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)

Oral budesonide in adult studies is a potent corticosteroid with decreased systemic bioavailability and an improved adverse effect profile in comparison with prednisone. It has recently been introduced for the treatment of inflammatory bowel disease in Europe, Canada, and Israel. Benign intracranial hypertension has rarely been associated with corticosteroid therapy but has not been reported in association with budesonide therapy. Three adolescents with Crohn's disease and poor nutritional status developed benign intracranial hypertension while receiving oral budesonide. All three patients had previously received multiple courses of prednisone during the course of their disease, without developing intracranial hypertension. Benign intracranial hypertension resolved after medication withdrawal and did not recur with subsequent use of prednisone. Evaluation for benign intracranial hypertension should be considered in patients with inflammatory bowel disease who develop headache while receiving oral budesonide. This side effect may be associated with poor nutritional status.
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PMID:Benign intracranial hypertension associated with budesonide treatment in children with Crohn's disease. 1141 18

Retroperitoneal fibrosis has been described as a rare occurrence during the course of inflammatory bowel disease, mainly Crohn's disease. This is the third report on retroperitoneal fibrosis occurring during the course of ulcerative colitis. A 62-year-old male patient with a 5-year history of ulcerative colitis developed stenosis of the left ureter due to retroperitoneal fibrosis. Treatment consisted in surgically releasing the ureter from the mass and steroids. During a 2.5-year follow-up, renal function was stable and ulcerative colitis in remission. Important aspects of this case are the moderate course of ulcerative colitis, ultrasound confirmation of normal kidney structure before manifestation of fibrosis, hypertension diagnosed four years before retroperitoneal fibrosis, a non-functioning kidney at diagnosis, and reduction of retroperitoneal mass after steroid treatment. Retroperitoneal fibrosis, although a rare disease entity should be considered when a patient with ulcerative colitis develops otherwise unexplained renal insufficiency.
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PMID:Retroperitoneal fibrosis during the course of ulcerative colitis. A simple coincidence? 1181 49

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

An increased incidence of ischemic stroke has been reported in patients with Crohn's disease. Cerebral infarcts are usually considered as a complication of the hypercoagulable state associated with this inflammatory bowel disease (IBD). The association between Crohn's disease, hyperhomocysteinemia and large-artery stroke of the young has rarely been reported. A 39-year-old woman, with prior medical history of Crohn's disease and hypertension, presented with an ischemic stroke of the left internal carotid artery (ICA) territory. Etiological workup disclosed bilateral high-grade ICA stenosis and atheroma of the subclavian and vertebral arteries. Exhaustive search for prothrombotic factors showed inflammation, with an increased level of fibrinogen and factor IX, and a marked hyperhomocysteinemia. Both vitamin B1 and vitamin B6 plasmatic levels were decreased. Heterozygous C677T methylene-tetrahydrofolate reductase gene mutation was present. This observation highlights the combined proatherogenic effect of vitamin B deficiency-induced hyperhomocysteinemia and inflammation leading to large-artery stroke of the young in the setting of Crohn's disease. Our case report stresses the importance of vitamin deficiency screening in patients with IBD in terms of stroke prevention.
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PMID:Large-artery stroke in a young patient with Crohn's disease. Role of vitamin B6 deficiency-induced hyperhomocysteinemia. 1517 25

