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)

Genes for the small human glandular kallikrein gene family were isolated. Members of this family include renal/pancreatic kallikrein, prostate-specific antigen and a kallikrein encoded by the first gene that was isolated and completely sequenced, hGK-1. All share strong nucleotide sequence homology, although hGK-1 and the prostate-specific antigen gene are more closely related (86% identity in coding nucleotides). Renal/pancreatic kallikrein has 77% nucleotide homology to prostate-specific antigen, but only 60% amino acid homology. There is strong homology in the 5'-flanking DNA with mouse kallikrein genes, suggesting common regulatory mechanisms. In the rat one-kidney, one clip model of hypertension, renal kallikrein messenger (m)RNA increased during the initial transient rise in plasma renin, and then decreased.
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PMID:Kallikrein genes: cloning in man and expression in rat renal hypertension. 324 Dec 25

The Behavioral Risk Factor Surveillance System (BRFSS) is widely used by state health agencies to measure the prevalence of chronic disease risk factors. We completed a test-retest study to assess the reliability of the Missouri Behavioral Risk Factor Surveillance System. We conducted telephone reinterviews for 222 respondents of completed Behavioral Risk Factor Surveillance System interviews from March and April 1993. The second interview was completed between 6 and 30 days after the first interview. Agreement was high for sociodemographic variables (kappa values from 0.85 to 1.00). Reliability of information on chronic conditions and risk factors was also high, with kappa values from 0.82 for hypertension to 1.00 for current smoking status. Regarding cancer screening practices, reliability was lower for knowledge of the prostate-specific antigen test (kappa = 0.21) than for women's cancer screening practices (that is, the mammogram and Papanicolaou smear). Questions on attitudes toward environmental tobacco smoke showed lower reliability than did questions on individual actions to reduce exposure to environmental tobacco smoke.
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PMID:Reliability of information on chronic disease risk factors collected in the Missouri Behavioral Risk Factor Surveillance System. 798 71

The first vasectomy operation was carried out 100 years ago in patients with prostate hyperplasia with symptoms. Then it became extensively used for hereditary hygiene purposes/eugenics, especially after the passing of the sterilization law in Denmark in 1935. In Nazi Germany, vasectomies and castrations were also used for forced sterilization of undesired races. Vasectomy has become a popular method of fertility control, especially in the US. In Denmark it is also popular, and since the 1973 sterilization law, approximately 100,000 procedures have been performed with a 95% rate of satisfaction. Vasectomy seems not to be as harmless as previously thought. The blockage of the transport route from the testes does not stop spermatogenesis. Spermatozoa are a certain kind of foreign matter which are first produced in puberty and act as antigens vis-a-vis other organisms. Certain immune complexes are formed that can have implication for a number of autoimmune diseases. Later in life vasectomy can be a potentiating factor in arteriosclerosis according to rhesus monkey experiments. Men with hypertension, hyperlipidemia, or heavy smokers should not undergo vasectomy. On the other hand, a 1990 epidemiological study showed no increased risk of cardiovascular diseases in vasectomized men. Yet the immune complexes could have other, more serious biological consequences. In large cohort studies the connection to testicular cancer has not been proven with certainty, but there may be an increased risk of prostate cancer among the vasectomized. The American Urological Association (AUA) has recently recommended that men over 40 who had been vasectomized should undergo examination and tests for prostate-specific antigen every year for early detection of cancer. There has been no indication of an increased mortality from prostate cancer among vasectomized men in the above epidemiological studies, but the AUA advises counseling patients about the possible connection.
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PMID:[Vasectomy]. 800 96

