Urge urinary incontinence, is caused by uninhibited contractions of the detrusor muscle, a condition known as overactive bladder syndrome. It is characterized by leaking of large amounts of urine in association with insufficient warning to get to the bathroom in time. Men
Urge incontinence is the most common type of incontinence in men. Similar to women, urine leakage happens following a very intense feeling of urination, not allowing enough time to reach the bathroom, a condition called overactive bladder syndrome. In men, the condition is commonly associated with benign prostatic hyperplasia (an enlarged prostate), which causes bladder outlet obstruction, a dysfunction of the detrusor muscle (muscle of the bladder), eventually causing overactive bladder syndrome, and the associated incontinence.Stress urinary incontinence is the other common type of incontinence in men, and it most commonly happens after prostate surgery. Prostatectomy, transurethral resection of the prostate, prostate brachytherapy, and radiotherapy can all damage the urethral sphincter and surrounding tissue, causing it to be incompetent. An incompetent urethral sphincter cannot prevent the urine from leaking out of the urinary bladder during activities that increase the intraabdominal pressure, such as coughing, sneezing, or laughing. Continence usually improves within 6 to 12 months after prostate surgery without any specific interventions, and only 5 to 10% of people report persistent symptoms. Both
Age is a risk factor that increases both the severity and prevalence of UI
Polyuria (excessive urine production) of which, in turn, the most frequent causes are: uncontrolled diabetes mellitus, primary polydipsia (excessive fluid drinking), central diabetes insipidus and nephrogenic diabetes insipidus.
These cases of HLH are classified as belonging to the class of Epstein–Barr_virus–associated_lymphoproliferative_diseases and termed EBV+ HLH. Genetics
Five genetic subtypes (FHL1, FHL2, FHL3, FHL4, and FHL5) are described, with an estimated overall prevalence of one in 50,000 and equal gender distribution. Molecular genetic testing for four of the causative genes, PRF1 (FHL2), UNC13D (FHL3), STX11 (FHL4), and STXBP2 (FHL5), is available on a clinical basis. Symptoms of FHL are usually evident within the first few months of life and may even develop in utero. However, symptomatic presentation throughout childhood and even into young adulthood has been observed in some cases.The five subtypes of FHL are each associated with a specific gene:

FHL1: HPLH1
FHL2: PRF1 (Perforin)
FHL3: UNC13D (Munc13-4)
FHL4: STX11  (Syntaxin 11)
FHL5: STXBP2 (Syntaxin binding protein 2)/UNC18-2Nearly half of the cases of type 2 familial hemophagocytic lymphohistiocytosis are due to bi-allelic PRF1 mutations. Pathophysiology
The underlying causes, either inherited or acquired, lead to an unchecked immune response when exposed to triggers. Impaired NK-cell cytotoxicity is the hallmark of HLH. All genetic defects for familial HLH are related to granule-dependent cytotoxicity. This inability to remove infected and antigen-presenting cells and terminate the immune response leads to uncontrolled proliferation and activation of the immune system with release of excessive cytokines. These cells then infiltrate organs, releasing more cytokines, which gives the clinical picture. The fever is caused by IL-1, IL-6 and TNF-alpha; the cytopenia is due to the suppressive effect on hematopoiesis by TNF-alpha and TNF-gamma. TNF-alpha and TNF-gamma may also lead to inhibition of lipoprotein lipase or stimulate triglyceride synthesis.