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)

Iris neovascular tufts are biomicroscopic capillary outgrowths from the pupillary margins. Iris tufts have been reported to occur in the elderly, in diabetes patients, and in myotonic dystrophy patients. Three cases have also been described in association with retinal vein occlusion. This paper describes a patient with unilateral acute retinal branch vein occlusion who had bilateral iris neovascular tufts. The bilaterality of this elderly patient's tufts suggested an underlying acquired systemic disorder. The patient denied medical illness, except for hypertension. Medical evaluation disclosed an insulin tolerance test diagnostic of diabetes, although a glucose tolerance test was not markedly abnormal. Iris tufts appeared to be associated with abnormal insulin secretion. Their occurrence with branch vein occlusion may be coincidental.
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PMID:Iris neovascular tufts. 616 13

Patients with neuromuscular disease may suffer from nocturnal respiratory failure despite normal daytime respiratory function. The physiological reduction in muscle tone during sleep may be life-threatening in a patient with impaired muscle strength. Nocturnal respiratory failure may occur in patients with the postpolio syndrome, amyotrophic lateral sclerosis, myasthenia gravis, myotonic dystrophy, and muscular dystrophy. Diagnosis of obstructive, central and mixed apneas, hypopneas, and hypoventilation is best made using polysomnography. Therapeutic options include noninvasive ventilation such as continuous positive airway pressure, bilevel positive airway pressure, intermittent positive pressure ventilation and, rarely, tracheostomy, oxygen, or protriptyline. Evaluation by a sleep specialist should be initiated in any neuromuscular patient with nocturnal symptoms such as air hunger, intermittent snoring or breathing, orthopnea, cyanosis, restlessness, and insomnia. Daytime symptoms may include morning drowsiness, headaches and excessive daytime sleepiness. Polycythemia, hypertension, and signs of heart failure may also be seen. Effective treatment is available, and may improve the quality of life, and possibly increase survival.
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PMID:Nocturnal respiratory failure as an indication of noninvasive ventilation in the patient with neuromuscular disease. 967 Mar 10

Post-traumatic stress-induced disorders are still the focus of interest and most recently discussions are under way whether stress-induced cortisol excess leads to atrophy of the brain. In investigation on carcinogenesis the first reports were published on the use of antisense-oligonucleotides during inhibition of the development of tumours by a humoral mechanism and on the gene-based neuroendocrine differentiation of the lungs, perhaps associated with the basis for the development of small cell carcinoma. The oncogenic action of superoxides has also humoral mediators. Interest in nitrogen oxide is focused on two areas: inflammations and hypertension. Intraluminal NO concentrations increase in asthma 2-10x, in cystitis 30-100x, in Crohn's disease 20-200x. Humoral mechanisms in asthma offer new drugs--inhibitors of the development or action of leucotrienes. The basal NO production is reduced in "essential" hypertension but it is not known whether it is the cause or consequence. IGF-I increases the formation of NO in the vascular wall and thus perhaps reduces vascular contractility. As far as IGF is concerned, it is obvious that if recombinant preparations will be available, they will be tested in amyotrophic lateral sclerosis, myotonic dystrophy, multiple sclerosis, catabolic conditions, osteoporosis, in renal failure and to promote wound healing. STH may also prove useful in cardiac failure, in particular in cardiac cachexia. That TRH has receptors in the gut is not surprising, it acts, however, even there via TSH. Thrombopoietin is being tested in clinical trials. Neocytolysis is a new phenomenon: when erythropoietin secretion declines new erythrocytes disappear and only old ones remain in the blood stream. Alpha-adducin is a renal tubular protein, regulating the sodium balance.
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PMID:[Endocrinology 1996-1997]. 965 Mar 40

