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 14 year old Bangladeshi boy presented with obesity, reduced vision, mental retardation, hypogonadism, delayed development and learning difficulty. On examination, he had polydactyly, moon face, bilateral gynaecomastia, small penis and undescended testes. Retinitis pigmentosa was found on fundoscopy. With typical features, he was diagnosed as a case of Laurence-Moon-Bardet-Biedl syndrome. It is a rare autosomal recessive disorder with mutation in 6 loci identified so far. It is commonly found in communities with high inter-family marriage. Clinical features appear early in childhood and diagnosis is usually done by puberty. Prominent features include rod-cone dystrophy leading to blindness, postaxial polydactyly, central obesity, learning disability, hypogonadism in males and renal dysfunction. Relatives with a single affected gene may have obesity, hypertension, diabetes and renal disease. There is increased risk of renal cell carcinoma. There is no definite treatment. Early diagnosis and symptomatic, supportive and rehabilitative measures can reduce the disability. These include dietary modification, oral hypoglycaemic drugs, testosterone supplement etc. Relatives of the patient should be screened for renal abnormality.
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PMID:Laurence Moon Bardet Biedl Syndrome. 1937 20

Recent studies using genetically modified mice, such as FGF23-/- and Klotho-/- mice that exhibit altered mineral homeostasis due to a high vitamin D activity showed features of premature aging that include retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism and short lifespan. The phenotype reversed by normalizing vitamin D and/or mineral homeostasis. Thus, hypervitaminosis D due to an increased 1alpha-hydroxylase activity seems to be a cause of the premature aging. In several studies, we have described that a complete or partial lack of vitamin D action (VDR-/- mice and CYP27B1-/-) show almost similar phenotype as FGF23-/- or Klotho-/- mice. VDR mutant mice have growth retardation, osteoporosis, kyphosis, skin thickening and wrinkling, alopecia, ectopic calcification, progressive loss of hearing and balance as well as short lifespan. CYP27B1-/- mice do not show alopecia nor balance deficit, which might be apoVDR-dependent or calcidiol-dependent. The features are typical to premature aging. The phenotype is resistant to a normalization of the mineral homeostasis by a rescue diet containing high calcium and phosphate. Taken together, aging shows a U-shaped dependency on hormonal forms of vitamin D suggesting that there is an optimal concentration of vitamin D in delaying aging phenomena. Our recent study shows that calcidiol is an active hormone. Since serum calcidiol but not calcitriol is fluctuating in physiological situations, calcidiol might determine the biological output of vitamin D action. Due to its high serum concentration and better uptake of calcidiol-DBP by the target cells through the cubilin-megalin system, calcidiol seems to be an important circulating hormone. Therefore, serum calcidiol might be associated with an increased risk of aging-related chronic diseases more directly than calcitriol. Aging and cancer seem to be tightly associated phenomena. Accumulation of damage on DNA and telomeres cause both aging and cancer, moreover the signalling pathways seem to converge on tumour suppressor protein, p53, which seems to be regulated by vitamin D. Also, the insulin-like growth factor signalling pathway (IGF-1, IGFBPs, IGFR) and fibroblast growth factor-23 (FGF-23) regulate growth, aging and cancer. Vitamin D can regulate these signalling pathways, too. Also NF-kappaB and telomerase reverse transcriptase (TERT) might be molecular mechanisms mediating vitamin D action in aging and cancer. Calcidiol serum concentrations show a U-shaped risk of prostate cancer suggesting an optimal serum concentration of 40-60 nmol/L for the lowest cancer risk. Therefore, it is necessary to study several common aging-associated diseases such as osteoporosis, hypertension and diabetes known to be vitamin D-dependent before any recommendations of an optimal serum concentration of calcidiol are given.
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PMID:Vitamin D and aging. 1944 37