Turner syndrome is due to haploinsufficiency of X chromosome genes that escape inactivation and associates female phenotype, short stature, gonadal dysgenesis, somatic stigmata, cardiovascular and renal anomalies and a large spectrum of other disorders (autoimmune thyroiditis, osteoporosis, inflammatory bowel disease, chronic liver diseases). The increased mortality in Turner syndrome is primarily a result of its cardiovascular complications. Congenital cardiac anomalies (coarctation of the aorta, bicuspid aortic valve, anomalous venous drainage) are present in 23-40% of patients; there is an increased risk of aortic dilation (42%) and dissection, ischemic heart disease and the risk of hypertension is increased three fold. In addition, insulin resistance may be present in up to 50% of women with Turner syndrome and an atherogenic lipid profile (increased cholesterol, triglycerides) favors the development of coronary artery disease. Our study was aimed to reveal anomalies in Turner syndrome that may increase cardiovascular risk. We studied a group of 62 Turner patients aged 16-67 years (mean age 26.8 years, SD = 11.1 years) comparatively to 62 age matched controls. Glycemia over 100 mg% was found in 11.3% of Turner patients vs 1.6% of controls and cholesterolemia over 200mg% was found in 51.2% of Turner patients vs 14.5% of controls; 24.2% of Turner patients were overweight vs 17.8% of controls and 6.4% were obese vs 4.8% of controls. In the Turner group we found congenital cardiac anomalies in 17.8%, hypertension in 6.5%, renal anomalies 11.3%, and hypothyroidism 29.2%.
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PMID:Cardiovascular risk factors in Turner syndrome. 1552 27

There is evidence from both observational studies and clinical trials that calcium malnutrition and hypovitaminosis D are predisposing conditions for various common chronic diseases. In addition to skeletal disorders, calcium and vitamin D deficits increase the risk of malignancies, particularly of colon, breast and prostate gland, of chronic inflammatory and autoimmune diseases (e.g. insulin-dependent diabetes mellitus, inflammatory bowel disease, multiple sclerosis), as well as of metabolic disorders (metabolic syndrome, hypertension). The aim of the present review was to provide improved understanding of the molecular and cellular processes by which deficits in calcium and vitamin D cause specific changes in cell and organ functions and thereby increase the risk for chronic diseases of different aetiology. 1,25-Dihydroxyvitamin D(3) and extracellular Ca(++) are both key regulators of proliferation, differentiation and function at the cellular level. However, the efficiency of vitamin D receptor-mediated intracellular signalling is limited by the negative effects of hypovitaminosis D on extrarenal 25-hydroxyvitamin D-1alpha-hydroxylase activity and thus on the production of 1,25-dihydroxyvitamin D(3). Calcium malnutrition eventually causes a decrease in calcium concentration in extracellular fluid compartments, resulting in organ-specific modulation of calcium-sensing receptor activity. Hence, attenuation of signal transduction from the ligand-activated vitamin D receptor and calcium-sensing receptor seems to be the prime mechanism by which calcium and vitamin D insufficiencies cause perturbation of cellular functions in bone, kidney, intestine, mammary and prostate glands, endocrine pancreas, vascular endothelium, and, importantly, in the immune system. The wide range of diseases associated with deficits in calcium and vitamin D in combination with the high prevalence of these conditions represents a special challenge for preventive medicine.
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PMID:Vitamin D and calcium deficits predispose for multiple chronic diseases. 1586 41

Turner syndrome (TS) is a common genetic disorder, resulting from the partial or complete absence of one sex chromosome, and occurring in approximately 50 per 100,000 liveborn girls. TS is associated with reduced adult height and with gonadal dysgenesis, leading to insufficient circulating levels of female sex steroids and to infertility. Morbidity and mortality are increased in TS but average intellectual performance is within the normal range. A number of recent studies have allowed new insights to be gained with respect to epidemiology, genetics, cardiology, endocrinology and metabolism. Elucidation of the effects of short stature homeobox protein deficiency has explained some of the phenotypic characteristics in TS, principally short stature. Treatment with growth hormone during childhood and adolescence allows a considerable gain in adult height, although the consequences of this treatment in the very long term are not clear. Puberty must be induced in most cases, and female sex hormone replacement therapy (HRT) is given during adult years. The optimal dose of HRT has not been established and, likewise, the benefits and drawbacks of HRT have not been thoroughly evaluated. The risks of type 2 diabetes, type 1 diabetes, hypothyroidism, osteoporosis, congenital heart disease, hypertension, ischemic heart disease, aortic dilatation and dissection, inflammatory bowel disease and celiac disease are clearly elevated, and proper care during adulthood is important. Currently no firm guidelines for diagnosis exist. In conclusion, TS is a condition associated with a number of diseases and conditions that are reviewed in the present paper. Individuals with TS need life-long medical attention.
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PMID:Clinical practice in Turner syndrome. 1692 65

