ABSTRACT
BACKGROUND: Changing voiding patterns, volume and frequency, may sometimes be mistaken for anxiety, stress or increase in fluid consumption. In the aging male population, the commencement of lower urinary tract symptoms (LUTS) may be silent and perceived as "normal" and unrelated to Benign prostatic enlargement (BPE). The purpose of the study was to determine the prevalence of apparently "silent LUTS" (perceived asymptomatic LUTS) in men in a Ghanaian Community as well as its underlying risk factors. METHODS: One hundred and eleven (111) men (40-70 years) were recruited from a community in Ghana. The International Prostate Symptoms Score (IPSS) questionnaire (administered in the local language and English) and ultrasonographic imaging of the prostate volume (PV) were utlized to collect data. IPSS score >7 plus PV > 30 cm3 was definitive of lower urinary tract symptoms. Eighty-one (81) participants were classified "LUTS Negative" (LN) and 30, "LUTS Positive" (LP). Risk factors i.e., cholesterol (CHOL), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), very low-density lipoprotein (VLDL), coronary risk (CR), BMI and Blood Pressure were also determined. RESULTS: The prevalence of LUTS using only IPSS definition alone was 42.3%. However, IPSS in combination with Prostate Volume gave a prevalence of 27.0%. LN subjects had enlarged prostate (41.98%) and LP, 100%. Quality of life (QoL) was better in the LUTS Negative than LUTS Positive group (p < 0.001). In the univariant analysis coronary risk, triglyceride and VLDL contributed to LUTS (p = 0.023, 0.22, 0.22, respectively). In a multivariant analysis HDL-C (p = 0.027), BMI (p = 0.047) and triglyceride (p = 0.019) significantly contributed to LUTS. CONCLUSIONS: The prevalence of LUTS (42.3%) is high. Components of Metabolic Syndrome- HDL-C, BMI, and coronary risk were associated with LUTS. This emphasizes the need for community education.
ABSTRACT
BACKGROUND: Oxidative stress and antioxidants have been implicated in many diseases including prostate cancer and benign prostatic hyperplasia (BPH). Lipid peroxidation contributes to oxidative stress. However, new and emerging antioxidants such as paraoxonase 1 (PON1) and arylesterase (ARE) associated with lipoprotein peroxidation have not been examined in BPH patients. PON1 and ARE, a high-density lipoprotein (HDL) cholesterol-bound enzyme system of antioxidants, protect low-density lipoprotein (LDL) cholesterol and HDL from oxidation by hydrolysis. The study primarily determined paraoxonase (PON1) and ARE activities in BPH treatment-naïve patients. MATERIALS AND METHODS: Sixty newly diagnosed patients (treatment-naïve) alongside 30 apparently healthy controls were recruited. Blood examinations included lipid profile (total cholesterol, triglycerides, LDL, HDL), glutathione peroxidase, PON1, ARE, and prostate specific antigen (PSA).Prostate volume and International Prostate Symptoms Score (IPSS) were determined. RESULTS: PSA was significantly different between patient and control groups (P < 0.0001). Total cholesterol, triglycerides, and LDL were significantly higher in the patient group (P = 0.002, P < 0.001, P = 0.003, respectively). Glutathione peroxidase was very low in the patient group compared to the control group (5.65 ± 2.30 ng/mL and 17.43 ± 10.98 ng/mL, respectively). Although PON1 was higher in the patient group (50.22 ± 19.68/61.30 ± 29.55 ng/mL; P > 0.05), ARE was significantly lower in the patient group (61.31 ± 21.76/49.30 ± 19.82 ng/mL; P = 0.0098). No correlation was established between antioxidants and the lipid profile except for the LDL and PON1 patient group (r = 0.1486, P = 0.0374). Similarly, a weak correlation was also established between PSA and LDL in the patient group (r = -0.275, P = 0.033). PON1/HDL ratio was not significantly different. However, the ARE/HDL ratio was significantly lower in the patient group (P < 0.0001). CONCLUSION: These results signify the presence of a higher lipoprotein peroxidation activity and lower lipid-associated antioxidant activity in the patient group. The ARE/HDL ratio is a better indicator of the HDL associated antioxidant than the PON1/HDL ratio or the individual antioxidants (PON1 and ARE) as reported by others.