We analyzed the late outcomes of 429 long-term survivors post allogeneic hematopoietic SCT (allo-HSCT) who received transplant in our center between 1981 and 2002, and were free of their primary disease for > or =2 years after allo-HSCT. Late recurrent primary malignancy was found in 58 (13.5%) patients and was the primary cause of late death. A total of 37 (8.6%) patients died of non-relapse causes at a median of 5.5 years (range, 2-15.6 years) post allo-HSCT. The major non-relapse causes of death were chronic GVHD (cGVHD), secondary malignancy and infection. The probabilities of OS and EFS were 85% (95% cumulative incidence (CI) (81-89%)) and 79% (95% CI (74-83%)) at 10 years, respectively. Long-term allo-HSCT survivors were evaluated for late complications (median follow-up, 8.6 years (range, 2.3-22.8 years)). cGVHD was diagnosed in 196 (53.1%) survivors. The endocrine and metabolic complications were hypogonadism in 134 (36.3%) patients, osteopenia/osteoporosis in 90 (24.4%), dyslipidemia in 33 (8.9%), hypothyroidism in 28 (7.6%) and diabetes in 28 (7.6%). Hypertension was diagnosed in 79 (21.4%), renal impairment in 70 (19.0%), depression in 40 (10.8%) and sexual dysfunction in 33 (8.9%) survivors. We conclude that in patients who receive allo-HSCT as treatment for hematological malignancy and who are free of their original disease 2 years post transplant, mortality is low and the probability of durable remission is high. Lifelong surveillance is recommended.
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PMID:Long-term outcome after allo-SCT: close follow-up on a large cohort treated with myeloablative regimens. 1959 25

The prevalence of hypogonadism has been found to be increased in certain chronic illnesses, especially diabetes, hypertension and obesity. Recently, the prevalence of hypogonadism in primary care practices mirrored that in our population of men with erectile dysfunction (ED). In this study, the prevalence of hypogonadism in nearly 1000 men with ED was tabulated, using a retrospective chart review, and analyzed for association with the various contributing medical and psychological factors. The prevalence of hypogonadism was determined in men with a variety of chronic illnesses, and was further characterized by decade. We observed an association between hypertension (P=0.025), tobacco abuse (P=0.0059), sleep apnea (P=0.0001), work stress (P=0.041) and hypogonadism. These data were further analyzed for the odds ratio and confidence interval (Forest plot), which showed strong association for sleep apnea and work stress. We did not observe any significant association between diabetes, atherosclerosis, alcohol abuse, multiple medications, asthma, seizure disorder, anxiety/depression and hypogonadism (P values for Cochran-Mantel-Haenszel general association were 0.48, 0.97, 0.25, 0.69, 0.22, 0.76 and 0.98, respectively). We suggest that a host of chronic illnesses have a high prevalence of secondary hypogonadism. Men who have chronic medical or psychological illnesses should have their testosterone level checked, especially when sexual dysfunction symptoms or signs are present.
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PMID:Hypogonadism in men with erectile dysfunction may be related to a host of chronic illnesses. 1979 59

Changing lifestyles and an excess of food supply in developed countries have resulted in an increasing prevalence of overweight and obesity. As a consequence, a disorder of complex pathophysiology involving visceral adipose tissue as an endocrine organ, dyslipidemia, insulin resistance and hypertension has emerged-the so-called metabolic syndrome. This disorder can lead to the manifestation of type 2 diabetes mellitus and cardiovascular disease. In men, testosterone deficiency may contribute to the development of the metabolic syndrome. In turn, states of hyperinsulinemia and obesity lead to a reduction of testicular testosterone production. Testosterone has reciprocal effects on the generation of muscle and visceral adipose tissue by influencing the commitment of pluripotent stem cells and by inhibiting the development of preadipocytes. Insulin sensitivity of muscle cells is increased by augmenting mitochondrial capacity and fostering expression of oxidative phosphorylation genes. Testosterone has a protective effect on pancreatic beta cells, which is possibly exerted by androgen-receptor-mediated mechanisms and influence of inflammatory cytokines. As some, but not all, epidemiological and interventional studies indicate, testosterone substitution might be helpful in preventing or attenuating the metabolic syndrome in aging men with late-onset hypogonadism and in hypogonadal patients with type 2 diabetes mellitus, but larger controlled trials are needed to confirm such hypotheses.
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PMID:Testosterone deficiency, insulin resistance and the metabolic syndrome. 1985 74