Since fiscal year 1991, the U.S. Human Genome Project has spent $170.6 million in federal funds to help isolate genes associated with Huntington's disease, amyotrophic lateral sclerosis, neurofibromatosis types 1 and 2, myotonic dystrophy, and fragile X syndrome and to localize genes that predispose people to breast cancer, colon cancer, hypertension, diabetes, and Alzheimer's disease. Now comes the hard part. Biology's 21st century megaproject starts to look relatively manageable compared to another challenge facing the enterprise: sorting out ethical, legal, and social issues associated with using this information. "The Human Genome Project," wrote Senior Editor Barbara Jasny in the October 1 Science editorial, stretches "the limits of the technology and the limits of our ability to ethically and rationally apply genetic information to our lives."
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PMID:Ethical, legal, and social issues of the Human Genome Project: what to do with what we know. 971 68

190 patients with diabetes mellitus (DM) were examined: 24 patients with DM type 1 and 166 with DM type 2. Frequency of arterial hypertension (AH) in diabetics is higher than in population. AH in different DM types varies by pathogenesis. Symptomatic renal AH is typical for DM1, essential AH combining with renal one in 1/3 of cases--for DM2. Treatment of AH and DM often provokes hypothyroidism which can be iatrogenic because of continuous intake of sugar reducing and antihypertensive drugs with antithyroid and strumogenic actions. Hypothyroidism aggravates an AH course: arterial pressure becomes high and resistant to hypotensive therapy. DM makes difficulties in selection of hypotensive drugs as many of them alter metabolism and due to negative attitude of the patients to continuous intake of sugar reducing, antihypertensive drugs, thyroid hormones. Therefore, hypertensive diabetics should be prepared for treatment psychologically and receive only prolonged hypotensive drugs. In DM with AH medication of choice is ACE inhibitors as they are nephroprotective, had no negative effect on carbohydrate, fat metabolism and thyroid system.
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PMID:[Role of thyroid pathology in pathogenesis of arterial hypertension in diabetes]. 1247 32

Insulin-like growth factor-I (IGF-I) has endocrine, autocrine and paracrine properties. Receptors for IGF-I are present on virtually all cell types but are located mainly on cells of mesenchymal origin, such as fibroblasts, chondrocytes and osteoblasts. Growth hormone (GH)-dependent and GH-independent actions of IGF-I have been implicated in normal and abnormal bone growth, diabetes mellitus, malnutrition, cancer, thyroid disease and hematological diseases. The availability of recombinant human IGF-I (rhIGF-I) has led to new treatments for GH-resistant Laron dwarfism and certain diseases associated with severe insulin resistance. IGF-I has recently been investigated as a neurotrophic factor. Phase II efficacy trials with patients with neurological disease such as traumatic brain injury, myotonic dystrophy and amyotrophic lateral sclerosis have shown that rhIGF-I has efficacy on various outcome parameters. Treatment with rhIGF-I may result in reversible side effects of which increased heart rate, papilledema, ophthalmologic and intracranial hypertension, facial and generalized edema, and weight gain are noteworthy.
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PMID:Insulin-like growth factor-I: clinical studies. 1509 66

In obese humans and rodents there is increased expression of the key glucocorticoid (GC) regenerating enzyme, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), in adipose tissue. This increased expression appears to be of pathogenic importance because transgenic mice overexpressing 11beta-HSD1 selectively in adipose tissue exhibit a full metabolic syndrome with visceral obesity, dyslipidemia, insulin-resistant diabetes, and hypertension. In this model, while systemic plasma GC levels are unaltered, GC delivery to the liver via the portal vein is increased. 11beta-HSD1 is most highly expressed in liver where inhibition or deficiency of its activity improves glucose and lipid homeostasis. To determine the potential contribution of elevated intrahepatic GCs alone toward development of insulin-resistant syndromes we generated transgenic mice expressing increased 11beta-HSD1 activity selectively in the liver under transcriptional control of hepatic regulatory sequences derived from the human apoE gene (apoE-HSD1). Transgenic lines with 2- and 5-fold-elevated 11beta-HSD1 activity exhibited mild insulin resistance without altered fat depot mass. ApoE-HSD1 transgenic mice exhibited fatty liver and dyslipidemia with increased hepatic lipid synthesis/flux associated with elevated hepatic LXRalpha and PPARalpha mRNA levels as well as impaired hepatic lipid clearance. Further, apoE-HSD1 transgenic mice have a marked, transgene-dose-associated hypertension paralleled by incrementally increased liver angiotensinogen expression. These data suggest that elevated hepatic expression of 11beta-HSD1 may relate to the pathogenesis of specific fatty liver, insulin-resistant, and hypertensive syndromes without obesity in humans as may occur in, for example, myotonic dystrophy, and possibly, the metabolically obese, normal-weight individual.
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PMID:Metabolic syndrome without obesity: Hepatic overexpression of 11beta-hydroxysteroid dehydrogenase type 1 in transgenic mice. 1511 95

