History Of Prostatic Hyperplasia Research Articles

ACUTE MESENTERIC ISCHEMIA: CASE REPORT

Acute mesenteric ischemia (AMI) is a rare cause for hospital admissions of abdominal pain with incidence of less than 0.1% but due to delay in diagnosis results in a high 40% to 80% mortality rate. Small intestine ischemia occurs due to blood supply interruption of the superior mesenteric artery (SMA) which can happen due to embolism, arterial or venous thrombosis or non occlusive ischemia. AMI is most commonly caused by SMA thrombosis, which is precipitated by dehydra­tion, low cardiac output and hypercoagulation, or SMA embolic occlusion, which mostly occurs due to acute myocardial infarction. We present a 74-year-old man who complained of acute chest pain and pressure, black stools that started 4 hours ago. The patient had a history of prostatic hyperplasia and aortic surgery complica­ted by intestinal necrosis. Computed tomography (CT) showed bleeding in the duodenum, which was stopped using adrenaline. Coronary angiography was performed after cessation of bleeding. The patient began to com­plain of severe abdominal pain. Abdominal and pelvic contrast CT showed SMA thrombosis. The patient un­derwent small intestine resection, ileostomy and cystos­tomy. Histopathological examination revealed ischemic and necrotic changes. Despite the treatment the patient died. Physicians should be aware of AMI as a possible cause of abdominal pain, especially in elderly patients with cardiovascular comorbidities. Contrast enhanced CT should be the first-line imaging modality for diffe­rential diagnosis. Thorough assessment of symptoms and risks, timely use of diagnostic and interventional measures can help to reduce high mortality.

An unusual cause of delayed hematoma after carotid endarterectomy: a case report

BackgroundNeck hematoma is a complication of carotid endarterectomy, usually occurring in the comparatively early stage postoperatively.Case presentationWe described a patient developing life-threatening hemorrhage and non-clotting hematoma at a comparatively later stage after CEA. DIC was diagnosed according to the lab results, and the patient underwent re-operation and was supported with blood products until the coagulopathy was corrected. The patient had a history of prostatic hyperplasia and experienced malaise during the hospitalization. Prostate cancer with bone metastases was diagnosed.ConclusionsThis case report describes a rare underlying cause of hematoma after CEA, which reminds us to pay attention to prostate symptoms or related medical history, especially malignancy, in surgical patients, which may result in severe complications.

Prevalence and heritability of benign prostatic hyperplasia and LUTS in men aged 40 years or older in Zhengzhou rural areas.

Benign prostate hyperplasia (BPH) is the most common disease among aging males, but no reports have addressed the prevalence of BPH in Zhengzhou. Therefore, we aimed to understand the prevalence of BPH in men aged 40 years or older in Zhengzhou's rural areas through a cross-sectional study and analyzed the correlation with epidemiologic factors and the heritability of the disease. A multistage sampling method was used to randomly select male respondents in Zhengzhou's rural areas. Men who were 40 years of age or older and their first-degree relatives were subjected to the International Prostate Symptom Score (IPSS) and related examinations. Heritability was calculated according to the prevalence of the first-degree relatives in the case and control groups. The prevalence of BPH was 10.04%. Its prevalence increased with age, from 2.17% in men aged 40-44 years to 31.11% in men aged 80 years or older. The average volume of the prostate was 17.16 ± 7.96 mL, and the average IPSS was 5.89 ± 5.91. The analysis of the correlation between the associated risk factors and BPH revealed that prostatitis and a history of prostatic hyperplasia were significant factors. Obesity, smoking, drinking, diabetes, and hypertension were not correlated with BPH. Of the 94 first-degree relatives of the cases, 53 had BPH (56.38%); of the 106 first-degree relatives of the controls, five had BPH (4.72%). Heritability appeared to account for 40.48% of BPH cases. The heritability of incomplete emptying, frequency, intermittency, urgency, weak stream, straining, and nocturia was 43.28, 71.37, 9.67, 5.67, 2.70, 53.36, and 19.12%, respectively. The total prevalence of BPH in men aged 40 years or older in Zhengzhou's rural areas was 10.04%, and the heritability of prostatic hyperplasia was 40.48%.