Long-term allograft survival poses a major problem in pediatric renal transplantation, with allograft nephropathy being the principal cause of graft failure after the first post-transplant year. The mechanisms of nephron loss resulting in graft dysfunction are multiple, comprising both immunologic factors such as acute and chronic antibody- or T-cell-mediated rejection and non-immunologic components. The latter include peri-transplant injuries and renovascular lesions (renal artery stenosis, thrombosis) as well as cardiovascular risk factors such as arterial hypertension and hyperlipidemia. Another relevant issue leading to progressive nephron loss and declining kidney transplant function is acute and chronic nephrotoxicity induced by the calcineurin inhibitors (CNIs) ciclosporin (cyclosporine microemulsion) and tacrolimus. Furthermore, the presence of an abnormal lower urinary tract as well as bacterial (recurrent pyelonephritis) and viral (cytomegalovirus [CMV], polyomavirus [BK virus; BKV]) infections are crucial factors involved in the incidence of chronic allograft dysfunction and graft failure. Renovascular lesions and lower urinary tract obstruction are typical indicators for surgical intervention. The aim of treatment in pediatric patients with renal failure secondary to a dysfunctional lower urinary tract is to create a sterile, continent, and nonrefluxive reservoir. Surgical techniques such as bladder augmentation and the introduction of intermittent catheterization and anticholinergic therapy have significantly improved graft outcome. Arterial hypertension, another factor responsible for graft function deterioration in pediatric renal transplant recipients, is controlled preferably by the use of angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor antagonists, which are known to possess nephroprotective properties in addition to their potent antihypertensive effects. Although treatment of subclinical rejection with augmented immunosuppression has been associated with better graft survival, an increase of the immunosuppressive level to avoid subclinical rejection should be weighed against the risk of infection. The majority of viral infections affecting kidney allografts are caused by CMV and BKV. Antiviral CMV prophylaxis or pre-emptive therapy with ganciclovir has been shown to have beneficial effects in the pediatric renal transplant population. Treatment of BKV-induced nephropathy is based on reduction of the immunosuppressant therapy, although specific antiviral agents such as cidofovir and leflunomide are known to inhibit BKV. However, cidofovir itself is nephrotoxic and should therefore be administered cautiously to pediatric renal transplant patients. Since CNIs are likewise known for their nephrotoxic effects, especially with long-term use, alteration of the immunosuppressant regimen is necessary in case of deteriorating graft function due to CNI-induced histopathologic changes. Complete CNI avoidance seems inappropriate because, in this situation in pediatric renal transplant recipients, other relatively potent immunosuppressant agents such as lymphocyte-depleting antibodies, which are frequently accompanied by a higher incidence of infections, are needed for rejection prophylaxis. CNI withdrawal and switching of the immunosuppressant regimen from CNI therapy to sirolimus may be an option for some pediatric renal transplant patients with less advanced graft function deterioration. Nevertheless, potential adverse events such as aggravation of proteinuria, hyperlipidemia, myelosuppression, and hypergonadotropic hypogonadism have to be considered, and controlled studies are lacking. At present, an immunosuppressant maintenance therapy composed of low-dose tacrolimus or ciclosporin (CNI minimization) and mycophenolate mofetil with low-dose corticosteroids appears to be the most promising strategy to adopt in pediatric renal transplant recipients at low or normal immunologic risk.
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PMID:Treatment strategies to minimize or prevent chronic allograft dysfunction in pediatric renal transplant recipients: an overview. 1987 24

