Marlex Mesh Gastric Banding: A 7-12 Year Follow-Up

This paper presents a 7-12 year (mean 9.8 years) follow-up of 92 extremely obese patients treated with Marlextrade mark mesh gastric banding (GB). The follow-up rate was 92% (85 patients). Weight loss was initially good (an average reduction in BMI of 13 during the first year), but late weight gain has been a common complaint and a reason for reoperation. Other complications that necessitated reoperation were severe vomiting and esophagus not amenable to medical treatment. Four patients have developed signs of Barrett's esophagus at late follow-up. Forty-six patients (50%) were reoperated 70 times for correction of the band or conversion to vertical banded gastroplasty (VBG). The most common reoperative procedure was conversion to VBG (38 patients). Only 25 (31%) of the 80 patients with long-term follow-up have an intact band. Our results show the need of long follow-up and that this GB cannot be recommended for the treatment of morbid obesity.     

Are patients with liver cirrhosis hypermetabolic?

Hypermetabolism is not a constant feature of liver cirrhosis. It may occur in up to 18% of cirrhotics. Most of the deviations are due to increases in resting energy expenditure (REE). Dietary induced thermogenesis (DIT) is normal or slightly increased whilst the thermic effect of exercise TEE is of minor importance in cirrhosis. The increase in REE which reflects a systemic manifestation of liver disease cannot be identified by the clinical and biochemical measures of liver function. An increased REE is frequently seen in malnourished patients and this is mainly due to disproportional loss in muscle mass. Some cirrhotic patients cannot reduce REE in response to weight loss. This problem is not specific for liver cirrhosis but is also seen in other cachectic groups of patients. Adjustment of REE per kg fat free mass (FFM) may lead to erroneous conclusions (i) because of the non linearity of REE over the range of FFM and (ii) the different contributions of muscle mass and non-muscle body cell mass (BCM) to FFM over the range of FFM. There is circumstantial evidence that the metabolic rate per kg BCM is increased in malnourished cirrhotics. More specifically, cirrhosis increases in REE are associated with a deterioration in hepatic circulation. Increased sympathetic nervous system activity is frequently seen in cirrhosis and may provide a link between between reduced nutritive portal flow and increased whole body oxygen consumption. Increased REE is also associated with weight loss, a poorer liver function and a higher mortality after liver transplantation and thus may have prognostic value. Taken together, REE is variable in patients with cirrhosis. Hypermetabolism is seen in malnourished patients and those with impaired splanchnic hemodynamics. Hypermetabolism is associated with a poorer outcome after liver transplantation.     

Evaluation of nutritional counselling in HIV-associated malnutrition

In HIV-infected patients, the outcome of counselling as the first step of a nutritional intervention programme was evaluated, in order to identify clinical and nutritional predictors for its efficacy. 75 HIV-infected patients were investigated, most with advanced disease. Nutritional status was determined by body weight, bioelectrical impedance and 7-day food intake record. Prior mean weight loss was 10% (range = +4% to -31%). Counselling facilitated weight gain in 40 75 patients (1-4 months later, overall mean difference +1.4 +/- 6.2%) and in 14 34 patients (8-11 months later, overall mean difference -1.4 +/- 9.0%). Weight changes correlated with changes in body cell mass (r(2) = .69, p < .001) and in body fat (r(2) = .29, p < 0.05), but not extracellular mass. Underlying conditions such as AIDS definition, fever, and diarrhoea correlated to prior weight loss (p < .001) but not to the outcome of counselling. Low energy intake (before counselling, < 31.5 kcal/kg) did not correlate to prior weight loss but it predicted further weight loss (p < 0.05 towards normal intake). High energy intake (> 38.5 kcal/kg) correlated (p < 0.05) with more prior weight loss but not with further weight changes. Nutritional counselling may be an effective first-line intervention for malnourished HIV infected patients. More than half of patients gain weight without other nutritional treatment. Whereas the severity of malnutrition is influenced by the underlying disease, fever, and diarrhoea, the course of weight change after nutritional intervention is not. Counselling may reduce the nutritional impact of these risk factors. In patients with low spontaneous intake, efficacy of counselling alone is limited, but it may help to identify those who require more invasive nutritional treatment.     