We experienced an anesthetic management for a patient of myotonic dystrophy with pheochromocytoma. Much attention is required to manage myotonic dystrophy on surgical manipulation. This disease interacts with anesthetic drugs. It may cause prolongation of drug action used during anesthesia compared with the usual case. It also may cause dangerous interactions such as severe arrhythmia and malignant hyperthermia. That is why we were faced with serious limitation in choosing anesthetic and adjuvant drugs. At the same time, the case of pheochromocytoma must be handled with scrupulous care. Pheochromocytoma causes severe hypertension and sometimes tachycardia leading to intracranial hemorrhage or adrenaline-induced severe hypovolemia. Besides, laparoscopic operation was scheduled to resect the pheochromocytoma. This operation demanded the anesthetic management with artificial ventilation. It must be difficult to cope with these conditions by limited number of drugs. This time, we managed this case by epidural anesthesia with propofol and nitrous oxide without opioid and muscular relaxant. Though, this patient was not fully awake from anesthesia and could not take enough breaths on his own. We extended the period of spontaneous breathing with careful check whether the patient has resumed spontaneous breathing. It took us fourteen days till extubation.
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PMID:[Anesthetic management for a patient of myotonic dystrophy with pheochromocytoma]. 1558 84

Type 1 diabetes mellitus (DM1) commonly occurs in childhood, although many pediatric centers are now seeing more cases of type 2 diabetes (DM2). Kidney failure caused by either type of diabetes is uncommon during childhood, but these years of hyperglycemia contribute to long-term complications. All children with diabetes warrant screening of glomerular filtration rate, blood pressure, and urine albumin excretion. Screening should begin after 5 years of DM1 or at puberty. A similar screening strategy should start at the time of diagnosis of DM2. Atypical features such as dipstick positive proteinuria or active urine sediment may warrant referral to a nephrologist for evaluation, including biopsy. The first line of treatment in either form of diabetes is achieving the best glycemic control possible. Patients developing microalbuminuria or hypertension should receive antiangiotensin II drugs. Adult studies suggest blood pressure goals should be lower in diabetes than in the general population. Although direct evidence is not yet available in children, achieving blood pressure below the 90th percentile for age, height, and gender seems prudent. Longitudinal studies and new screening tests may allow detection of susceptible children earlier in the course of DM1 or DM2, perhaps allowing prevention of diabetic kidney disease.
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PMID:Pediatric aspects of diabetic kidney disease. 1582 59

Autosomal dominant polycystic kidney disease (ADPKD) is the most common life-threatening, hereditary disease. The prevalence of ADPKD is more common than Huntington disease, haemophilia, sickle cell disease, cystic fibrosis, myotonic dystrophy and Down syndrome combined. In recent years there have not only been advances in the understanding of the genetic and molecular events involved in ADPKD, but some diagnostic and therapeutic advances have also emerged. In the genetics area, the gene for PKD1 was localised to chromosome 16, is associated with polycystin-2 protein, and found to account for approximately 85% of patients with ADPKD. The gene for PKD2, found in chromosome 4, accounts for approximately 15% of ADPKD, and is associated with the polycystin-2 protein. While these genetic and molecular biology findings have stimulated a great deal of exciting basic research in ADPKD, therapies to decrease morbidity and mortality in ADPKD patients have yet to emerge from these findings. In contrast, the early diagnosis and treatment of hypertension with inhibitors of the renin-angiotensin-aldosterone system have the potential to decrease or prevent left ventricular hypertrophy cardiac complications and slow the progression of the renal disease.
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PMID:Optimal care of autosomal dominant polycystic kidney disease patients. 1688 82


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