Missed Coronary Artery Dissection Post-Blunt Chest Trauma.

Cardiac contusion is rarely diagnosed in patients with blunt chest trauma in the emergency department, especially if patients are asymptomatic. We present a case of a 43-year-old man whose diagnosis of left anterior descending artery (LAD) dissection after blunt chest trauma was delayed. The patient presented to the emergency department of a remote district hospital after a motorcycle accident, asymptomatic with a mildly reduced level of consciousness due to a very small subdural hemorrhage. Ten days later, when he developed a syncopal attack due to a massive pulmonary embolism (PE), his first performed electrocardiogram (ECG) showed sinus rhythm with QS waves and slight ST elevation in leads V2-V6. The subsequent coronary angiography showed left anterior descending artery dissection, and the diagnosis was nicely depicted with optical coherence tomography (OCT). A drug-eluting stent was implanted with a good angiographic result. This case highlights the significance of early recognition of traumatic coronary dissection, which should be excluded even in asymptomatic patients with a plain ECG acquisition, for the appropriate management and prevention of unfavorable outcomes.

Population pharmacokinetics of colistin and the relation to survival in critically ill patients infected with colistin susceptible and carbapenem-resistant bacteria.

OBJECTIVES: The aim was to analyse the population pharmacokinetics of colistin and to explore the relationship between colistin exposure and time to death. METHODS: Patients included in the AIDA randomized controlled trial were treated with colistin for severe infections caused by carbapenem-resistant Gram-negative bacteria. All subjects received a 9 million units (MU) loading dose, followed by a 4.5 MU twice daily maintenance dose, with dose reduction if creatinine clearance (CrCL) < 50 mL/min. Individual colistin exposures were estimated from the developed population pharmacokinetic model and an optimized two-sample per patient sampling design. Time to death was evaluated in a parametric survival analysis. RESULTS: Out of 406 randomized patients, 349 contributed pharmacokinetic data. The median (90% range) colistin plasma concentration was 0.44 (0.14-1.59) mg/L at 15 minutes after the end of first infusion. In samples drawn 10 hr after a maintenance dose, concentrations were >2 mg/L in 94% (195/208) and 44% (38/87) of patients with CrCL ≤120 mL/min, and >120 mL/min, respectively. Colistin methanesulfonate sodium (CMS) and colistin clearances were strongly dependent on CrCL. High colistin exposure to MIC ratio was associated with increased hazard of death in the multivariate analysis (adjusted hazard ratio (95% CI): 1.07 (1.03-1.12)). Other significant predictors included SOFA score at baseline (HR 1.24 (1.19-1.30) per score increase), age and Acinetobacter or Pseudomonas as index pathogen. DISCUSSION: The population pharmacokinetic model predicted that >90% of the patients had colistin concentrations >2 mg/L at steady state, but only 66% at 4 hr after start of treatment. High colistin exposure was associated with poor kidney function, and was not related to a prolonged survival.

Impact of Toll-like receptor-4 and tumour necrosis factor gene polymorphisms in patients with hidradenitis suppurativa.

BACKGROUND: Recent evidence has suggested that deranged immune responses play a role in the pathogenesis of hidradenitis suppurativa (HS). OBJECTIVES: To investigate the role of single nucleotide polymorphisms (SNPs) of the tumour necrosis factor (TNF) and Toll-like receptor 4 (TLR4) genes in the physical course of HS; these genes encode for proteins implicated in the immune response of the host. METHODS: DNA was isolated from 190 patients with HS and 84 healthy controls. SNPs at the promoter regions -376G/A, -238G/A and -308G/A of the TNF gene and the Asp299Gly and Thr399Ile SNPs of the TLR4 gene were determined by polymerase chain reaction (PCR) and digestion of the PCR product by restriction enzymes; after electrophoresis on 2·0% agarose gel, products were visualized on under ultraviolet radiation. RESULTS: The presence of the -238 TNF gene polymorphism was associated with a predisposition to HS (P = 0·027). Susceptibility to the disease was strongly correlated with the presence of AGG/GGA/AGA/GAA TNF haplotypes in 32 (17%) patients compared with two (2%) controls (P < 0·001, odds ratio 8·30, 95% confidence interval 1·94-35·52). The frequency of HS exacerbations and disease severity were greater in patients carrying any of the GAG/AGG/GGA/AGA/GAA haplotypes of the TNF gene. Thirty-two patients were given TNF antagonists. Nineteen of these patients were carriers of the GGG haplotype of the TNF gene, whereas 13 were carriers of other haplotypes; favourable responses as evidenced by the Sartorius score were registered in 15 (79%) and five (38%, P = 0·025), respectively. Carriage of the TLR4 gene alleles was not associated with any disease parameter. CONCLUSIONS: A significant role of SNPs at the promoter region of the TNF gene is indicated for susceptibility to HS and for response to TNF antagonists.