Metabolic and thermogenic response to continuous and cyclic total parenteral nutrition in traumatised and infected patients

16 traumatised or infected patients on mechanical ventilation were randomised to continuous TPN or to cyclic TPN after a 24-h period of glucose infusion (1.25 kJ x kg BW(-1) x h(-1)). Energy supply was equivalent to 1.3 x baseline energy expenditure. Glucose, fat and amino acids were administered at a constant rate over 24 h in the continuous TPN group and over 12 h, followed by glucose (1.25 kJ x kg BW(-1) x h(-1)), in the cyclic TPN group. Nutrient-induced thermogenesis was lower during continuous than during cyclic TPN (5 +/- 4 vs. 12 +/- 7%, mean +/- SD, p < 0.05), as was the increase in CO(2) elimination (13 +/- 11 vs. 30 +/- 7%, respectively, p < 0.01). Energy balance was more positive during continuous TPN. In both groups, energy expenditure reached a plateau during the first 12 h of TPN infusion. The lower nutrient-induced thermogenesis and more positive energy balance, indicates a more efficient utilisation of nutrients during continuous than during cyclic TPN. The lower CO(2) production during continuous TPN, may be advantageous when respiratory function is compromised. The plateau in energy expenditure in response to TPN infusion may be useful as a guideline for nutritional therapy.     

Immunohistochemistry of anterior proliferative vitreoretinopathy

Anterior proliferative vitreoretinopathy is characterized by epiretinal proliferation that extends anteriorly over the vitreous base, and may, in addition to the cells usually contributing to proliferative vitreoretinopathy, also contain cells of ocular structures located in that area. We examined 11 complete globes with aPVR that were enucleated after previous severe trauma or perforating injuries (n=8) and complicated retinal detachment (n=3) by a panel of immunohistochemical markers. We found presence of RPE, glial cells, macrophages and fibrocytes, as consistently reported in PVR membranes. In addition, T-cell lymphocytes were present in 6 of the cases, and cells expressing the common leucocyte antigen on 8 cases. Cells staining positive for the intracytoplasmic contractile filament-smooth muscle actin were present in 5 cases and cells staining for desmin in one case. Collagen type IV was part of most of the membranes, and vessels with leakage of plasma factors were present in more than half of the cases.This paper was presented in part at the First Annual Meeting of the European Community Ophthalmic Research Association (ECORA), Bonn, Germany, 6.10.1993.     

H3 receptor-mediated inhibition of noradrenaline release: an investigation into the involvement of Ca2+ and K+ ions,G protein and adenylate cyclase

The effects of ₂-adrenoceptor agonists (dexmedetomidine, oxymetazoline), alone or in combination with various -adrenoceptor subtype-selective antagonists (CH-38083, idazoxan, WB4101, BRL44408, ARC-239, prazosin), on noradrenaline- and isoprenaline-induced lipolysis were investigated in human isolated abdominal subcutaneous fat cells. The rank order of potency of antagonists in preventing dexmedetomidine- and oxymetazoline-evoked suppression of isoprenaline-induced lipolysis was (pA₂-values): CH-38083 (7.69 and 7.48) idazoxan (7.5 and 7.41) > BRL 44408 (7.23 and 7.19) WB 4101 (7.13 and 7.12) > prazosin (5.18 and 5.17) > ARC-239 (4.72, 4.9). While CH-38083 and idazoxan, non-subtype selective ₂-adrenoceptor antagonists and BRL44408, a selective a_2A-adrenoceptor antagonist as well as WB4101 potentiated the lipolytic effect of noradrenaline, ARC-239, the selective _2B-adrenoceptor antagonist failed to affect it. In addition since the _2A-adrenoceptor selective agonist, oxymetazoline concentration dependently inhibited the lipolytic effect of isoprenaline, and WB4101 and BRL44408 (a_2A-adrenoceptor antagonists) antagonised the effect of oxymetazoline in a competitive manner, it is concluded that the a_2A-adrenoceptor subtype is involved in antilipolysis. In addition, functional evidence was obtained that there is an interaction between _2A- and -adrenoceptors located on the cell surface of adipocytes, through which locally released noradrenaline and/or circulating circulating adrenaline influence lipolysis.On leave from Institute of Medical Pharmacology, University of Pisa, Via Roma 55, I-5626 Pisa, Italy Correspondence to: E. S. Vizi at the above address     