ABSTRACT
Background: Croton membranaceus extract has apoptotic effects on BPH-1 cells. This study determined if the apoptotic effects were created through the ceramide pathway. Methods: The study was a follow-up to a previous observational study of 30 histologically confirmed patients with benign prostatic hyperplasia (BPH) who were on C. membranaceus ethanolic extract at 20 mg t.i.d orally for 3 mo. Thereafter, total and free prostate-specific antigen (PSA), lipid profile plus Apo lipoprotein A and B, ceramide/Sphingophospho-kinase 1 (SphK1) and 2 (SphK2), sphingosine lyase (SPL), the cytotoxic adducts of oxidative stress 4-hydroxy-2-nonenal (4HNE) and malondialdehyde (MDA), were determined. Results: Total and free PSA were significantly (p < 0.05) different after treatment. Apo lipoprotein A was significantly different (p = 0.024). The SphK1/SphK2 ratio reduced significantly (p = 0.049). Furthermore, SPL, ceramide, and MDA increased significantly after treatment (p = 0.05, p = 0.004, and p = 0.007, respectively). A weak positive correlation was found between high-density lipoprotein (HDL) cholesterol and SphK1, and HDL and ceramide before treatment (p = 0.036, r = 0.3826; p = 0.018, r = 0.4286, respectively. Conclusions:C. membranaceus uses the ceramide pathway by modulating the SphK1/SphK2 ratio and increasing SPL to generate oxidative stress and consequently apoptosis.
ABSTRACT
ETHNOPHARMACOLOGICAL RELEVANCE: Croton membranaceus leaf extracts are used in the Bahamas to aromatize tobacco. In Nigeria it is used to improve digestion and in Ghana, the root extract is used for the treatment of benign prostatic hyperplasia (BPH). Despite claims of efficacy no data exists to support this. The aim of this study was to determine if Croton membranaceus aqueous root extract (CMARE) could attenuate the development of BPH in an animal model. MATERIALS AND METHODS: Fifty (50) adult male Sprague-Dawley rats weighing 200-250g were randomly divided into 5 groups. Group 1 served as the control and received normal saline p.o. Groups 2-5 were castrated and injected with 5mg/kg b.wt. testosterone propionate subcutaneously for 28 days. Group 2 (model group) had no further treatment. Group 3 was simultaneously given 0.5mg/kg b.wt. finasteride p.o. throughout. Groups 4 and 5 received 30mg/kg b.wt. [low dose (LD)] and 300mg/kg b.wt. [high dose (HD)] CMARE, respectively, for 28 days. Rats were sacrificed at the end of the study and all prostate organs harvested. Wet weights, volumes and prostatic index (PI) were determined. Tissues were histologically examined. Serum prostate specific antigen (PSA) and dihydrotestosterone (DHT) levels were determined. RESULTS: Prostate volume of the control group was 0.67±0.23cm(3). The model, finasteride, CMARE LD and HD groups had the following volumes: 0.92±0.12, 0.84±0.16, 0.79±0.16 and 0.80±0.19cm(3), respectively. Only the model group showed significant statistical differences with the control (p=0.007). PI for control, model, finasteride, LD and HD groups was as follows: 0.19±0.04, 0.30±0.04, 0.25±0.04, 0.21±0.05 and 0.22±0.05. No statistical differences between the control PI and the CMARE treated groups were observed. Histologically, the model group had massive growth of columnar stromal and epithelial cells. CMARE and finasteride attenuated this growth with a resultant thin layer of stromal and epithelial cells similar to the control. PSA levels were significantly lower in the treatment groups. CONCLUSION: CMARE reduces stromal and epithelial cell growth, and subsequently shrinks enlarged prostate. This is the first scientific proof validating the anecdotal evidence of CMARE efficacy in the management of BPH.
