XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.

Standards of Medical Care in Diabetes

Section I: Anatomy Surgical Anatomy of the Retroperitoneum, Kidneys, and Ureters Anatomy of the Lower Urinary Tract and Male Genitalia Section II: Clinical Decision Making Evaluation of the Urologic Patient: History, Physical Examination, and Urinalysis Urinary Tract Imaging: Basic Principles Outcomes Research Section III: Basics of Urologic Surgery Basic Instrumentation and Cystoscopy Basics of Laparoscopic Urologic Surgery Section IV: Infections and Inflammation Infections of the Urinary Tract-A. Schaeffer Inflammatory Conditions of the Male Genitourinary Tract Interstitial Cystitis and Related Disorders Sexually Transmitted and Associated Diseases Urological Implications of AIDS and Related Conditions Cutaneous Diseases of the External Genitalia Tuberculosis and Other Opportunistic Infections of the Genitourinary System Section V: Molecular and Cellular Biology Basic Principles of Immunology Molecular Genetics and Cancer Biology Tissue Engineering Perspectives for Reconstructive Surgery Section VI: Reproductive and Sexual Function Male Reproductive Physiology Male Infertility Surgical Management of Male Infertility Physiology of Erectile Dysfunction: Pathophysiology, Evaluation, Nonsurgical Management Epidemiology, Evaluation, and Nonsurgical Management of Erectile Dysfunction Prosthetic Surgery for Erectile Dysfunction Vascular Surgery for Erectile Dysfunction Peyronie's Disease Priapism Androgen Deficiency in the Aging Male Female Sexual Function and Dysfunction Section VII: Male Genitalia Neoplasms of the Testis Surgery of Testicular Tumors Tumors of the Penis Surgery of Penile and Urethral Carcinoma Surgery of the Penis and Urethra Surgery of the Scrotum and Seminal Vesicles Section VIII: Renal Physiology and Pathophysiology Renal Physiology and Pathophysiology Renovascular Hypertension Section IX: Upper Urinary Tract Obstruction and Trauma Pathophysiology of Obstruction Management of Upper Urinary Tract Obstruction Upper Urinary Tract Trauma Section X: Renal Failure and Transplantation Renal Transplantation Etiology, Pathogenesis, and Management of Renal Failure Section XI: Urinary Lithiasis and Endourology Urinary Lithiasis: Etiology, Epidemiology, and Pathophysiology Evaluation and Medical Management of Urinary Lithiasis Surgical Management of Upper Urinary Tract Calculi Ureteroscopy and Retrograde Ureteral Access Percutaneous Approaches to the Upper Urinary Tract Section XII: Neoplasms of the Upper Urinary Tract Renal Tumors Urothelial Tumors of the Upper Urinary Tract Urothelial Tumors of the Renal Pelvis and Ureter Open Surgery of the Kidney Laparoscopic Surgery of the Kidney Ablative Therapy for Renal Tumors Section XIII: The Adrenals Pathophysiology, Evaluation, and Medical Management of Adrenal Disorders Surgery of the Adrenals Section XIV: Urine Transport, Storage, and Emptying Physiology and Pharmacology of the Renal Pelvis and Ureter Physiology and Pharmacology of the Bladder and Urethra Pathophysiology, Categorization, and Management of Voiding Dysfunction Urodynamic and Video dynamic Evaluation of Voiding Dysfunction Neuromuscular Dysfunction of the Lower Urinary Tract Urinary Incontinence: Epidemiology, Pathophysiology, Evaluation, and Overview of Management The Overactive Bladder Pharmacologic Management of Storage and Emptying Failure Conservative Management of Urinary Incontinence: Behavioral and Pelvic Floor Therapy, Urethral and Pelvic Devices Electrical Stimulation and Neuromodulation in Storage and Emptying Failure Retropubic Suspension Surgery for Incontinence in Women Vaginal Reconstructive Surgery for Sphincteric Incontinence Pubovaginal Slings Tension-Free Vaginal Tape Procedures Injection Therapy for Urinary Incontinence Additional Treatment for Storage and Emptying Failure Geriatric Voiding Dysfunction and Urinary Incontinence Urinary Tract Fistulae Bladder and Urethral Diverticula Surgical Procedures for Sphincteric Incontinence in the Male: The Artificial Genitourinary Sphincter Perineal Sling Procedures Section XV: Bladder Lower Genitourinary Calculi and Trauma Urothelial Tumors of the Bladder Management of Superficial Bladder Cancer Management of Metastatic and Invasive Bladder Cancer Surgery of Bladder Cancer Laparoscopic Bladder Surgery Use of Intestinal Segments in Urinary Diversion Cutaneous Continent Urinary Diversion Orthotopic Urinary Diversion Genital and Lower Urinary Tract Trauma Lower Urinary Tract Calculi Section XVI: Prostate Molecular Biology, Endocrinology, and Physiology of the Prostate and Seminal Vesicles Etiology, Pathophysiology, and Epidemiology of Benign Prostatic Hyperplasia Natural History, Evaluation, and Nonsurgical Management of Benign Prostatic Hyperplasia Minimally Invasive and Endoscopic Management of Benign Prostatic Hyperplasia Retropubic and Superpubic Open Radical Prostatectomy Epidemiology, Etiology, and Prevention of Prostate Cancer Pathology of Prostatic Neoplasms Ultrasonography and Biopsy of the Prostate Tumor Markers in Prostate Cancer Early Detection, Diagnosis, and Staging of Prostate Cancer Definitive Therapy of Localized Prostate Cancer: Outcomes Expectant Management of Prostate Cancer Anatomic Retrograde Retropubic Prostatectomy Radical Perineal Prostatectomy Laparoscopic and Robotic Radical Prostatectomy and Pelvic Lymphadenectomy Radiation Therapy for Prostate Cancer Cryotherapy of Prostate Cancer Treatment of Locally Advanced Prostate Cancer Management of Rising Prostate-Specific Antigen after Definitive Therapy Hormonal Therapy for Prostate Cancer Management of Hormone-Resistant Prostate Cancer Section XVII: Pediatric Urology Normal and Anomalous Development of the Urinary Tract Renal Function in the Fetus Congenital Obstructive Uropathy Perinatal Urology Evaluation of Pediatric Urologic Patient Renal Disease in Childhood Urinary Tract Infections in Infants and Children Anomalies of the Kidney Renal Dysplasia and Cystic Disease of Kidney Anomalies and Surgery of the Ureteropelvic Junction Ectopic Ureter Vesicoureteral Reflux Prune-Belly Syndrome Exstrophy and Epispadias Complex Surgical Technique for One-Stage Exstrophy Reconstruction Bladder Anomalies in Children Posterior Urethral Valves and Other Urethral Anomalies Voiding Dysfunction in Children: Neurogenic and Non-neurogenic Urinary Tract Reconstruction Hypospadias Abnormalities of External Genitalia in Boys Abnormalities of Testis and Scrotum: Surgical Management Sexual Differentiation: Normal and Abnormal Surgical Management of Intersex Pediatric Oncology Pediatric Endourology and Laparoscopy Pediatric Genitourinary Trauma

