Which patients with ischaemic priapism require further investigation for malignancy?

Ischaemic priapism (IP) is characterised by a persistent, painful penile erection lasting for >4 h. Many causes of IP have been identified including haematological dyscrasias (particularly, sickle cell disease), drugs and rarely malignancy. There are also a large proportion of men, in which no aetiology is identified. Identification of men at risk for malignancy provides a diagnostic challenge to the clinicians looking after these patients. All cases of IP between 2007 and 2017 at a single tertiary andrology unit were identified. The case notes and electronic records of these patients were reviewed to identify cases of malignant priapism. Men with idiopathic IP were used as a control group for comparative statistics. In total, 412 men with IP were identified, 202 of which had idiopathic IP. Within this group, the prevalence of malignant priapism was 3.5% (n = 11). MP secondary to local invasion or penile metastases occurred in seven of the 11 men (bladder × 3, prostate, lung, urethral and chondrosarcoma of the pelvis). MP secondary to haematological malignancy occurred in the remaining four (chronic myeloid leukaemia × 2, chronic lymphocytic leukaemia, and myelodysplasia). IP was the initial presentation of malignancy in seven of the patients (64%). An abnormally low haemoglobin value (reference range 130-180 g/dl) was found in 82% (n = 9) of the men with MP. The mean haemoglobin value in men with MP was 109.64 ± 20.30 g/dl compared to the control of 131.87 ± g/dl. This difference was considered highly significant p = 0.0046. Men with MP also appear to have a very poor prognosis with an 18-month mortality of 64% (n = 7). Malignancy is a rare and important cause of IP. A low haemoglobin is a predictor of malignancy and warrants further investigation in IP.

An analysis of the frequency of Y-chromosome microdeletions and the determination of a threshold sperm concentration for genetic testing in infertile men.

OBJECTIVE: To describe the prevalence of Y-chromosome microdeletions in a multi-ethnic urban population in London, UK. To also determine predictive factors and a clinical threshold for genetic testing in men with Y chromosome microdeletions. PATIENTS AND METHODS: A retrospective cohort study of 1473 men that were referred to a tertiary Andrology centre with male factor infertility between July 2004 and December 2016. All had a genetic evaluation, hormonal profile and 2 abnormal semen analyses. Those with abnormal examination findings also had targeted imaging performed. RESULTS: The prevalence of microdeletions was 4% (n = 58) in this study. These microdeletions were partitioned into the following regions: Azoospermia factors (AZF); AZFc (75%), AZFb+c (13.8%), AZFb (6.9%), AZFa (1.7%), and partial AZFa (1.7%). A high follicle-stimulating hormone level (P < 0.001) and a low sperm concentration (P < 0.05) were both found to be significant predictors for the identification of a microdeletion. Testosterone level, luteinising hormone level and testicular volume did not predict the presence of a microdeletion. None of the men with an AZF microdeletion had a sperm concentration of >0.5 million/mL. Lowering the sperm concentration threshold to this level retained the high sensitivity (100%) and increased the specificity (31%). This would produce significant cost savings when compared to the European Academy of Andrology/European Molecular Genetics Quality Network and European Association of Urology guidelines. The surgical sperm retrieval (SSR) rate after microdissection testicular sperm extraction was 33.2% in men with AZFc microdeletion. CONCLUSIONS: The prevalence of Y-chromosome microdeletions in infertile men appears to vary between populations and countries. A low sperm concentration was a predictive factor (P < 0.05) for identifying microdeletions in infertile males. A threshold for genetic testing of 0.5 million/mL would increase the specificity and lower the relative cost without adversely affecting the sensitivity. The rate of SSR was lower than that previously described in the literature.

Abnormal deep dorsal vein resulting in veno-occlusive erectile dysfunction.

A 59-year-old man with a 6-year history of erectile dysfunction presented to the andrology outpatient clinic. Multimodality assessment with ultrasound, MRI venography and fluoroscopic venography demonstrated an aberrant emissary vein arising from the corporal bodies causing venogenic erectile dysfunction. Selective coil embolisation of the collateral vein resulted in an almost immediate and sustained improvement in his erections.