A comparison between fluoroscopically guided radiofrequency energy delivery and conventional technique in an animal model of fundoplication failure

Background The use of radiofrequency energy (RFe) treatment at the gastroesophageal junction (GEJ) has been considered an alternative to surgery after fundoplication disruption. It is unknown whether the recommended delivery technique for primary gastroesophageal reflux disease applies to an anatomically altered GEJ following fundoplication. The aim of this study was to determine whether modifications to the standard technique using fluoroscopic guidance more accurately localizes ablation zones compared with standard technique alone. Methods Ten pigs were randomized to either conventional or fluoroscopically guided RFe ablation. All pigs had a laparoscopic Nissen fundoplication that was subsequently disrupted by severing all but the most cranial fundoplication stitch. Conventional RFe delivery included usage of markers located on the Stretta catheter. After labeling the z-line via submucosal contrast injection, fluoroscopic guidance involved using fluoroscopic markers to guide RFe ablation. Ablations were acutely marked, measured, and agreed upon by a panel of three researchers analyzing harvested tissue. Distances from the target zone for each ablation line (e.g., 1 cm was the target zone for line 1) were calculated and analyzed using Mann-Whitney and Fischer’s tests. Results Fluoroscopic guidance was significantly more accurate than the conventional technique (0.2 ± 0.2 cm vs. 1.8 ± 0.8 cm, p < 0.0001). Analyzing the individual distances for each of the six ablation lines revealed that all within Group B were closer than Group A (p < 0.01 for all except lines 1 and 2). Overall, the total ablation treatment length for conventionally treated animals was 4.48 ± 0.7 cm and for those who underwent fluoroscopic guidance it was 2.92 ± 0.5 cm (p < 0.001). Conclusion In a porcine model of fundoplication disruption, fluoroscopic guidance improved RFe accuracy.     

Hypothalamic-pituitary-adrenocortical axis dysregulation in patients with major depression is influenced by the insertion/deletion polymorphism in the angiotensin I-converting enzyme gene

The Dex/CRH test is one of the most reliable neuroendocrine function tests for hypothalamic-pituitary-adrenocortical (HPA) system dysregulation in depression. Persistent overdrive of HPA system activity after successful antidepressant treatment predicts an enhanced risk for relapse of a depressive episode. As the renin-angiotensin system has been shown to play a role in HPA system activity, we investigated the impact of the angiotensin converting enzyme (ACE) gene insertion (I)/deletion (D) polymorphism, which determines ACE plasma concentrations, on HPA system dysregulation. We performed repeated combined Dex/CRH tests in 115 patients suffering from major depression. Dex/CRH test results were related to the I/D polymorphism within the ACE gene, which was assessed by PCR. Genotype frequencies were comparable to those in the general population (I/I 16.8%, I/D 59.3%, D/D 23.9%). D/D genotypes showed a higher cortisol stimulation during the first Dex/CRH test after admission than homozygous I-allele carriers (repeated measurement ANOVA: P=0.034). Cortisol area under the curve values were highest in those with the D/D genotype (mean+/-SEM [nmol/l*75 min]: 12700+/-2220), intermediate in those with the I/D genotype (9570+/-1000), and lowest in those with the I/I genotype (5160+/-1000; ANOVA: P=0.04). After successful antidepressive treatment and attenuation of HPA system overdrive these differences were no more detectable. The HPA axis stimulating properties of higher ACE and consecutively higher AT-II and/or lower substance P concentrations may be crucial factors for the HPA system hyperactivity during major depressive episodes.     