Identified risk factors for atherosclerosis include diet, age, gender, family history, stress, lifestyle, smoking, diabetes, dyslipidemias, hypertension, and HIV. The mechanistic rationale to explain these associations remains poorly understood. We believe that these seemingly unrelated entities may promote atherosclerosis through a common pathway by inducing adventitial autonomic dysfunction, specifically as an adventitial stress dysfunction of neurogenic origin. Atherosclerosis may represent a local vascular manifestation of the global autonomic dysfunction induced by age, smoking, hypertension, HIV, and diabetes. Atherosclerosis may also participate in a feed-forward cycle as aging, diabetes, dyslipidemia, and hypertension may also represent independent downstream consequences of global sympathetic bias. Chronic physiologic stress and behavioral stress can shift the autonomic balance towards a state of sympathetic predominance. The highly communicable nature of behavioral stress may partially implicate the familial association of atherosclerosis as an epigenetic phenomenon, independent of putative genetic mechanisms. Host stress, global autonomic dysfunction, and sympathetic bias may also arise from chronic maladaptive consumption of stressed foods, as organisms detect and assimilate the stress phenotypes of their dietary constituents through a process called xenohormesis. The benefits of exercise may operate through reduction of chronic physiologic stress associated with global sympathetic bias. The neurogenic adventitial stress response may explain the local tissue remodeling seen in atherosclerosis, including adventitial adipose dysfunction, inflammation, adventitial angiogenesis, thrombosis, and endothelial dysfunction. We believe that the locations of atherosclerotic lesions correspond to regions of neurogenic adventitial autonomic dysfunction, in similar fashion to the segmental patterns of involvement found in inflammatory bowel disease. The diffuse atherosclerosis exhibited in transplanted hearts may reflect a diffuse sympathetic bias of the donor heart, since tissues and organs exhibit an intrinsic sympathetic bias in the absence of an extrinsic source of autonomic hegemony. Once we regard atherosclerosis as a neurogenic phenomenon manifested in adventitial autonomic dysfunction, novel diagnostic and therapeutic paradigms become evident.
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PMID:Is atherosclerosis a neurogenic phenomenon? 1740 Mar 98

Vitamin D as a part of the endocrine system is an important component in the interaction between the kidney, bone, parathyroid hormone, and the intestine, which maintains extracellular calcium level within normal limits, in order to keep the vital physiologic process and skeletal integrity. Vitamin D is also associated with hypertension, muscular function, immunity, and ability to encounter infection, autoimmune disease, and cancer. The role of vitamin D in immunity is a feedback reaction of paracrine to eliminate inflammation or to influence CD4 T-cell differentiation and or to increase the function of T suppressor cell or combination between both. The active form of vitamin D produces and maintains self immunologic tolerance, some studies show that 1,25(OH)2D inhibits induction of disease in autoimmune encephalomyelitis, thyroiditis, type-1 diabetes mellitus, inflammatory bowel disease (IBD), systemic lupus erythematosus, and collagen-induced arthritis and Lyme arthritis.
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PMID:Vitamin D and autoimmune disease. 1769 36

Hepatic portal venous gas is most often associated with extensive bowel necrosis due to mesenteric infarction. Mortality exceeds 75% with this condition. The most common precipitating factors include ischemia, intra-abdominal abscesses and inflammatory bowel disease. In this report, we present a 75-year-old woman with extensive hepatic portal and mesenteric venous gas due to colonic diverticulitis. She had a 10-year history of type II diabetes mellitus and hypertension. She was treated by sigmoid resection and Hartmann's procedure and discharged from the hospital without any complications.
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PMID:Extensive hepatic-portal and mesenteric venous gas due to sigmoid diverticulitis. 1923 52


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