Prospective Evaluation of Ischemia in Brachial–Basilic and Forearm Prosthetic Arteriovenous Fistulas for Hemodialysis

Ischemia is a devastating complication after arteriovenous fistula (AVF) creation. When not timely corrected, it may lead to amputation. Symptomatic ischemia occurs in 3.7–5% of the hemodialysis population. Upper arm AVFs have a higher incidence of ischemia compared to forearm AVFs. As more patients may need upper arm AVFs in the growing and older hemodialysis population, occurrence of symptomatic ischemia may increase. The purpose of this study is to identify predictors for occurrence of ischemia.MethodsA prospective evaluation of ischemia was performed in patients randomised for either a brachial–basilic (BB-) AVF or a prosthetic forearm loop AVF. Clinical parameters, preoperative vessel diameters, access flows, digital blood pressures, digit-to-brachial indices (DBI) and interventions for ischemia were recorded.ResultsSixty-one patients (BB-AVF 28) were studied. Seventeen patients (BB-AVF 8) developed ischemic symptoms. Six patients (BB-AVF 3) needed interventions for severe symptoms. Age, history of peripheral arterial reconstruction and radial artery volume flow were significant predictors for the occurrence of ischemia.ConclusionSymptomatic ischemia occurred in 28% of patients with brachial–basilic and prosthetic forearm AVFs. Age, history of peripheral arterial reconstruction and radial artery volume flow might be important for prediction of ischemia

Gain of chromosome 7, as detected by in situ hybridization, strongly correlates with shorter survival in astrocytoma grade 2.

The clinical course of astrocytoma grade 2 (A2) is highly variable and is not reflected by morphological characteristics. Earlier studies using small series of A2 cases suggest that in situ hybridization (ISH) with chromosome-specific DNA probes allows for frequent detection of aneusomy 1, trisomy 7, and monosomy 10. The role of trisomy 7 in astrocytoma carcinogenesis is disputed, however, because of its presence in non-neoplastic brain tissue, as detected by karyotyping. Our objective was to investigate whether there was a correlation between chromosomal aberrations and survival in a series of 47 cases of A2. All cases were evaluated for numerical aberrations of chromosomes 1, 7, and 10 by ISH. Chromosomal aberrations were detected in 68% of cases of A2. Trisomy/polysomy 7 was seen in 31 cases (66%), 22 of which (47%) had a high percentage of this numerical aberration. Only 11 of these 22 cases also showed aneusomy for I or 10. No cells or only a few cells with aberrations were detected in non-neoplastic control samples. Using Kaplan-Meier analysis, trisomy/polysomy 7 correlated significantly with shorter survival. Hence, as determined by ISH, trisomy/polysomy 7 is absent in non-neoplastic brain tissue and is frequently detected in A2, correlating with the malignant progression of the disease

Dopamine transporter in attention-deficit hyperactivity disorder normalizes after cessation of methylphenidate

Attention-deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder of childhood, which is frequently treated with methylphenidate. The short-term response to treatment with methylphenidate is a substantial decrease in dopamine transporter density, with improvement in neuropsychological tests. In this study, single-photon emission computed tomography was used to investigate possible long-term alterations in the cerebral dopamine system after cessation of treatment with methylphenidate in five children with ADHD. Three months after initiation of treatment with methylphenidate, a reduction of the dopamine transporter in the striatal system was observed. Methylphenidate was administered for a period of 9 to 20 months. Follow-up with single-photon emission computed tomography after withdrawal of methylphenidate medication disclosed an increase of dopamine transporter activity comparable with pretreatment values. The observed upregulation of dopamine transporter activity might support the assumption that methylphenidate does not lead to permanent damage of the nigrostriatal dopaminergic pathways