Campbell-Walsh urology

Childhood trauma confers higher risk of adulthood physical and mental illness; however, the biological mechanism mediating this association remains largely unknown. Recent research has suggested dysregulation of the immune system as a possible biological mediator. The present paper conducted a meta-analysis to establish whether early-life adversity contributes to potentially pathogenic pro-inflammatory phenotypes in adult individuals. A systematic search of Pubmed, PsycINFO, EMBASE, Scopus and Medline identified 25 articles for the meta-analysis, including 18 studies encompassing a sample of 16 870 individuals for C-reactive protein (CRP), 15 studies including 3751 individuals for interleukin-6 (IL-6) and 10 studies including 881 individuals for tumour necrosis factor-α (TNF-α). Random-effects meta-analysis showed that individuals exposed to childhood trauma had significantly elevated baseline peripheral levels of CRP (Fisher's z=0.10, 95% confidence interval (CI)=0.05-0.14), IL-6 (z=0.08, 95% CI=0.03-0.14) and TNF-α (z=0.23, 95% CI=0.14-0.32). Subgroup analyses for specific types of trauma (sexual, physical or emotional abuse) revealed that these impact differentially the single inflammatory markers. Moreover, meta-regression revealed greater effect sizes in clinical samples for the association between childhood trauma and CRP but not for IL-6 or TNF-α. Age, body mass index (BMI) and gender had no moderating effects. The analysis demonstrates that childhood trauma contributes to a pro-inflammatory state in adulthood, with specific inflammatory profiles depending on the specific type of trauma.

