Objective While attention bias modification (ABM) is a promising novel treatment for anxiety disorders, clinical trial data remain restricted to adults. The authors examined whether ABM induces greater reductions in pediatric anxiety symptoms and symptom severity than multiple control training interventions. Method From a target sample of 186 treatment-seeking children at a hospital-based child anxiety clinic, 40 patients with an ongoing anxiety disorder who met all inclusion criteria were enrolled in the study. Children were randomly assigned to one of three conditions: ABM designed to shift attention away from threat; placebo attention training using stimuli identical to those in the ABM condition; and placebo attention training using only neutral stimuli. All participants completed four weekly 480-trial sessions (1,920 total trials). Before and after the attention training sessions, children’s clinical status was determined via semistructured interviews and questionnaires. Reduction in the number of anxiety symptoms and their severity was compared across the three groups. Results Change in the number of anxiety symptoms and their severity differed across the three conditions. This reflected significant reductions in the number of anxiety symptoms and symptom severity in the ABM condition but not in the placebo attention training or placebo-neutral condition. Conclusions ABM, compared with two control conditions, reduces pediatric anxiety symptoms and severity. Further study of efficacy and underlying mechanisms is warranted.
Primary hypomagnesemia with secondary hypocalcemia is a rare autosomal recessive disorder characterized by profound hypomagnesemia associated with hypocalcemia. Pathophysiology is related to impaired intestinal absorption of magnesium accompanied by renal magnesium wasting as a result of a reabsorption defect in the distal convoluted tubule. Recently, mutations in the TRPM6 gene coding for TRPM6, a member of the transient receptor potential (TRP) family of cation channels, were identified as the underlying genetic defect. Here, the results of a TRPM6 mutational analysis of 21 families with 28 affected individuals are presented. In this large patient cohort, a retrospective clinical evaluation based on a standardized questionnaire was also performed. Genotype analysis revealed TRPM6 mutations in 37 of 42 expected mutant alleles. Sixteen new TRPM6 mutations were identified, including stop mutations, frame-shift mutations, splice-site mutations, and deletions of exons. Electrophysiologic analysis of mutated ion channels after heterologous expression in Xenopus oocytes proved complete loss of function of TRPM6. Clinical evaluation revealed a homogeneous clinical picture at manifestation with onset in early infancy with generalized cerebral convulsions. Initial laboratory evaluation yielded extremely low serum magnesium levels, low serum calcium levels, and inadequately low parathyroid hormone levels. Treatment usually consisted of acute intravenous magnesium supplementation leading to relief of clinical symptoms and normocalcemia, followed by lifelong oral magnesium supplementation. Serum magnesium levels remained in the subnormal range despite adequate therapy. This is best explained by a disturbed magnesium conservation in the distal convoluted tubule, which emerged in all patients upon magnesium supplementation. Delay of diagnosis resulted in permanent neurologic damage in three patients.
We describe a boy with a neonatally diagnosed primary nonfamilial hypomagnesemia. Oral supplementation of large quantities of magnesium salts was required to maintain low normal serum magnesium levels. Lately, a further increase in the oral supplementation had to be administered in order to avoid seizures. A thorough investigation was conducted. Both an intestinal and urinary magnesium wasting was noticed. The rarity of this simultaneous double transport defect merit its description.
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