A case of ureteral reflux identified by ultrasound

Reflux nephropathy is known to be a major cause of renal failure in children. Vesico-ureteral reflux is usually diagnosed by voiding cysto-urethrography (VCG). However, it has been observed that conventional VCG is not always reliable for the diagnosis of ureteral reflux. In the case of a 5 year old girl with recurrent febrile urinary tract infection, VCG showed no ureteral reflux. Urodynamic study revealed a large bladder capacity and significant residual urine. Renal scintigram delineated a right renal scar. Simple ultrasound examination with videotape recording during voiding definitely demonstrated the presence of significant ureteral reflux when she voided, that is, there was marked dilatation of the right distal ureter and ballooning of the right renal pelvis on voiding, and quick refilling of the bladder concomitantly with the disappearance of the pelvic ballooning. Therefore, an ultrasound during voiding may be useful for diagnosing ureteral reflux in patients where a VCG does not reveal reflux.     

Vasopressin plus oxygen vs vasopressin alone in cirrhotic patients with portal-hypertensive gastropathy: Effects on gastric mucosal haemodynamics and oxygenation

The effects of vasopressin plus oxygen and vasopressin alone on gastric mucosal perfusion and oxygenation were studied using reflectance spectrophotometry and laser Doppler velocimetry in 23 cirrhotic patients with portal-hypertensive gastropathy. The measurements were performed under basal conditions and after double-blinded administration of placebo (n= 7), vasopressin (0.3 U/min; n= 8) or vasopressin (0.3 U/min) plus nasal oxygen (4 L/min; n= 8). No significant effects on gastric mucosal haemodynamics and oxygenation were observed after placebo. In contrast, vasopressin and vasopressin plus oxygen induced a similar reduction in haemoglobin content (-26 ± 2 and -21 ± 4%, respectively P < 0.01) and laser Doppler signal (-23 ± 2 and -22 ± 2%, respectively, P < 0.01). Although each treatment induced a significant reduction in oxygen saturation (-21 ± 2 and -7 ± 1%, respectively P < 0.01), the effect was less pronounced in patients receiving the combination than in those receiving vasopressin alone (P < 0.01). These data suggest that vasopressin and vasopressin plus oxygen reduce gastric mucosal hyperaemia and that the oxygen supplement partially protects against gastric mucosal hypoxia during vasopressin infusion in cirrhotic patients with portal-hypertensive gastropathy.     

Bile acid composition in primary hepatocellular carcinoma

Bile acid composition in human primary hepatocellular carcinoma (HCC) tissues from eight non-hyperbilirubinaemic patients was compared with that in the neighbouring liver tissues. Quantitation of bile acids was carried out using selected ion monitoring. Significant amounts (>14 pmol/mg liver) of bile acids were found to be present in HCC tissues of all patients. In four patients, the concentration of chenodeoxycholic acid was higher in HCC than the corresponding neighbouring liver tissues, whereas those of other bile acids were less. The ratio of cholic to chenodeoxycholic acid was lower in HCC than in adjacent liver tissues in seven out of eight patients. This may indicate predominant synthesis of chenodeoxycholic acid in HCC tissues. The large inter-individual variation in bile acid concentration and composition of HCC tissues may result from the grade of anaplasia of HCC cells. 3β-Hydroxy-5-cholenoic acid, thought to be excreted in increased amounts in the urine of HCC patients, was shown to be a minor constituent of HCC tissues and of the neighbouring liver tissues in most patients, indicating that the C26-hydroxylation pathway plays a minor role. Unusual bile acids, such as 23-nor-3α,7α,12α-trihydroxy-5β-cholanoic, 3β,7β-dihydroxy-5β-cholanoic, 7-oxo-3α,12α-dihydroxy-5β-cholanoic and 12-oxo-3α,7α-dihydroxy-5β-cholanoic acids, were found in trace amounts in HCC tissues but their significance is not clear at present.     

Intracellular Calcium Dynamics,Shortened Action Potential Duration,and Late‐Phase 3 Early Afterdepolarization in Langendorff‐Perfused Rabbit Ventricles

