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Posters 316 stress (serious quarrel with classmates, physical activities) have been observed. The patients had no coronary risk factors. Their average blood pressure was 150/90 mmHg and heart rate was 120 beats/ min. ST-segment elevations and T-wave inversions were registered on electrocardiograms of teenagers. Dysfunction and dyskinesia of the left ventricle apex and interventricular septum was detected on echocardiography. The levels of creatine kinase-MB and troponin I did not increase. Occlusions and anomalies of vessels were not demonstrated by aortocoronarography. Tako-Tsubo cardiomyopathy was diagnosed in all cases. Symptomatic medical treatment had been administered and the function of heart was normalized within 3-4 weeks. Conclusions:Tako-Tsubo cardiomyopathy may occur not only in adults, but in teenagers too. Therefore increased awareness of Tako-Tsubo cardiomyopathy will lead to its more frequent diagnosing, which will result in adequate medical management. (3) and Branch Pulmonary Stenosis( 2). 6 of these (31%) with significant lesions were referred to tertiary cardiac centre for further assessment/intervention. 617 Conclusion:Childhood murmurs are sometimes transient and vast majority of persistent murmurs are innocent. Asymptomatic murmurs after infancy could be reviewed by paediatricians and persistent or symptomatic ones referred to paediatric cardiac clinic. Facility to perform an echocardiography at district general hospital will help in confirming innocent murmurs and more importantly reassuring anxious parents. It also has a role in detecting few, yet significant, congenital heart conditions that could then be referred on to tertiary centre. SIGNIFICANCE OF MURMURS IN INFANCY

Introduction Inclusion of ethnic/racial minorities in clinical trials is essential to fully assess therapeutic efficacy. It is well-known that populations respond dissimilarly to interventions. This concept has been research ed thoroughly in the context of urologic oncology research, however research into the impact of demographic characteristics in andrology trials is lacking. Objective To analyze the inclusion of historically under-represented minority men in clinical trials for Erectile Dysfunction (ED) in comparison to Prostate Cancer (PC) trials. Methods We searched ClinicalTrials.gov for the disease keyword: “Erectile Dysfunction” and used “Prostate Cancer” trials for comparison. Completed trials that had available demographic data were included for analysis. Literature was reviewed to determine the prevalence of ED and PC diagnosed among Hispanic, Black, White, and Asian men. The proportion of individuals of each group that participated in trials is divided by the proportion of each group in the disease population to calculate the “Participation to Prevalence Ratio” (PPR). PPRs between 0.8-1.2 indicates adequate representation, 1.2 is over-representation. Results A total of 312 trials were assessed: 289 for prostate cancer and 23 for ED. Hispanic men comprised 11.8% of ED trial participants and 4.61% of prostate cancer trial participants, yet represented 18% of ED patients and 7.3% of PC patients. Black/African-American (AA) men accounted for 10.2% of ED trial participants and 9.4% of PC trial participants, but comprised 16% of ED patients, and 16.3% of PC patients. Hispanic and AA men are under-represented in trials for ED and Prostate Cancer (Hispanic ED PPR=0.66; Hispanic PC PPR=0.63; AA ED PPR=0.42; AA PC PPR=0.58). Conclusions Our findings show that both Hispanic and AA men are underrepresented in both ED and PC clinical trials. A greater emphasis must be placed on achieving representative enrollment in clinical trials for ED and PC in order to address this disparity and improve generalizability of the findings. Disclosure No

Abstractsnods and other seizure types. He was then investigated for possible GLUT1 deficiency. Results The initial investigations revealed a CSF sugar of 2.4 when the blood sugar was 5.9 (ratio of 0.4) which was low but not low enough for GLUT1 deficiency. Genetic testing revealed a mutation in the Exon 5 of the SLC2A gene c.647T>C (p.lle216Thr) not previuosly reported. Conclusion GLUT1 deficiency should be suspected in a child with developmental delay, epilepsy and movement disorder. Novel mutations can result in the condition. Our case is one such example for novel mutation as well as refusal of ketogenic diet from late diagnosis. CEREBRAL PALSY AND CHEMOKINE CCL18 POLYMORPHISM IN VERY PRETERM INFANTS