Use of femur length/abdominal circumference ratio in detecting the macrosomic fetus

The femur length/abdominal circumference ratio, expressed as FL/AC X 100, was determined in 156 fetuses and evaluated as a predictor of fetal macrosomia within one week prior to delivery. The normal range (mean +/- 2 SD) in the 105 normal-weight fetuses was 22.0 +/- 2, while the normal range in the 51 macrosomic fetuses was 20.5 +/- 2; these differences were highly significant (P = less than .0001). The predictive power of a positive ratio was 68%, with a sensitivity of 63%. This ratio was particularly useful in the subset (n = 9) of macrosomic fetuses whose mothers were diabetic, correctly identifying 89% of this group. Because it is age independent, this ratio should prove most helpful in identifying fetuses at risk for macrosomia in patients whose dates are not known, since it may become abnormal before the fetal weight falls above the 90th percentile at term (3,900 g). In patients whose dates are known, early fetal macrosomia is best predicted by evaluating the abdominal circumference against normal standards for age.     

Ketamine-induced vesicopathy

We report about a 25-year-old patient with transnasal ketamine abuse over years presenting with severe irritative urinary dysfunction (imperative urinary urgency, pollakisuria, dysuria) and severe alguria. Cystoscopia showed ketamine-induced vesicopathy with errosive cystitis; other etiologies could be excluded. Despite serious effort the patient was not motivated for abstinence from ketamine. After two ineffecient therapies with botulinum toxin A (200 and 400?I.?E.) injected into the bladder, a prostate preserving cystectomia and ileum neobladder were mandatory.     

Psychotic and non-psychotic denial of pregnancy

We report about two patients with denial of pregnancy. While the first patient was free of psychopathological symptoms besides denial of pregnancy until rupture of the membranes, and was able to accomodate the new born, the second patient with psychotic denial of pregnancy could not accomodate the child because of the schizophrenia, so that an adoption was necessary. On the basis of the two cases aetiological, epidemiological, clinical und prognostic implications of psychotic and non-psychotic denial of pregnancy are discussed.     

Influence of a functional polymorphism within the angiotensin I-converting enzyme gene on partial sleep deprivation in patients with major depression

Partial sleep deprivation (PSD) exerts transient antidepressant efficacy. As a potential mechanism of action an enhancement of dopaminergic neurotransmission within the CNS is discussed. Because genetic variations influencing neurotransmission could have an impact on therapeutic outcome and stability of improvement, we investigated the functional insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene to examine a possible influence on the dopaminergic pathway. We included 56 patients with major depression (DSM-IV). Psychiatric ratings including the HAM-D6 scale were assessed prior to and after PSD and related to the different genotypes. The ACE I/D polymorphism was determined following PCR amplification using genomic DNA. A total of 58.1% of the patients were PSD responders. As expected, the therapeutical effect of PSD was transient and most patients experienced an exacerbation of depressive symptoms on day 2. Subdivision according ACE gene variants showed a significantly less pronounced relapse of symptoms in ACE gene D-allele carriers (P=0.02). Our results give first hints that the ACE I/I genotype, probably influencing dopaminergic neurotransmission, could be an indicator for relapse after PSD. This should result in earlier and more intense additional therapeutic interventions in this group of patients.     

Lack of association of serotonin‐2A receptor gene polymorphism (T102C) with suicidal ideation and suicide

Serotonergic dysfunction has been implicated in the pathophysiology of affective disorders and suicidality. Especially the density of the 5‐HT2A receptor was claimed as being increased in suicidality, proposed as an adaptive upregulation due to reduced serotonergic transmission. Recent studies have shown an association of allele C of the 5‐HT2A‐T102C polymorphism with suicidal ideation in patients with major depression. The purpose of this study was to test whether this proposed marker indicates susceptibility not only to suicidal ideation in depressed patients but also to suicidality as a syndrome. We investigated the 5‐HT2A‐T102C polymorphism in 131 suicide victims with unknown underlying psychiatric diagnoses, 84 patients with major depression with or without suicidal ideation, and 125 healthy controls. We were unable to find any association of genotype or allele frequencies to major depression, suicidal ideation, or suicide as a syndrome. Thus, our results suggest that this polymorphism may not commonly be involved in the susceptibility to suicidality. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:831–835, 2000. © 2000 Wiley‐Liss, Inc.