Bladder calculus, as one of the most common complications of BPH, the incidence is approximately 10% [1]. BOO, urinary tract infection, neurogenic bladder, bladder diverticula, bladder augmentation, or the bladder foreign body have been shown may be associated with the occurrence of bladder calculus [12]. Combining bladder stones is also an absolute surgical indication of BPH. In undeveloped areas, many patients with BPH hesitate to receive surgical treatment, insisting on drug conservative treatment even when bladder calculus has formed, which causes great harm to physical health and severely affects the quality of life during disease progression. Researchers have been troubled by the problem of why some BPH patients have a higher possibility accompany bladder calculus for many years. Though few studies have explored some risk factors of bladder calculus formation in patients with BPH, which indicated IPP seems to be the most important potential risk factor, the result is still uncertain [9, 10].
In this study, we aimed to determine the risk factor that influences the presence of bladder calculus in patients with BPH.
The concept of IPP was proposed by Jean Casimir Félix Guyon in 1888 in Paris [13]. After two centuries of research, IPP has emerged as a novel prostatic morpho-metric parameter of significance to help the clinicians in many aspects of managing the patients with some diseases of the lower urinary tract and the prostate [14]. Topazio et al found that IPP was significantly and inversely correlated with treatment success in patients with lower urinary tract symptoms (LUTS) and BPH under alpha-blockers therapy. IPP can be used as a predictor of alpha-blockers response [15]. A recent study indicated that IPP was a good predictor of clinically significant BOO due to BPH [16]. Lee also showed that even in men with good flow, high grades of IPP were more likely to have BOO [17]. Lim et al reported that a long IPP would cause BOO by creating a “ball-valve” effect during voiding, which destroy the funneling effect of the bladder neck [18]. Chia et al also demonstrated that IPP was caused by the enlarging lateral lobes and the median lobe, and that the protrusion of the enlarged lobes caused a “ball-valve” type of obstruction, thus disrupting the funneling effect of the bladder neck and causing dyskinetic movement of the bladder during voiding [19]. In this study, the mean length of the IPP was 12.7 mm in group 1 and 9 mm in group 2. The statistically significant association between these two groups shows that IPP was a risk factor for bladder calculus formation in BPH patients. In a prospective clinical study, Mariappan et al indicated that IPP can be divided into three levels based on the length of the IPP [20]. Grade I, the length of IPP was less than 5 mm; Grade II, the length of IPP was 5 to 10 mm; and Grade III, the length of IPP was longer than 10 mm. In our study, all patients in group 1 and 2 were classified into Grade II and III.
ROC curve revealed that the cut-off value of IPP that caused the highest risk of bladder calculus formation was 11.5 mm. Kim et al reviewed data of 271 BPH patients, the median length of IPP was 11.5 mm in patients combing with bladder stones, while the average length was 3.4 mm in patients without bladder stones [9]. In another study, the median length of IPP was 11 mm in BPH patients with bladder calculus, while 4 mm in patients without calculus [10]. Lu et al indicated that, for IPP, the cut-off value of the highest risk of hydronephrosis was 1.95 cm. Interestingly, the median length of IPP in their study receiving TURP was longer than ours [11]. In our study, the length of all IPP was ≥ 5 mm, and all patients received surgical intervention. These results make the length of IPP ≥ 5 mm the potential to become a novel indication for TURP surgery. Inconsistent with previous studies, univariate, multivariate analyses, and the ROC curve indicated that IPP was an important independent risk factor for the presence of bladder calculus in BPH patients [9, 10].
AUR is a urological emergency, it usually presents as a sudden inability to urinate with the symptom of lower abdominal pain [21]. The risk is cumulative and increases with age. About 10% of old men in their 70 s and 30% in their 80 s will develop AUR within 5 years [22]. AUR is significantly associated with morbidity, mortality, and cost to the public health service. On the basis of the guidelines of the European Association of Urology, initial management of AUR should consist of bladder decompression with an indwelling catheter followed by trial without catheter [23]. The pathogenesis of AUR can be multifactorial. Chen et al revealed that BPH causes the most AUR, and the incidence is estimated to be as high as 53% [24]. AUR is also associated with bladder calculus. When bladder calculus causes posterior urethral obstruction, AUR also occurs. A common manifestation in children is interrupted urination, and urination can continue after changing positions or rubbing the penis. In our study, the AUR rate was significantly higher in group 2 than in group 1. 3 patients (9.1%) in group 1 had AUR, while 21 patients (30%) in group 2 had AUR. The results of our study showed that AUR was an independent risk factor for the occurrence of bladder calculus in patients with BPH. Further ROC curve demonstrated that AUR was the second most important risk factor compared with IPP. A similar AUR rate was also found in a previous study. Huang et al reported that the AUR rate was 10.6% in patients with BPH and bladder calculus, lower than 37.4% in patients with BPH. However, AUR was not an independent risk factor in their study [10]. Confusingly, in spite of bladder calculus or BPH can cause AUR, the AUR rate in group 1 was lower. We hypothesized that it may be attributed to patients with BPH developed AUR early and received standardized medications, the probability of complications with bladder stones was greatly reduced. From our perspectives, severe BPH symptoms and no history of AUR may be an important sign of combining with bladder calculus. Due to the limited number of patients in our study, further studies are still warranted to be explored this problem.
Now few studies have focused on the relationship between serum creatinine and bladder calculus. Univariate analyses showed serum creatinine was a potential risk factor, however, multivariate analyses revealed that it was not an independent risk factor in comparison with IPP and AUR. A lower level of serum creatinine was found in group 1. Li et al indicated that lower levels of serum creatinine and uric acid, and lower percentages of diabetes mellitus were local factors in the formation of bladder uric acid stone [25]. Interestingly, the level of uric acid was also lower in group 1, though results showed it was not an independent risk factor. Older age and higher rates of urinary tract infection have also been considered as independent risk factors in previous studies [9, 10]. In our study, patients in group 1 were a little younger and the rate of urinary tract infection was a little higher than patients in group 2. However, age and urinary tract infection were proven not to be independent risk factors. Moreover, our results also first demonstrated that serum albumin, hemoglobin, diabetes, hypertension, smoking, and drinking were not independent risk factors for the occurrence of bladder calculus in patients with BPH.
The limitations of this study should be noted. First, it has a retrospective design with a relatively small sample size and its inherent retrospective and non-randomized nature may have led to selection bias. Second, all patients enrolled in our study were Chinese, so we cannot eliminate the influence of ethnic diversity. Third, all patients did not have accurate uroflow parameters and urodynamic results, making the study hard to further exploring whether urodynamic indicators are risk factors. A prospective randomized controlled trial is urgently needed in the future.