Prostate-specific antigen kallikrein is not a marker of non-ST elevation acute coronary syndrome

We have read with great interest the letter entitled “Prostatespecific antigen (PSA) kallikrein and acute myocardial infarction (AMI): Where we are. Where are we going?”, recently published by Patane S and Marte F [1] where the authors very concisely reviewed the role of the PSA in AMI. Currently, a growing interest has been directed towards PSA and the cardiovascular system [2]. The investigation of novel circulating serum and plasma biomarkers in patients with cardiovascular disease has been accelerating at a remarkable place. For example, a Medline search that uses the terms “biomarkers” and “acute coronary syndromes” (ACS) reveals an approximate doubled in the number of published reports during the 2-year interval from 2005 to 2006 compared with the period from 2003 to 2004. Although this expanding body of research has established firm evidence for the value of biomarkers, such as for diagnosis and risk assessment among patients with suspected ACS [3], it has also deluged the clinical and research communities with candidate biomarkers, very few of which are likely to survive the test of time as useful clinical tools [3]. It is thus increasingly important for researchers, manufacturers, regulators, and clinicians to critically appraise the value of new biomarkers as they emerge as candidates for further investigation and possible clinical application. PSA is a 33Kda single chain glycoprotein that was first identified in seminal plasma [4] andwas subsequently isolated from prostate tissue [5]. It has been identified as a member of the human kallikrein family of serine proteases [2] and was initially considered only as a marker for the detection of prostate cancer [6]. Recently, attention has been focused on PSA serum levels and the PSA unspecificity to prostate, semen, and gender has been demonstrated [2]. Increased PSA serum level, are a common finding in patients with nonprostatic illnesses including AMI [7–11]. In this line, we have conducted a pilot study to determine the ability of PSA to predict ACS. In contrast to previous published studies, our data do not support PSA as a biomarker of ACS. Since April 2010 to the end of December 2010 we included one hundred and ten male patients with a first non-ST elevation ACS (STEACS). Thirty three patients were excluded from analysis for the following reasons: history of adenocarcinoma of the prostate gland, n=11 and history of prostatic hyperplasia, n=22. Hence, the data from 77 patients were analyzed. We also recruited 55 apparently healthy men as controls. The study was approved by the local research ethics committee and all subjects gave written informed consent before study entry. We obtained venous blood samples to determine PSA. The assay for total PSA is based on microparticle enzyme immunoassay technology and was performed on the Abbott IMx System (Abbott Laboratories). The analytical sensitivity of this method was calculated to 0.02 ng/mL at the 95% confidence interval. Results of normally distributed continuous variables are expressed as the mean value± SD. Continuous variables with a non-normal distribution are presented as median value (interquartile interval) and qualitative variables are presented as frequencies. Analysis of normality of the continuous variables was performed with the Kolmogorov–Smirnov test. Differences between non-STEACS and control subjects were assessed by unpaired t test for continuous variables and χ testing was used for discrete variables. We assessed differences in PSA levels between non-STEACS and controls using a binary logistic regression analysis. This analysis was performed adjusting by age, given the known correlation between PSA levels and age. Differences were considered to be significant if the null hypothesis could be rejected with N95% confidence. The SPSS 11.5 statistical software package (SPSS Inc, Chicago, Illinois, USA) was used for all calculations. Baseline characteristics of subjects enrolled in the study are shown in the Table 1. There were significant differences between groups regarding age, hypertension, hypercholesterolemia and diabetes mellitus. Glucose levels were higher in patients than in controls. PSA levels did not differ between the non-STEACS group and control group after adjusting by age (1.17 [0.56-2.93] vs 1.01 [0.43-1.64]μg/L, P=0.79) (Table 1 and Fig. 1). In our study, we found that PSAmay not be an idealmarker for ACS. Crook et al. [12] have reported that mean serum PSA concentration during AMI was significantly lower on day 2 compared to days 1 or 3, suggesting that these results could reflect several factors, such as thrombolysis treatment, reduced physical activity, or an acute-phase response. In our study, PSA concentration was analyzed in the nonSTEACS group on day 3. Previous preliminary observations have

Occupational and Other Risk Factors for Clinically Overt Familial Amyloid Polyneuropathy

Amyloidosis is associated with the deposition of amyloid substance in various tissues of the body. In several forms of familial amyloid polyneuropathy, mutated transthyretin is the main fibril component. The disease is inherited as an autosomal dominant trait with onset in adult life, but few carriers develop symptoms. The aim of the present investigation was to screen for additional factors that might be necessary for the development of familial amyloid polyneuropathy. We conducted a case-control study involving 51 male and 30 female cases of clinically overt familial amyloid polyneuropathy and 306 male and 317 female population controls. We considered occupational exposures, disease histories, and medical treatments as potential determinants of risk for clinically overt disease. We found an odds ratio of 5.4 for dressmakers. Low and high levels of exposure to organic solvents resulted in an odds ratio of 2.1 and 11.8, respectively. A history of prostatic hyperplasia, cholecystic disease, or appendectomy was also a risk factor, possibly as a consequence of anesthesia.