International Journal of Methods in Psychiatric Research, 2005; Vol.14, No.3, 158–166

The original article to which this Erratum refers was published in International Journal of Methods in Psychiatric Research, 2005; Vol.14, No.3, 158–166. Copyright © 2005 John Wiley & Sons, Ltd.     

Improved diagnostic effectiveness with a sequential diagnostic paradigm in idiopathic pediatric sensorineural hearing loss.

OBJECTIVES: To determine whether a stepwise diagnostic paradigm is more diagnostically efficient and cost-effective than a simultaneous testing approach in the evaluation of idiopathic pediatric sensorineural hearing loss (SNHL). DESIGN: Prospective prevalence study. SETTING: Tertiary referral children's hospital. PATIENTS: Consecutive children (n = 150) presenting with idiopathic SNHL in the last 2 years. INTERVENTIONS: All children were evaluated with full diagnostic evaluations including GJB2 screens, temporal bone computed tomography scans, and laboratory investigations. MAIN OUTCOME MEASURES: 1) Diagnostic yields of GJB2 screens, imaging, and laboratory results per SNHL category; 2) Cost analysis comparing a sequential versus a simultaneous testing approach. RESULTS: Overall, 12.0% of patients had biallelic mutations in the GJB2 gene, whereas 30% of patients had an abnormality on temporal bone scan. Laboratory testing did not reveal the SNHL etiology in any patient. While maintaining diagnostic accuracy, significant cost savings were inferred by using a sequential diagnostic algorithm. Our data show children with severe to profound SNHL should first be tested with a GJB2 screen, as opposed to those with milder SNHL, who should undergo imaging as the initial testing step. In patients with initially positive GJB2 or imaging screens, logistic regression analysis significantly predicted negative results on further testing. CONCLUSIONS: A stepwise diagnostic paradigm tailored to the level of the hearing loss in children with bilateral SNHL is more diagnostically efficient and cost effective than the more commonly used full, simultaneous testing approach. Laboratory investigation should not be routine but based on clinical history.     

Primary hyperaldosteronism caused by adrenocortical carcinoma

Since the syndrome of primary hyperaldosteronism was described by Jerome Conn in 1955, over 300 patients with this disorder have been identified in the medical centers of Vanderbilt University and the University of Michigan. The most frequent cause of this endocrinopathy has been a solitary adenoma of the adrenal cortex (72%); bilateral adrenocortical hyperplasia has been the cause of primary hyperaldosteronism in 27% of cases; less frequently, the cause has been multiple and/or bilateral adenomas (1%). During the last 4 years in these 2 medical centers, we have encountered 3 patients who have had biochemically proven primary hyperaldosteronism due to adrenocortical carcinoma. Each of these unusual cases is summarized with review of the recent literature.

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Resumen Desde la descripción del síndrome de hiperaldosteronismo primario por Jeremo Conn en 1955, más de 300 pacientes con esta entidad han sido identificados en nuestros 2 centros médicos, la Universidad de Vanderbilt (Nashville) y la Universidad de Michigan (Ann Arbor). La causa más frecuente de esta endocrinopatía ha sido el adenoma solitario de la corteza suprarrenal (72%); la hiperplasia adrenocortical bilateral ha sido la causa del hiperaldosteronismo primario en 27% de los casos; con menor frecuencia se han presentado los adenomas multiples y/o bilaterales (1%). En los 4 últimos años hemos encontrado 3 pacientes con hiperaldosteronismo primario comprobado bioquímicamente producido por carcinoma adrenocortical. Se presenta cada uno de estos casos poco usuales junto con una revisión de la literatura reciente.

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Résumé Depuis que le syndrome d'hyperaldostéronisme primitif a été décrit par Jerôme Conn en 1955 plus de 300 sujets qui en étaient victimes ont été identifiés à la Vanderbilt University de Nashville et à l'University of Michigan de Ann Arbor. La cause la plus fréquente de cette endocrinopathie répond à un adénome solitaire de la cortico-surrénale (72%) alors que l'hyperplasie corticale des 2 surrénales est plus rarement à son origine (27%), les adénomes multiples et/ou bilatéraux étant rarissimes (1%). Au cours des 4 dernières années 3 cas d'hyperaldosteronisme dû à un cancer de la cortico-surrénale ont été observés dans les 2 centres. Chacun de ces cas exceptionnels est exposé cependant que la littérature récente concernant l'hyperalderosteronisme est analysée.

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Presented at the International Association of Endocrine Surgeons in Paris, September 1985.     

Modification of Blood Vessel Diameter Following Perivascular Application of Botulinum Toxin-A

The purpose of this study was to demonstrate that perivascularly applied botulinum toxin-A (BTX) increases the diameter of treated blood vessels in a rat femoral vessel exposure model. Six adult Sprague–Dawley rats were used and bilateral femoral artery and vein exposures were performed. Five units of BTX were applied to the experimental side and an equal volume of sterile saline was applied to the control side. Digital images of the vessels were obtained at the following time points: pretreatment, immediately posttreatment, and postoperative days (POD) 1, 14, and 28. Vessel diameters were equivalent at baseline and immediately following application of BTX and saline. The BTX artery was significantly larger than the control artery on POD 1 and 14. The BTX treated artery was significantly larger than all other vessels on POD 14 (p < 0.05) as well as all prior time points (p < 0.01). Direct perivascular application of BTX increases the diameter of rat femoral vessels as early as POD 1. The affect is most robust on POD 14 where the artery was significantly larger than all other vessels at all time points. It is likely that the increased diameter of blood vessels results in an increased blood flow across the area of dilation. Such an increase in flow may serve to improve end-organ perfusion in microvascular procedures.     

Prostate cancer: Prevalence and treatment in African men

Epidemiological data from the United States of America (USA) indicate that the incidence and mortality of prostate cancer is higher among Black African-American men (AAM) than among White (Caucasian) American men (CAM). Earlier studies suggesting that prostate cancer is relatively rare among indigenous Black men in Africa are probably flawed by underreporting because recent studies indicate that the incidence rates among Black men are similar to those of White men living in Africa. The higher incidence of prostate cancer among AAM has been ascribed to racial differences in genetic susceptibility, dietary factors, or androgen metabolism. However, it may also be due to registration artefacts because in Africa the reported incidence rates of prostate cancer in different countries correlate directly with the per capita gross national product, suggesting improved access to medical facilities is responsible for higher reported incidence rates.

The greater prostate cancer mortality among AAM may result from higher tumour grade and stage and higher serum PSA at presentation, but it has also been suggested that prostate cancer is biologically more aggressive in AAM than in CAM. However, recent studies indicate that tumour grade and stage and serum PSA at presentation are similar in the races, with no difference in survival after multivariate analysis controlling for pretreatment cancer severity. This suggests that the higher prostate cancer mortality among AAM results from socio-economic factors and limited access to healthcare. Black men living inside as well as outside of Africa still tend to present with locally advanced or metastatic prostate cancer due to lack of early detection programmes.