Surrogate Alcohol or Nonbeverage Alcohol Consumption: The Surrogate Alcohol Questionnaire (SAQ).

BACKGROUND: Diagnosis and treatment of alcohol use disorders and their sequelae are common clinical questions for the consultation-liaison psychiatrist. At an urban, academic medical center, the authors consulted on several patients whose consumption of alcohol included nonbeverage forms of alcohol, (described in the literature as surrogate alcohols, nonbeverage alcohols, e.g., mouthwash). METHODS: The authors describe 4 patients who presented with surrogate alcohol consumption. The authors review the clinical issues and literature related to surrogate alcohol use. The authors describe the array of substances, which either contain ethanol, but are not intended for drinking, or which contain other intoxicating alcohols (e.g., methanol), that are consumed in lieu of traditional beverage alcohol. Furthermore, the authors discuss standard medical treatment interventions for ethanol and non-ethanol based alcohols. The authors propose a screening tool, the surrogate alcohol questionnaire, a tool to facilitate better recognition of surrogate alcohol use.

Hospital care of childhood traumatic brain injury in the United States, 1997-2009: a neurosurgical perspective.

OBJECT: The goal in this paper was to study hospital care for childhood traumatic brain injury (TBI) in a nationwide population base. METHODS: Data were acquired from the Kids' Inpatient Database (KID) for the years 1997, 2000, 2003, 2006, and 2009. Admission for TBI was defined by any ICD-9-CM diagnostic code for TBI. Admission for severe TBI was defined by a principal diagnostic code for TBI and a procedural code for mechanical ventilation; admissions ending in discharge home alive in less than 4 days were excluded. RESULTS: Estimated raw and population-based rates of admission for all TBI, for severe TBI, for death from severe TBI, and for major and minor neurosurgical procedures fell steadily during the study period. Median hospital charges for severe TBI rose steadily, even after adjustment for inflation, but estimated nationwide hospital charges were stable. Among 14,932 actual admissions for severe TBI captured in the KID, case mortality was stable through the study period, at 23.9%. In a multivariate analysis, commercial insurance (OR 0.86, CI 0.77-0.95; p = 0.004) and white race (OR 0.78, CI 0.70-0.87; p < 0.0005) were associated with lower mortality rates, but there was no association between these factors and commitment of resources, as measured by hospital charges or rates of major procedures. Increasing median income of home ZIP code was associated with higher hospital charges and higher rates of major and minor procedures. Only 46.8% of admissions for severe TBI were coded for a neurosurgical procedure of any kind. Fewer admissions were coded for minor neurosurgical procedures than anticipated, and the state-by-state variance in rates of minor procedures was twice as great as for major procedures. Possible explanations for the "missing ICP monitors" are discussed. CONCLUSIONS: Childhood brain trauma is a shrinking sector of neurosurgical hospital practice. Racial and economic disparities in mortality rates were confirmed in this study, but they were not explained by available metrics of resource commitment. Vigilance is required to continue to supply neurosurgical expertise to the multidisciplinary care process.

Detection of a novel exon 4 low-density lipoprotein receptor gene deletion in a swiss family with severe familial hypercholesterolemia.

Familial hypercholesterolemia (FH) is an autosomal dominant disease which results in 2-3-fold elevated cholesterol levels and in accelerated atherosclerosis. FH is caused by small mutations or larger rearrangements in the low-density lipoprotein receptor (LDLR). Here, we report that screening the LDLR gene in a Swiss family (n = 15) with clinical symptoms of FH by combined single strand conformation polymorphism and long-distance PCR identified a novel 1.3 kb deletion in the LDLR. The deletion eliminated exon 4 of the LDLR presumably by recombination between two identical 25 bp repeats present in intron 3 and 4. The 25 bp sequence in intron 3 is part of an Alu repeat, whereas no homology to Alu repeats was found for the intron 4 region. This 1.3 kb LDLR deletion allele cosegregated with elevated cholesterol levels over three generations. Even on high-dose statin therapy, carriers of the deletion averaged 1.6 times higher cholesterol levels and 1.9 times higher apolipoprotein B-100 (apoB-100) levels than non-carriers who had lipid and apoB-100 levels within the range of the Swiss population. Most affected members of the first and second generation of this family had experienced a first myocardial infarction (MI) before the age of 55 years and most LDLR gene deletion carriers older than 40 years showed severe coronary artery disease (CAD). Hence, we conclude that deletion of exon 4 in the LDLR gene drastically decreases low-density lipoprotein binding leading to severe hypercholesterolemia.