Significance of vomiting for hyperamylasemia and sialadenosis in patients with eating disorders

The authors investigated the significance of vomiting for hyperamylasemia and sialadenosis in patients with bulimia nervosa. Hyperamylasemia was found in 61% of the bulimics and in 20% of the restrictor anorectics but in no patients with binge-eating syndrome. In more than three fourths of the bulimics there was a close positive correlation between the frequency of vomiting and total serum amylase levels. Both frequency and type of vomiting seem to be relevant to the extent of salivary gland enlargement. The significance of vomiting for the etiopathology of hyperamylasemia and for the diagnosis of eating disorders will be discussed. © 1993 by John Wiley & Sons, Inc.     

Rationale and design of the AdaptResponse trial: a prospective randomized study of cardiac resynchronization therapy with preferential adaptive left ventricular‐only pacing

The AdaptResponse trial is designed to test the hypothesis that preferential adaptive left ventricular‐only pacing with the AdaptivCRT^® algorithm reduces the incidence of the combined endpoint of all‐cause mortality and intervention for heart failure (HF) decompensation, compared with conventional cardiac resynchronization therapy (CRT), among patients with a CRT indication, left bundle branch block (LBBB) and normal atrioventricular (AV) conduction. The AdaptResponse study is a prospective, randomized, controlled, single‐blinded, multicentre, clinical trial ( ClinicalTrials.gov Identifier: NCT02205359), conducted at up to 200 centres worldwide. Following enrolment and baseline assessment, eligible subjects will be implanted with a CRT system containing the AdaptivCRT algorithm, and randomized in a 1:1 fashion to either a treatment (‘AdaptivCRT’) or control (‘Conventional CRT’) group. The study is designed to observe a primary endpoint in 1100 patients (‘event‐driven’) and approximately 3000 patients will be randomized. The primary endpoint is the composite of all‐cause mortality and intervention for HF decompensation; secondary endpoints include all‐cause mortality, intervention for HF decompensation, clinical composite score (CCS) at 6 months, atrial fibrillation, quality of life measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), health outcome measured by the EQ‐5D instrument, all‐cause readmission after a HF admission, and cost‐effectiveness. The AdaptResponse clinical trial is powered to assess clinical endpoints and is expected to provide definitive evidence on the incremental utility of AdaptivCRT‐enhanced CRT systems.     

Weisheitszähne — Stationär behandlungsbedürftige Komplikationen

Background

In view of the conflicting guidelines issued by national and international scientific societies, debate about the indications for prophylactic extraction of wisdeom teeth is ongoing. This prospective study was therefore set up to explore the complications associated with wisdom teeth and requiring in-patient treatment.

Patients and Methods

From January /2003 to December 2003, 21 subjects were admitted for treatment of complications associated with wisdom teeth. The medical history was recorded for each of these patients, as were the cause and type of the complications. The parameter used to quantify the severity of any infections was the CRP, and the overall clinical complexity level of each case was assessed by the length of stay in hospital (and the duration of intensive care if this had been necessary). The characteristics of patients in the group with postoperative complications were compared to those of patients with complications attributable to pericoronitis. Moreover, complications in patients who had undergone prophylactic extraction of wisdom teeth that had not been causing any symptoms were compared with those in patients whose wisdom teeth had been extracted because of morbidity.

Results

Overall, 18 deep-space infections (15 abscesses, 2 inflammatory infiltrations, 1 case of phlegmonous cellulitis), 2 mandibular fractures and 1 lingual nerve injury were noted within 1 year. The complications resulted from surgical procedures in 15 of the 21 cases, while in 6 they had their origin in pericoronitis. Extensive surgery or intensive care was required only for patients with postoperative complications. The length of stay in hospital was significantly greater for patients with postoperative complications (p= 0.007, U-test). However, 9 of these 15 patients reported preoperative episodes of infection. Thus, more than two thirds of the complications could be traced back to wisdom teeth that were causing symptoms.