This study assessed the survival of a nationally representative sample of older Canadian men, taking into account common comorbid conditions. Mortality follow-up between 1978 and 1989 was conducted for male participants of the Canada Health Survey who were at least 60 years of age at baseline. The proportional hazards model and life table methods were used to examine survival by comorbidity status. Comorbid conditions examined included history of stroke and/or heart disease, high blood pressure, chronic bronchitis or emphysema, diabetes and smoking status, but excluded cancer because of small numbers. For those subjects aged 80 and older, comorbidity was not a significant predictor of survival. A large portion of men between the ages of 60 and 79, even those with pre-existing comorbid conditions, survived at least 10 years after interview. In a clinical setting, more detailed information on comorbid conditions can be obtained to better estimate long-term survival. Notwithstanding, our findings may have implications for the administration of population-based health interventions (e.g. the use of prostate-specific antigen [PSA] blood tests for the early detection of prostate cancer). In particular, our results suggest that there may be little benefit in restricting access to PSA screening based on survival probability in men under age 80.
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PMID:Comorbid survival among elderly male participants of the Canada health survey: relevance to prostate cancer screening and treatment. 982 Aug 31

A 70-year-old man is referred to a urologist for recommendations on the management of metastatic prostate cancer. His cancer was diagnosed 5 years ago, and he underwent radical prostatectomy at that time. The tumour was confined to the prostate gland (Gleason score 7), and during surgery the lymph nodes were assessed as being clear of cancer. Before the surgery, the patient's prostate-specific antigen (PSA) level had been 8 ng/mL. After the prostatectomy, PSA was at first undetectable, but recently the PSA level rose to 2 ng/mL and then, at the most recent test, to 16 ng/mL. A bone scan was ordered to investigate back discomfort, which has been persistent but easily controlled with acetaminophen. Unfortunately, the bone scan shows several sites of metastatic disease. The man's medical history includes type 2 diabetes, which has developed during the past 3 years and which is controlled by diet, as well as asymptomatic hypertension, which is managed by means of a thiazide diuretic. The patient asks what treatments are available, what impact they are likely to have on his disease and what risks are associated with the therapies.
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PMID:Prostate cancer: 9. Treatment of advanced disease. 995 46

The purpose of this study was to test the hypothesis of a causal relationship between high insulin levels and the development of benign prostatic hyperplasia (BPH) and to determine the clinical, anthropometric, metabolic and insulin profile in men with fast-growing BPH compared with men with slow-growing BPH. The present study was designed as a risk factor analysis of BPH in which the estimated annual BPH growth rate was related to components of the metabolic syndrome. Two hundred and fifty patients referred to the Urological Section, Department of Surgery, Central Hospital, Varberg, Sweden, with lower urinary tract symptoms with or without manifestations of the metabolic syndrome were consecutively included. The prevalences of atherosclerotic disease manifestations, non-insulin-dependent diabetes mellitus (NIDDM) and treated hypertension were obtained. Data on blood pressure, waist and hip measurement, body height and weight were collected and body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn from fasting patients to determine insulin, total cholesterol, triglycerides, HDL and LDL cholesterol, uric acid, alanine aminotransferase (ALAT) and prostate-specific antigen (PSA). The prostate gland volume was determined using ultrasound. The median annual BPH growth rate was 1.04 ml/year. Men with fast-growing BPH had a higher prevalence of NIDDM (p = 0.023) and treated hypertension (p = 0.049). These patients were also taller (p=0.004) and more obese as measured by body weight (p<0.001), BMI (p=0.026), waist measurement (p <0.001), hip measurement (p = 0.006) and WHR (p=0.029). Moreover, they had elevated fasting plasma insulin levels (p = 0.018) and lower HDL cholesterol levels (p = 0.021) than men with slow-growing BPH. The annual BPH growth rate correlated positively with diastolic blood pressure (rs = 0.14; p = 0.009), BMI (rs = 0.24; p < 0.001) and four other expressions of obesity and fasting plasma insulin level (rs = 0.18; p = 0.008), and negatively with the HDL cholesterol level (rs = -0.22; p = 0.001). In conclusion, the data suggest that NIDDM, hypertension, tallness, obesity, high insulin and low HDL cholesterol levels constitute risk factors for the development of BPH. The results also suggest that BPH is a component of the metabolic syndrome and that BPH patients may share the same metabolic abnormality of a defective insulin-mediated glucose uptake and secondary hyperinsulinaemia, as patients with the metabolic syndrome. The findings support the hypothesis of a causal relationship between high insulin levels and the development of BPH, and give rise to a hypothesis of increased sympathetic nerve activity in men with BPH.
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PMID:Clinical, anthropometric, metabolic and insulin profile of men with fast annual growth rates of benign prostatic hyperplasia. 1041 80

