Turner syndrome with a karyotype of 46,X,i(X)(q10) visited for hypertension and mild headache. Transthoracic echography (TTE) showed no definite persistent ductus arteriosus shunt flow

Full Text available with Trip Pro

2018 BMC Endocrine Disorders

56. Baicalein Ameliorates Pulmonary Arterial Hypertension Caused by Monocrotaline through Downregulation of ET-1 and ET<sub>A</sub>R in Pneumonectomized Rats. (PubMed)

Baicalein Ameliorates Pulmonary Arterial Hypertension Caused by Monocrotaline through Downregulation of ET-1 and ETAR in Pneumonectomized Rats. Baicalein (BE) extracted from Scutellaria baicalensis Georgi is able to alleviate various cardiovascular and inflammatory diseases. However, the effects of BE on pulmonary arterial hypertension (PAH) remain unknown. Therefore, the present study aimed to examine whether BE ameliorates pneumonectomy and monocrotaline-induced PAH in rats

2018 American Journal of Chinese Medicine

57. IgG4-related disease of pulmonary artery causing pulmonary hypertension. (PubMed)

IgG4-related disease of pulmonary artery causing pulmonary hypertension. IgG4-related disease (IgG4-RD) is recognized as an immune-mediated condition with pathology features of lymphoplasmacytic infiltrate, storiform fibrosis, and obliterative phlebitis, accompanied with or without elevated serum IgG4 concentrations. However, few of pulmonary artery IgG4-RD causing pulmonary hypertension (PH) was reported.The medical records of 3 patients with pulmonary artery IgG4-RD inducing PH were analyzed (...) confirmed the diagnosis as IgG4-RD. Treated with glucocorticoids and cyclophosphamide or rituximab, 2 patients' IgG4 concentrations declined sharply and the lesions shrunk gradually. Another patient treated with glucocorticoids died of heart failure.IgG4-RD involved pulmonary artery causing PH was rare. A high index of awareness of this disease is required for early diagnosis and treatment. PET/CT might be a valuable approach to distinguish pulmonary artery IgG4-RD from pulmonary thrombus and malignant

Full Text available with Trip Pro

2018 Medicine

58. Mesalazine treatment causing resolution of intracranial hypertension secondary to ulcerative colitis: A case report. (PubMed)

Mesalazine treatment causing resolution of intracranial hypertension secondary to ulcerative colitis: A case report. The association between intracranial hypertension (ICH) and ulcerative colitis (UC) is rare. We report the unusual case of a male patient with UC and ICH in whom both conditions resolved with mesalazine therapy.A 48-year-old Caucasian man presented to our department in June 2016 for decreased vision, transient visual obscuration, pulsatile tinnitus and headaches of 7 months

2018 Medicine

59. Growth/differentiation factor 15 causes TGFβ-activated kinase 1-dependent muscle atrophy in pulmonary arterial hypertension. (PubMed)

Growth/differentiation factor 15 causes TGFβ-activated kinase 1-dependent muscle atrophy in pulmonary arterial hypertension. Skeletal muscle dysfunction is a clinically important complication of pulmonary arterial hypertension (PAH). Growth/differentiation factor 15 (GDF-15), a prognostic marker in PAH, has been associated with muscle loss in other conditions. We aimed to define the associations of GDF-15 and muscle wasting in PAH, to assess its utility as a biomarker of muscle loss

Full Text available with Trip Pro

2018 Thorax

60. Germline <i>BMP9</i> mutation causes idiopathic pulmonary arterial hypertension. (PubMed)

Germline BMP9 mutation causes idiopathic pulmonary arterial hypertension. Idiopathic pulmonary arterial hypertension (IPAH) is a rare disease with high heritability. Although several predisposing genes have been linked to IPAH, the genetic aetiology remains unknown for a large number of IPAH cases.We conducted an exome-wide gene-based burden analysis on two independent case-control studies, including a total of 331 IPAH cases and 10 508 controls. Functional assessments were conducted

2018 European Respiratory Journal

To help you find the content you need quickly, you can filter your results via the categories on the right-hand side >>>>