Implications for a role of interleukin-23 in the pathogenesis of chronic gastritis and of peptic ulcer disease.

The present study aimed to investigate the role of gastric mucosa for the secretion of interleukin (IL)-23 in chronic gastritis. One hundred and one patients were enrolled; 47 with duodenal ulcer, 33 with gastric ulcer and 31 with chronic gastritis. Biopsies were incubated in the absence/presence of endotoxins. Supernatants were collected and IL-23 and IL-1beta were measured by enzyme-linked immunosorbent assay. Scoring of gastritis was performed according to the updated Sydney score. Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis. IL-23 was higher in supernatants of tissue samples of Helicobacter pylori-positive than of H. pylori-negative patients. No differences were recorded in concentrations of IL-23 and IL-1beta between patients with duodenal ulcer, gastric ulcer and chronic gastritis. Positive correlations were found between IL-23 of patients with both duodenal and gastric ulcer and chronic gastritis and the degree of infiltration of neutrophils and monocytes. Similar correlations were observed between IL-23 and IL-1beta. IL-23 secreted by the gastric mucosa could be implicated in the pathogenesis of chronic gastritis. IL-23 was released in the presence of H. pylori from the inflamed gastric mucosa and followed the kinetics of IL-1beta.

Inherited retarded eruption in the permanent dentition.

The term retarded eruption, may be used in cases where eruption is inhibited, causing an interruption in the coordination of tooth formation and tooth eruption. The phenomenon may be local or general, and several etiological factors for retarded eruption have been listed, comprising a lack of space, ankylosis, cysts, supernumerary teeth, hormone and vitamin deficiencies and several developmental disturbances and syndromes. The present paper describes several cases of retarded eruption where no factors other than inheritance have been evident. So far 14 cases have been evaluated, 9 boys and 5 girls. In addition several cases have been registered among parents and grandparents of the probands. Typical features are: retarded eruption, defined as more than 3 SD beyond mean eruption figures, comprises all teeth in the permanent dentition, and in 5 cases also second primary molars. The chronology of tooth formation are within normal limits. Consequently the teeth finish development still laying deeply buried in the jaws, often in aberrant positions and with curves or hooks on the roots. When the teeth finally get the "signal" for eruption, 5-15 years beyond normal eruption time, they move rather quickly into right positions, despite the long eruption paths and the hooked roots. Permanent teeth without, as well as with predecessors, are affected. Extraction of predecessors does not seem to provoke eruption. The main features in management are to take care of the primary teeth, to improve-esthetics, and offer surgery and orthodontics when needed. Analyses of pedigrees indicates that the genetic transmittance may be autosomal dominant as both sexes are affected, about half of the siblings show the trait, and the trait shows continuity through generations.

Inherited primary failure of eruption in the primary dentition: report of five cases.

Unerupted primary teeth are a rare event and in most cases involve the second primary molars. The impaction may be primary, meaning that the teeth never have been erupted (also called primary failure of eruption), or it may be secondary, meaning that the teeth after eruption are reimpacted. The present report describes five cases (three boys and two girls) with primary failure of eruption of totally fourteen second primary molars. None of these teeth ever erupted and were removed surgically at an age of 10-11 yrs. Additionally, in all five cases the eruption of the entire permanent dentition was severely retarded. Consequences of the nonerupting primary molars put a more functional strain, with severe attrition, on the remaining teeth. The unerupted primary molars also seemed to prevent the development of the corresponding premolars. In addition the impacted primary molars were in some cases a threat to the eruption of first permanent molars. The etiology of the present primary failure of eruption seems to be inheritance, and the mode of transmission is judged to be autosomal dominant.