Prostatic infarcts are uncommon and in the past have only been reported on transurethral resections of the prostate. We reviewed 13 consults and 2 nonconsult cases of needle biopsies showing prostatic infarcts from two institutions. The incidence of infarcts on biopsy were 2 in 2958 (0.07%) and 1 in 108,586 (0.0009%) in our nonconsult cases. Men averaged 71 years of age (range, 57-84 yrs). No relationship was seen with histories of hypertension, diabetes, atherosclerotic coronary vascular disease, recent surgery, and steroid use. Four of 12 men with available information had acute urinary retention, with markedly enlarged prostates in three (90 cc, 92 cc, 94 cc); two of these men had hematuria. An additional two men also had large glands (84 cc, 150 cc), one also with hematuria. Of eight men without acute urinary retention, three had sudden prostate-specific antigen (PSA) rises (increases of 199 ng/mL, 219 ng/mL, 287 ng/mL). Infarcts were usually an isolated focus on one core and varied from 1 mm to 11 mm (mean, 6.3 mm). Six cases showed earlier-aged infarcts with coagulative necrosis and recent hemorrhage and six showed intermediate-aged infarcts with reactive stroma and epithelium without necrosis. In the remaining three cases, there were remote infarcts characterized by replacement of the stroma by dense fibrosis with metaplastic glands. Adjacent tissue revealed reactive nests of immature squamous metaplasia in 14 of 15 cases with visible nucleoli (12 cases), squamous atypia (7 cases), and mitoses ranging from 1-10 (7 cases). Pathologists sent in 10 of 13 consult cases (77%) for problems with interpretation of the infarcts; remaining consults had other pathology of concern. One case was misdiagnosed as urothelial cancer. Features helpful in recognizing infarcts' benign nature were cyst formation containing cellular debris with or without neutrophils (73%), corpora amylacea (20%), and rings of collagen around squamous islands (40%). Infarcts are typically, although not exclusively, found in large prostates and may result in sudden rises in serum PSA. Infarcts' distinctive histology must be recognized and distinguished from necrosis resulting from infection and prior cryotherapy, as we have seen such misdiagnoses. Pathologists' awareness of prostatic infarcts on needle biopsy and their potential for atypical histology can prevent the misdiagnosis of cancer.
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PMID:Infarct of the prostate gland: experience on needle biopsy specimens. 1102 99

We describe a 72-year-old man with prostate enlargement, prostate-specific antigen level of 35 ng/dl, mild polyarthritis, and constitutional symptoms. Prostatic ultrasonography suggested neoplasm; however, transrectal biopsy revealed findings consistent with polyarteritis nodosa (PAN). The patient went on to develop leg paresthesia and dysesthesia, increased serum creatinine, and systemic hypertension. Steroids and intravenous cyclophosphamide were administered, followed by improvement. Our case emphasizes the protean onset of PAN, and provides a new differential diagnosis of prostatic diseases related to elevated prostate-specific antigen.
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PMID:Polyarteritis nodosa mimicking prostatic cancer. 1103 51

