Alloimmunization due to anti-M antibodies are rare since they present as naturally occurring immunoglobulin M antibodies, which do not cross the placenta. Very rarely, these may convert to immunoglobulin G antibodies and cause hemolytic disease of the fetus and newborn. We present the case of a fifth gravida, with previous two miscarriages and an unexplained stillbirth, booked with us for the 8 weeks. At booking, she was found to have anti-M antibodies with titers of 1:2, which was stable throughout pregnancy. At 35 weeks, there was evidence of severe fetal anemia and features of hydrops on the ultrasound scan, requiring delivery. Neonatal direct Coombs test was positive. Baby had a hemoglobin of 8.8 mg/dL and a reticulocyte count of 5.5% at birth, requiring two units of blood transfusion. He also required 6 days of intensive phototherapy. Alloimmunization due to anti-M antibodies should be suspected in women with previous bad obstetric history. The maternal antibody titers may not be a true reflection of the severity of fetal affection, and hence not reliable for monitoring in pregnancy

Context:Avanafil is a smooth muscle relaxant that is clinically used to treat erectile dysfunction. It is an inhibitor of phosphodiesterase-5 (PDE5), the enzyme that catalyzes the metabolism of cyclic guanosine monophosphate (cGMP). The inhibitory effect of avanafil on isolated detrusor muscle contractility has not been studied.Aims:This study investigated the inhibitory effect of avanafil on isolated caprine (goat) detrusor muscle contractility and the possible mechanisms involved.Settings and Design:80 mM potassium chloride (KCl)-induced contractility of the isolated goat detrusor was studied using a physiograph.Materials and Methods:Ten caprine detrusor strips were made to contract using 80 mM KCl before and after addition of three concentrations (10, 30, and 60 μM) of avanafil. Three reversal agents, ODQ, a guanylyl cyclase inhibitor; glibenclamide, an adenosine triphosphate (ATP)-sensitive potassium channel blocker; and iberiotoxin, a calcium-sensitive potassium (BKCa) channel blocker, were investigated for their ability to reverse the inhibitory effect of 30 μM avanafil on KCl-induced detrusor contractility.Statistical Analysis Used:The nonparametric statistical test, Kruskal–Wallis test, was used for the analysis of the data.Results:Avanafil caused a statistically significant inhibition of detrusor contractility at 30 and 60 μM concentrations. The inhibitory effect of 30 μM avanafil on detrusor contractility was significantly reversed by the addition of ODQ, glibenclamide, and iberiotoxin.Conclusions:Avanafil inhibits the contractility of the isolated detrusor by inhibiting PDE5, leading to raised cellular levels of cGMP. The raised levels of cGMP could have inhibited detrusor contractility by activating cGMP-dependent protein kinase, by opening ATP-sensitive potassium channels, and by opening BKCa. Avanafil could be evaluated for treating clinical conditions requiring relaxation of the detrusor like overactive bladder.