Conclusion

In our clinic’s catchment area, infectious complications were more frequent and more severe and required more intensive and longer treatment in hospital than complications arising from pericoronitis. However, complications of prophylactic extraction of wisdom teeth were decidedly less frequent than direct or indirect complications of extraction of symptomatic teeth. Thus, our data tend to support the concept of elective extraction of wisdom teeth with the aim of preventing serious infections.     

Intravenous DDAVP and factor VIII-von Willebrand factor concentrate for the treatment and prophylaxis of bleedings in patients With von Willebrand disease type 1, 2 and 3.

The current standard set of von Willebrand factor (VWF) parameters used to differentiate type 1 from type 2 VWD include bleeding times (BTs), factor VIII coagulant activity (FVIII:C), VWF antigen (VWF:Ag), VWF ristocetine cofactor activity (VWF:RCo), VWF collagen binding activity (VWF:CB), ristocetine induced platelet aggregation (RIPA), and analysis of VWF multimers in low and high resolution agarose gels and the response to DDAVP. The BTs and RIPA are normal in asymptomatic carriers of a mutant VWF allele, in dominant type 1, and in recessive type 2N VWD, and this category has a normal response of VWF parameters to DDAVP. The response of FVIII:C is compromised in type 2N VWD. The BTs and RIPA are usually normal in type Vicenza and mild type 2A VWD, and these two VWD variants show a transiently good response of BT and VWF parameters followed by short in vivo half life times of VWF parameters. The BTS are strongly prolonged and RIPA typically absent in recessive severe type 1 and 3 VWD, in dominant type 2A and in recessive type 2C (very likely also 2D) VWD and consequently associated with low or absent platelet VWF, and no or poor response of VWF parameters to DDAVP. The BTs are prolonged and RIPA increased in dominant type 2B VWD, that is featured by normal platelet VWF and a poor response of BT and functional VWF to DDAVP. The BTs are prolonged and RIPA decreased in dominant type 2A and 2U, that all have low VWF platelet, very low VWF:RCo values as compared to VWF:Ag, and a poor response of functional VWF to DDAVP. VWD type 2M is featured by the presence of all VWF multimers in a low resolution agarose gel, normal or slightly prolonged BT, decreased RIPA, a poor response of VWF:RCo and a good response of FVIII and VWF:CB to DDAVP and therefore clearly in between dominant type 1 and 2U. The existing recommendations for prophylaxis and treatment of bleedings in type 2 VWD patients with FVIII/VWF concentrates are mainly derived from pharmocokinetic studies in type 3 VWD patients. FVIII/VWF concentrates should be characterised by labelling with FVIII:C, VWF:RCo, VWF:CB and VWF multimeric pattern to determine their safety and efficacy in prospective management studies. As the bleeding tendency is moderate in type 2 and severe in type 3 VWD and the FVIII:C levels are near normal in type 2 and very low in type 3 VWD patients. Proper recommendations of FVIII/VWF concentrates using VWF:RCo unit dosing for the prophylaxis and treatment of bleeding episodes are proposed and has to be stratified for the severity of bleeding, the type of surgery either minor or major and for type 2 and type 3 VWD as well.     

Coexistence of foam cells and hypocholesterolemia in mice lacking the ABC transporters A1 and G1

The concept that macrophages can become foam cells as a result of a disturbed balance between the uptake of cholesterol from lipoproteins and cholesterol efflux is generally accepted. ABCA1 and ABCG1 are two cholesterol transporters that may act sequentially to remove cellular cholesterol, but currently their combined role in vivo is unknown. We report here that targeted disruption of both ABCA1 and ABCG1 in mice, despite severe plasma hypocholesterolemia, leads to massive lipid accumulation and foam cell formation of tissue macrophages. A complete ablation of cellular cholesterol efflux in vitro is observed, whereas in vivo macrophage-specific reverse cholesterol transport to the feces is markedly decreased. Despite the massive foam cell formation of tissue macrophages, no lipid accumulation was observed in the vascular wall, even in mice of 1 year old, indicating that the double knockout mice, possibly because of their hypocholesterolemia, lack the trigger to attract macrophages to the vessel wall. In conclusion, even under hypocholesterolemic conditions macrophages can be converted into foam cells, and ABCA1 and ABCG1 play an essential role in the prevention of foam cell formation.