The current trends in favor of androgen deprivation therapy (ADT) for nonmetastatic prostate cancer at the stage of biochemical recurrence or increasing prostate-specific antigen (PSA) raises the issue of exposing otherwise asymptomatic patients to potential side effects over the longer term. Some of these side effects can have deleterious effects on quality of life, and others may contribute to increased risks for serious health concerns associated with aging. Sexual side effects are the most well-recognized adverse effects from ADT and include loss of libido, erectile dysfunction (ED), and hot flashes. Loss of libido is distressing to many men, and they may not pursue treatments for ED. However, for those who do maintain sexual interest, various remedies are available. The incidence of hot flashes, which may not abate over the course of ADT, is close to 80%. Estrogens, progestin megestrol acetate, medroxyprogesterone acetate, venlafaxine, and cyproterone acetate have been shown to alleviate hot flashes and associated symptoms. Physiologic effects, including gynecomastia, changes in body composition (weight gain, reduced muscle mass, increase in body fat), and changes in lipids, are less commonly recognized as side effects of ADT. These may lead to an exacerbation of potentially more serious conditions, such as hypertension, diabetes, and coronary artery disease. Loss of bone mineral density, anemia, and hair changes also may occur. Additionally, both the diagnosis of prostate cancer and the hormonal therapy can cause psychological distress. These side effects need more systematic study in clinical trials. Physicians should be aware of far-reaching consequences of ADT and should incorporate strategies for preventing and managing toxicities into routine practice.
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PMID:Side effects of androgen deprivation therapy: monitoring and minimizing toxicity. 1266 85

Previous studies have suggested that hyperinsulinaemia and other components of metabolic syndrome are risk factors for clinical prostate cancer. This prospective study tested the hypothesis that hyperinsulinaemia and other components of metabolic syndrome are risk factors for lethal clinical prostate cancer. The clinical, haemodynamic, anthropometric, metabolic and insulin profile at baseline in men who had died from clinical prostate cancer during follow-up was compared with the profile of men who were still alive at follow-up. If the hypothesis is true, men with an unfavourable prognosis would have a higher profile at baseline than those with a favourable prognosis. A total of 320 patients in whom clinical prostate cancer, stages T2-3, had been diagnosed were consecutively included in the study during 1995-2003. Height, body weight, waist measurement, hip measurement and blood pressure were determined. Body mass index and waist/hip ratio (WHR) were calculated. Blood samples were collected to determine triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, uric acid, alanine aminotransferase and fasting plasma insulin level. The prostate gland volume was measured using transrectal ultrasound. The annual benign prostatic hyperplasia (BPH) growth rate was calculated. The diagnosis of prostate cancer was established using transrectal ultrasound-guided automatic needle biopsy of the prostate gland. All patients with clinical prostate cancer were followed up until their death or until the study was terminated on 31 December 2003. At follow-up, 54 patients had died from prostate cancer and 219 were still alive. The results showed that the men who died of clinical prostate cancer during the follow-up period were older (P < 0.001), had a larger prostate gland volume (P < 0.001), a faster BPH growth rate (P < 0.001), a higher prevalence of type 2 diabetes (P < 0.035) and treated hypertension (P < 0.023), a higher stage (P < 0.001) and grade (P = 0.028) of clinical prostate cancer, a higher prostate-specific antigen (PSA) level (P < 0.001) and a higher PSA density (P < 0.001) at baseline than men still alive with clinical prostate cancer at follow-up. These men also had a lower HDL-cholesterol level (P = 0.027), a higher fasting plasma insulin level (P = 0.004), a higher WHR (P = 0.097) of borderline significance and a higher uric acid level (P = 0.079) of borderline significance. Eliminating the effect on mortality of higher stage and grade of the clinical prostate cancer and PSA at baseline, the following statistically significant correlations remained: a higher fasting plasma insulin level (P = 0.010) and a lower HDL-cholesterol level of borderline significance (P = 0.065). In conclusion, hyperinsulinaemia and five other previously established components of metabolic syndrome are shown to be prospective risk factors for deaths that can be ascribed to prostate cancer. These findings confirm previous study, which indicate that prostate cancer is a component of metabolic syndrome. Moreover, these data indicate that hyperinsulinaemia and other metabolic disorders precede deaths caused by prostate cancer. Thus, our data support the hypothesis that hyperinsulinaemia is a promoter of clinical prostate cancer. Furthermore, our data suggest that the insulin level could be used as a marker of prostate cancer prognosis and tumour aggressiveness, regardless of the patient's prostate cancer stage, cancer grade and PSA level.
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PMID:Hyperinsulinaemia: a prospective risk factor for lethal clinical prostate cancer. 1624 13


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