Calcium Dynamics, APD Shortening, and Late‐Phase 3 EAD. Introduction: To elucidate the mechanism of late‐phase 3 early after depolarization (EAD) in ventricular arrhythmogenesis, we hypothesized that intracellular calcium (Ca_i) overloading and action potential duration (APD) shortening may promote late‐phase 3 EAD and triggered activity, leading to development of ventricular fibrillation (VF). Methods and Results: In isolated rabbit hearts, we performed microelectrode recording and simultaneous dual optical mapping of transmembrane potential (V_m) and Ca_i transient on left ventricular endocardium. An I_KATP channel opener, pinacidil, was used to abbreviate APD. Rapid pacing was then performed. Upon abrupt cessation of rapid pacing with cycle lengths of 60–200 milliseconds, there were APD₉₀ prolongation and the corresponding Ca_i overloading in the first postpacing beats. The duration of Ca_i transient recovered to 50% (DCaT₅₀) and 90% (DCaT₉₀) in the first postpacing beats was significantly longer than baseline. Abnormal Ca_i elevation coupled with shortened APD produced late‐phase 3 EAD induced triggered activity and VF. In additional 6 preparations, the heart tissues were treated with BAPTA‐AM, a calcium chelator. BAPTA‐AM significantly reduced the maximal Ca_i amplitude (26.4 ± 3.5% of the control; P < 0.001) and the duration of Ca_i transients in the mapped region, preventing the development of EAD and triggered activity that initiated VF. Conclusions: I _KATP channel activation along with Ca_i overloading are associated with the development of late‐phase 3 EAD and VF. Because acute myocardial ischemia activates the I_KATP channel, late‐phase 3 EADs may be a mechanism for VF initiation during acute myocardial ischemia. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1364‐1371, December 2012)     

Long-Term Follow-Up of Patients with Sick Sinus Syndrome: A Comparison of Clinical Aspects Among Unpaced, Ventricular Inhibited Paced, and Physiologically Paced Groups

To analyze the prognosis of the sick sinus syndrome (SSS), we compared the clinical aspects among unpaced, ventricular paced, and physiologically paced patients who were followed over a long period. Unpaced intrinsic SSS was not always progressive and patients did not necessarily require permanent pacing. The incidence of concomitant AV conduction disturbance was 65.6% before pharmacologic autonomic block, (PAB), but this was significantly reduced to 31.7% after PAB. Follow-up study of the physiologically paced groups revealed no development of either new or more than second degree AVB. The VVI group had significantly more complications (68%) than the physiologically paced groups, mainly chronic atrial fibrillation (36%) and thromboembolism (20%). In addition, cardiothoracic ratio (CTR) in the VVI group was significantly greater compared with that in the physiologic groups. Nine deaths occurred during the follow-up period in the pacing groups, including six with VVI and three with physiologic pacing. In the VVI pacing group, heart failure and thromboembolism were most commonly the causes of death, while in the physiologic pacing groups, the causes of death were noncardiac. Although the survival rate in the ventricular paced group was not significantly different from that in the physiologic pacing groups, cardiac deaths were fewer in the latter group. Considering our clinical data, the decision to use ventricular pacing needs to be carefully weighed in patients with sick sinus syndrome, and physiologic pacing is more highly recommended. (PACE, Vol. 11. November 1988)     

Regression of plane warts following spontaneous inflammation

This paper describes the clinical and histopathological features in ten cases of spontaneously involuting plane warts. In all, rapid regression occurred after the sudden development of an inflammatory reaction. At an early stage a degenerative change appears in the upper epidermis and the typic features of the warts are masked. At the height of the reaction an intense mononuclear cell infiltrate in the dermis associated with epidermal spongiosis, exocytosis cell necrosis and focal parakeratosis is found. It is suggested that the development of cell mediated immunity may be responsible for spontaneous involution of warts.     

Serial evaluation for myocardial performance in fetuses and neonates using a new Doppler index

BACKGROUND: Fetal echocardiography has been used for non-invasive evaluation of human fetal cardiac anatomy, function and hemodynamics. The Tei index, a new Doppler index known to be independent of both ventricular geometry and heart rate, has recently been applied to the evaluation of myocardial performance. METHODS: In the present study, the Tei index was prospectively and longitudinally determined in 50 normal fetuses, 35 fetuses with intrauterine growth retardation (IUGR), 30 fetuses of diabetic mothers (DM) and 20 normal infants. The Tei index of both left and right ventricles was calculated from a Doppler ventricular inflow and outflow trace using the following formula: Tei index = (ICT + IRT)/ET, where ICT is isovolumetric contraction time; IRT, isovolumetric relaxation time; and ET, ejection time). RESULTS: The Tei index of the left ventricle decreased linearly with advancing gestational age during 18-33 weeks and decreased acceleratively with increasing gestational age after 34 weeks. The index of the right ventricle decreased slightly and linearly with advancing gestational age during 18-41 weeks. In neonates, the Tci index of the left and right ventricle increased immediately and transitorily after birth and decreased and stabilized after 24 h of life. From 18 to 26 weeks of gestation, the Tei indices in fetuses with IUGR and of DM were not significantly different from controls. However, from 27 to 40 weeks of gestation, the Tei indices in both fetuses with IUGR and of DM were significantly greater than controls. CONCLUSIONS: This gradual decrease in the Tei index during gestation may represent the maturational or developmental alternation of myocardial performance in utero. Fetuses with IUGR and of DM may have abnormal myocardial performance in later gestation.