Signal transduction pathway of the muscarinic receptors mediating gallbladder contraction

In gallbladder smooth muscle, carbachol interacts with M₃ receptors to mediate contraction. To examine components of the intracellular second messenger system that is coupled to these receptors we have tested whether carbachol stimulates the formation of inositol phosphates (IP) to cause contraction. Guinea pig gallbladder muscle strips were prelabeled with [³H]inositol and were incubated with 0.1 mmol/l carbachol, a concentration causing maximal contraction. [³H]inositol monophosphates, [³H]inositol bisphosphates and [³H]inositol trisphosphates and contraction were measured at various times (0–90 s). To examine whether a pertussis toxin-sensitive guanine nucleotide binding protein is coupled to the muscarinic receptors, guinea pigs were pretreated with pertussis toxin (180 g/kg i.v./24 h). The effectiveness of pertussis toxin treatment was determined by measuring [³²P]ADP-ribosylation of a –40/41 kDa protein from gallbladder homogenates. Carbachol caused a significant time-dependent increase in the formation of [³H]inositol monophosphates, [³H]inositol bisphosphates and [³H]inositol trisphosphates. The time course of [³H]inositol trisphosphate turnover caused by carbachol was biphasic, and was detectable at 15 s and maximal at 60 s; at 75 s and 90 s formation of [³H]inositol trisphosphates decreased, whereas the time course of carbachol-induced contraction of the gallbladder smooth muscle strips reached a plateau after 90 s. The effects of carbachol on [³H]inositol trisphosphates and on contraction were abolished by atropine. Pretreatment with pertussis toxin resulted in ADP-ribosylation of a 40/41 kDa protein from gallbladder cell membranes but did not affect the concentration-response or time course of carbachol-induced contraction. These results indicate that carbachol-induced contraction of gallbladder smooth muscle cells is accompanied by the activation of inositol phosphate turnover and does not involve a pertussis toxin-sensitive G-protein.This article is based in part on the doctoral thesis of Burkhard Mackensen at the Faculty of Medicine, University of Hamburg, Germany. Some of the results were presented at the meeting of the American Gastroenterological Association (AGA) in San Francisco 1992 (von Schrenck et al. 1992) Correspondence to: T. von Schrenck at the above address     

Pharmacokinetics and bioavailability of benperidol in schizophrenic patients after intravenous and two different kinds of oral application

Pharmacokinetics and bioavailability of benperidol were determined in 13 schizophrenic patients after acute administration of 6 mg benperidol as an intravenous (i.v.) bolus injection, orally as liquid, and orally as tablets using a partially randomized cross-over design. Drug plasma levels were determined by high performance liquid chromatography with electrochemical detection and subjected to model independent pharmacokinetic analyses. After i.v. dosing the geometric means (mean-g) were 3.2 min for the distribution half-life, 5.80 h for the elimination half-life (t _1/2), 4.21 l/kg for the distribution volume, 7.50 h for the mean residence time (MRT), and 0.50 l/(h*kg) for the clearance. After oral administration as liquid and as tablet mean-g data for the time lag until the first appearance of measurable plasma concentrations were 0.33 and 1.1 h, mean-g t _1/2 values were 5.5 and 4.7 h, respectively, mean-g t _max data were 1.0 h and 2.7 h, mean-g MRT values were 8.44 and 8.84 h, and mean-g C _max ^maxvalues were 10.2 and 7.3 ng/ml. Differences between liquid and tablet administration were statistically significant for time lag,t _max, andC _max. Mean-g absolute bioavailabilities were computed as 48.6% after liquid and 40.2% after tablet administration respectively. All parameters studied exhibited large intersubject variation. The plasma concentrations of the presumed metabolite reduced benperidol were found to be very low.