/pdf/childhood-trauma-and-adulthood-inflammation-a-meta-analysis-2w3gsxpikj.pdf

Childhood Trauma and Adulthood Inflammation: A Meta-Analysis of Peripheral C-reactive Protein, interleukin-6 and Tumour Necrosis factor-α

Diagnosis and Treatment of Overactive Bladder (Non-Neurogenic) in Adults: AUA/SUFU Guideline

Diagnosis and Treatment of Interstitial Cystitis/Bladder Pain Syndrome: AUA Guideline Amendment

INTRODUCTION AND HYPOTHESIS Voiding dysfunction has gained interest due to its high prevalence in the elderly. This study characterized bladder dysfunction in women with voiding dysfunction using video urodynamic studies (VUDS) focused on detrusor underactivity (DU). METHODS We studied 1914 women in which first-line medical treatment failed. Age, comorbidities, and urodynamic parameters were analyzed to determine the association between bladder sensation and contractility. RESULTS VUDS were normal in 2.9% (n = 56) of patients and showed DU in 23.1% (n = 443), detrusor hyperactivity and impaired contractility (DHIC) in 12.0% (n = 231), hypersensitive bladder in 17.0% (n = 325), detrusor overactivity (DO) in 2.6% (n = 49) and bladder outlet obstruction in 42.3% (n = 810). The mean age of patients in the DU and DHIC groups was significantly older than in women with normal VUDS and those with hypersensitive bladders (p<0.01). Decreased bladder sensation and larger cystometric bladder capacity were noted in the DU group compared to the DHIC, HSB, and DO groups. Bladder sensation was negatively associated with the bladder contractility. Bladder contractility index and voiding efficiency were lower in the DU and DHIC groups compared to the normal group. CONCLUSIONS The bladder conditions of women with voiding dysfunction included DU, DHIC, HSB and DO. Bladder contractility index and voiding efficiency were significantly lowest in DU and DHIC groups and lower in HSB and DO groups than normal tracing group. Reduced bladder sensation was noted in DU and negatively associated with detrusor contractility.

/pdf/urodynamic-characteristics-of-detrusor-underactivity-in-35fbg3h0s1.pdf

Urodynamic characteristics of detrusor underactivity in women with voiding dysfunction.

Objectives

To investigate urothelial dysfunction, suburothelial inflammation, and muscarinic receptor expression in diabetic patients with overactive bladder (OAB).



Methods

A total 19 patients with OAB and diabetes mellitus (DM), 14 OAB patients without DM, and 10 healthy control subjects were enrolled in the study. Immunofluorescence staining of E-cadherin, zonula occludens-1 (ZO-1), tryptase (mast cell activation), and apoptosis tests on the bladder urothelium and suburothelium were performed. Tissue muscarinic receptor M2, M3, and purinergic receptor P2X3 levels were measured by Western blotting. Video urodynamic studies were analyzed in relation to immunofluorescence and western blotting results.



Results

The mean age of the controls, OAB patients without and with DM were comparable (62.9 ± 6.9, 58.4 ± 21.3, and 68.9 ± 11.3 years, respectively, P = 0.25). E-cadherin and mast cell expression in the bladder urothelium samples of the DM-OAB group and the OAB group without DM differed significantly from those of the control group (all P < 0.05). However, immunofluorescence analyses including E-cadherin, mast cells, apoptotic cell counts, and ZO-1 were comparable between OAB patients with and without DM. In addition, M3 muscarinic protein expression in the bladders of OAB patients with and without DM was significantly higher than that in the control subjects. The video urodynamic parameters did not correlate with the immunofluorescence data, M2 and M3 muscarinic receptor data, or P2X3 protein expression.