Nurses and nurse practitioners require information on the health problems faced by aging HIV-infected adults. In this descriptive, cross-sectional study, we reviewed the electronic medical records of 1,478 adult patients seen in an HIV clinic between May 2006 and August 2007 to examine patterns of comorbidities, and immunological and clinical characteristics across each decade of life. With increasing age, patients were found to have lower HIV viral loads, more prescribed medications, and a higher prevalence of comorbid conditions, including coronary artery disease, hypertension, hypercholesterolemia, hypogonadism, erectile dysfunction, diabetes, peripheral neuropathy, hepatitis C, esophageal gastric reflux disease, and renal disease. Fortunately, with increasing age, patients were also more likely to have public or private health insurance and tended to be more compliant to medical appointments. With growing interest in aging with HIV, this study highlights the vastly different comorbidity profiles across decades of life, calling into question what constitutes "older" with HIV.
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PMID:Aging with HIV: a cross-sectional study of comorbidity prevalence and clinical characteristics across decades of life. 2047 64

The metabolic syndrome is one of several patterns of risk for atherosclerotic cardiovascular disease. Although the concept of the metabolic syndrome has been known for 2 centuries or more, it is only recently that its individual components have been proposed. Visceral obesity is a central component but other major facets such as hypertension, dyslipidemia, or dysglycemia are often present. These components are well-established cardiovascular risk factors and therefore grouping them under a single entity, namely the metabolic syndrome, has questioned its clinical usefulness and its ability to predict cardiovascular disease. Depending on what criteria are used, the prevalence of this syndrome may be as much as 40% in those aged 60 years and older. Heredity, environmental factors, personal lifestyle habits and behavior, and clinical comorbidities all seem to be associated with the metabolic syndrome. In addition, hypogonadism in men and hypovitaminosis D are age-related issues associated with the metabolic syndrome. In ageing individuals the existence of the metabolic syndrome as a distinct entity is questioned although some studies report an association with diabetes mellitus, physical impairments, and cognitive dysfunction. Further studies that explore these factors over time are needed but for now, treatment remains focused on individual components and not on the syndrome as a whole.
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PMID:The metabolic syndrome in older persons. 2049 45

There is a high prevalence of hypogonadism in the older adult male population and the proportion of older men in the population is projected to rise in the future. As hypogonadism increases with age and is significantly associated with various comorbidities such as obesity, type 2 diabetes, hypertension, osteoporosis and metabolic syndrome, the physician is increasingly likely to have to treat hypogonadism in the clinic. The main symptoms of hypogonadism are reduced libido/erectile dysfunction, reduced muscle mass and strength, increased adiposity, osteoporosis/low bone mass, depressed mood and fatigue. Diagnosis of the condition requires the presence of low serum testosterone levels and the presence of hypogonadal symptoms. There are a number of formulations available for testosterone therapy including intramuscular injections, transdermal patches, transdermal gels, buccal patches and subcutaneous pellets. These are efficacious in establishing eugonadal testosterone levels in the blood and relieving symptoms. Restoration of testosterone levels to the normal range improves libido, sexual function, and mood; reduces fat body mass; increases lean body mass; and improves bone mineral density. Testosterone treatment is contraindicated in subjects with prostate cancer or benign prostate hyperplasia and risks of treatment are perceived to be high by many physicians. These risks, however, are often exaggerated and should not outweigh the benefits of testosterone treatment.
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PMID:A practical guide to male hypogonadism in the primary care setting. 2051 42

Within endocrinology, the long-term management of Turner syndrome (TS) in adults is fast becoming a specialist subject in its own right. The complications of TS can affect every system in the body, and the main reason why it falls to endocrinologists to coordinate health care is that many features are clearly within the endocrine remit: hypothyroidism, diabetes, hypertension, osteoporosis, hypogonadism. Endocrinologists as general physicians can often cover surveillance of problems in other areas such as congenital heart disease, inflammatory bowel disease and deafness, calling upon specialist input only if the need arises. In this way, a simple 'one stop shop' can offer a well-woman service for women with TS in a cost-effective manner. Such a service requires a multidisciplinary approach.
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PMID:How do you monitor the patient with Turner's syndrome in adulthood? 2071 75


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