Bacteria and inflammatory cells reduce chorioamniotic membrane integrity and tensile strength

Article Abstract:

Premature rupture of the membranes surrounding the fetus is associated with premature delivery and poor fetal outcome. The mechanism causing premature rupture of membranes (PROM) is poorly understood, but evidence now supports the theory that infection and inflammation play a role in causing PROM. Some laboratory studies have found that bacteria can produce substances called proteases, which tend to make the fetal membranes less elastic. By increasing the tensile strength and decreasing the elasticity, the integrity of the fetal membrane is compromised, predisposing it to rupture. Polymorphonuclear neutrophils (PMNs) are cells involved in the process of inflammation, which is associated with bacterial infection. The integrity of the fetal membrane was assessed using three parameters: bursting tension, work to rupture and elasticity. Fetal membranes, removed from women without PROM immediately after cesarean delivery, were studied in the laboratory. The membrane integrity was assessed after the membranes were exposed to group B streptococci and Staphylococcus aureus bacteria with and without the presence of neutrophils. Bursting tension, work to rupture, and elasticity were decreased with both groups of bacteria. The presence of neutrophils altered only the strength of the fetal membrane. When S. aureus bacteria was combined with neutrophils, the effects on the membrane were additive; this interaction did not occur with group B streptococcus. These results indicate that certain bacteria and neutrophils may work together to weaken the integrity of the fetal membranes, and predispose the membranes to premature rupture. Clinical studies are needed. (Consumer Summary produced by Reliance Medical Information, Inc.)

Infection, Physiological aspects, Bacteria, Pathogenic, Pathogenic bacteria, Fetal membranes, Premature rupture of membranes, Premature rupture of the membrane, Neutrophils, Chorioamnionitis

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Prazosin-induced stress incontinence

Article Abstract:

Stress incontinence occurs when urine involuntarily leaks from the bladder. Diagnosis of genuine stress incontinence can be made by cystometry, a technique of measuring changes in pressure within the bladder. The condition can be corrected by surgery. A healthy, active 59-year-old woman complained of urine leakage during exercise, jogging and coughing. Tests of bladder pressure and instability of the detrusor muscle surrounding the bladder were performed. Genuine stress incontinence was demonstrated with visible leakage of urine. Medication history included prazosin to treat high blood pressure and hormone replacement therapy to treat symptoms of menopause. Prazosin is a alpha-adrenergic antagonist which reduces high blood pressure by dilating blood vessels. It is also known to relax the bladder neck and urethra, the tube leading from the bladder. High blood pressure medication was switched to verapamil. The symptoms resolved within 36 hours of a change in medication. Although genuine stress incontinence was diagnosed in this patient, surgery was avoided by changing antihypertensive medication. (Consumer Summary produced by Reliance Medical Information, Inc.)

Case studies, Complications and side effects, Urinary stress incontinence, Prazosin

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