Conclusion

Urothelial dysfunction and chronic suburothelial inflammation may contribute to the pathogeneses of OAB. However, DM does not aggravate the severity of urothelial inflammation in OAB patients.

Urothelial Dysfunction and Chronic Inflammation in Diabetic Patients with Overactive Bladder.

Interstitial cystitis/bladder pain syndrome with Hunner's lesion (HIC) is characterized by chronic inflammation and nerve hyperplasia; however, the pathogenesis of HIC remains a mystery. In this study, we detected both Epstein–Barr virus (EBV) latency infection genes EBNA‐1 and LMP‐1 and EBV lytic infection BZLF‐1 and BRLF‐1 expression in the HIC bladders, indicating the coexistence of EBV persistence and reactivation in the B cells in HIC bladders. Upregulation of EBV‐associated inflammatory genes in HIC bladders, such as TNF‐α and IL‐6, suggests EBV infection is implicated in the pathogenesis of bladder inflammation. Nerve hyperplasia and upregulation of brain‐derived neurotrophic factor (BDNF) were noted in the HIC bladders. Double immunochemical staining and flow cytometry revealed the origin of BDNF to be EBV‐infected B cells. Inducible BDNF expression was noted in B cells upon EBV infection, but not in the T cells. A chromatin immunoprecipitation study revealed BDNF transcription could be promoted by cooperation between EBV nuclear antigens, chromatin modifiers, and B‐cell‐specific transcription. Knockdown of BDNF in EBV‐infected B cells resulted in the inhibition of cell proliferation and viability. Downregulation of phosphorylated SMAD2 and STAT3 after BDNF knockdown may play a role in the mechanism. Implantation of latent EBV‐infected B cells into rat bladder walls resulted in a higher expression level of CD45 and PGP9.5, suggesting tissue inflammation and nerve hyperplasia. In contrast, implantation of BDNF depleted EBV‐infected B cells abrogated these effects. This is the first study to provide insights into the mechanisms underlying the involvement of EBV‐infected B cells in HIC pathogenesis. © 2022 The Pathological Society of Great Britain and Ireland.

EBV infection mediated BDNF expression is associated with bladder inflammation in interstitial cystitis/bladder pain syndrome with Hunner's lesion

Stroke and lower urinary tract symptoms: A neurosurgical view

Purpose

To compare the differences in urinary nerve growth factor (NGF) and detrusor wall thickness (DWT) between patients with overactive bladder (OAB) and controls to evaluate their suitability as biomarkers in OAB.



Materials and Methods

A total of 81 patients including normal controls (n = 28), patients with OAB dry (n = 28) and OAB wet (n = 25) were enrolled in this study. Videourodynamic study was performed in 79 patients after confirmation of symptomatic classification by 3-day voiding diary. Urine NGF and DWT measurements were performed at full bladder and urge to void after natural-filling or catheter-filling during videourodynamic study. Urinary NGF level was measured by the ELISA method and DWT was measured by trans-abdominal ultrasound. These two parameters were compared among different symptomatic and urodynamic subgroups.



Results

DWT was not significantly different among subgroups at 250 ml bladder volume. Although patients with OAB wet had a significantly greater DWT at the maximal bladder volume, this difference was not significant from controls after correction of the volume factor. By contrast, urinary NGF levels were significantly increased in patients with OAB wet and those with urodynamic detrusor overactivity. However, elevated NGF levels in OAB wet were found only after natural-filling and not after catheter-filling.



Conclusions

Urinary NGF level in natural-filling urine sample is a better biomarker for assessment of OAB wet compared to DWT. Patients with OAB dry or hypersensitive bladder did not have an elevated urinary NGF level. Urine samples from catheter-filling do not have a detectably high NGF levels. Neurourol. Urodynam. 29:482–487, 2010. © 2009 Wiley-Liss, Inc.

Urinary nerve growth factor is a better biomarker than detrusor wall thickness for the assessment of overactive bladder with incontinence.

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