Biomedical subjects
Publications and source records attributed to T Andersen.
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Electrocardiograms, serum electrolytes, plasma concentrations of pre-albumin and retinol-binding globulin, and dietary intakes were analyzed in 22 women during weight loss after gastroplasty surgery for morbid obesity. QT interval corrected for heart rate (QTc) was prolonged (greater than 0.44 sec) in 32% (95% confidence limits 14-55%) on one or more occasions. No clinical or electrocardiographic complications were seen. Occurrence of QTc prolongation was significantly (p less than 0.05) associated with protein intake below recommendation and with low plasma pre-albumin concentrations. QTc prolongation was not associated with mineral intake and occurred in spite of normal serum levels of calcium (uncorrected and albumin-corrected), magnesium, potassium and sodium. Because QTc prolongation may precede fatal arrhythmias, adequate protein intake is mandatory during weight reduction.
A hundred patients scheduled for elective abdominal surgery were randomized to either general anaesthesia (low-dose fentanyl) and systemic morphine for postoperative pain or combined general anaesthesia and epidural analgesia with etidocaine 1.5% intraoperatively (T4-S5) and bupivacaine 0.5% 5 ml/4 h for 24 h and morphine 4 mg/12 h for 72 h. Postoperative pain was better controlled by the epidural regimen (P less than 0.0001). We found no significant reduction in postoperative mortality (6% to 2%), pneumonia (28% to 20%), cardiac dysrhythmia (10% to 5%) and wound complications (14% to 11%) by the epidural analgesic regimen. The incidence of deep venous thrombosis (125I-fibrinogen scan) was 32% after general anaesthesia and low-dose heparin and 34% after epidural analgesia with no prophylactic antithrombotic treatment (P greater than 0.9). Postoperative weight loss and decrease in serum-albumin and serum-transferrin, as well as the reduction in haemoglobin and the need for postoperative transfusions, were similar in the two groups. Convalescence, as assessed by postoperative fatigue, restoration of bowel function (flatus, bowel movement and food intake) and the time until the patients were self-aided at their preoperative level, was not reduced by epidural analgesia. Since 50% of the patients in each group suffered from one or more of the above-mentioned postoperative complications, this epidural regimen was not effective in reducing postoperative morbidity after major abdominal surgery despite the achievement of adequate pain relief.
To obtain information on possible determinants of weight loss after horizontal gastroplasty, pouch emptying was prospectively investigated in 27 morbidly obese patients. A scintigraphic method was used. Examinations were carried out every 6 months until 2 years after surgery. Pouch emptying was described by means of delay, time until half emptying, mean transit time, and emptying rate. The measures all showed a significant (p less than 0.05) acceleration of pouch emptying during the first 6 months after gastroplasty. Thereafter pouch emptying was unaltered. No significant association could be detected between measures of pouch emptying and weight loss. From calculation of 95% confidence intervals for coefficients of correlation it proved very unlikely that pouch emptying is an important determinant of weight loss.
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We compared the weight-reducing effect of diet and gastroplasty with that of diet alone in a randomized trial in 60 morbidly obese patients followed for two years. Initial median body weight was 120 kg in patients randomly assigned to gastroplasty plus diet and 115 kg in those assigned to diet alone. Maximum weight losses did not differ significantly between the groups (26.1 kg in the gastroplasty group and 22.0 kg in the group treated with diet alone, P greater than 0.05). The risk of a Type II error with a true difference larger than 9.5 kg was less than 5 per cent. However, the group treated with diet alone regained significantly more weight after maximum weight loss had been achieved, so that the gastroplasty group had a more favorable net outcome at two years (P less than 0.05).
Delayed hypersensitivity to four common antigens was assessed in 32 patients undergoing major abdominal surgery randomly allocated to either general anesthesia (fentanyl + O2/N2O + postoperative pain relief with systemic opiates) or general anaesthesia + epidural analgesia (local anaesthetics + morphine) continued for 72 h. Skin-test responses were performed 2 days before surgery and 1 day after surgery and compared to a similar retesting schedule in 16 comparable non-operative control patients. Cumulated mean skin-test responses increased from 1290 to 2330 mm2 (P less than 0.0001) during retesting in the non-operative control group. In contrast, mean skin-test responses in patients operated during general anaesthesia + systemic opiates for postoperative pain relief fell from 1422 to 1227 mm2 (P = 0.3) and in patients receiving epidural analgesia from 1228 to 890 mm2 (P = 0.06), without statistically significant differences between these two groups (P greater than 0.5). Thus, surgery leads to depression of delayed hypersensitivity and this impairment in immunofunction is not modified by an epidural analgesic regimen providing adequate pain relief.
An analysis was made of weight changes during treatment with valproate in 63 adult epileptic patients. 36 patients (57%) gained more than 4 kg in weight during treatment, while 27 patients (43%) were stable in weight with weight changes of less than +/- 4 kg. There were no significant differences between weight gainers and weight-stable patients with regard to age, sex, pretreatment overweight, duration of treatment, dosage or serum levels of valproate. From structured patient interviews, it appeared that the 2 groups of patients differed only insignificantly with regard to appetite, thirst and familial predispositions to obesity and diabetes. Consequently, no factors predictive for weight gain could be outlined. Presumable pathogenic mechanisms of importance are discussed.
Liver biopsies from 61 consecutive patients with morbid obesity (less than 60% overweight) and from 48 patients with alcoholic liver disease were examined for the presence of Mallory bodies. For the detection both routine haematoxylin and eosin stained sections and sections exposed to an immunohistochemical technique were employed. The latter uses an antiserum which recognizes antigenic determinants in Mallory bodies. Using haematoxylin and eosin staining. Mallory bodies were not detected in any of the biopsies from the obese patients, but found to be present in 63% of the patients with alcoholic liver disease. Using the immunohistochemical technique, Mallory bodies were found in the liver of 2 obese patients (3%) and in 36 patients with alcoholic liver disease (75%). None of the Mallory body positive obese patients showed signs of diabetes mellitus, cholestasis or hypocholesterolemia, but both patients admitted previous excessive alcohol consumption. It is concluded that the immunohistochemical detection of Mallory bodies is more sensitive than routine staining. Further, Mallory bodies are rare findings in livers of obese patients and may be related to excessive alcohol consumption.
Plasma fibronectin concentrations and liver morphology were investigated in 45 morbidly obese subjects (median overweight 88%) and in 42 normal weight controls, matched for sex and age. A significantly (P less than 0.01) raised plasma fibronectin concentration (median 464 mg/l, range 276-862 mg/l) was found in the obese subjects when compared with concentrations in the controls (median 348 mg/l, range 164-536 mg/l). Plasma fibronectin concentrations of the obese patients correlated significantly to their degree of overweight (r = 0.33, P less than 0.05) as well as to the degree of fatty change found in their liver biopsies (r = 0.33, P less than 0.05). Significantly (P less than 0.05) elevated plasma fibronectin concentrations even in obese subjects without hepatic fatty change indicate that liver fat accumulation is no prerequisite of the obesity-related elevation of plasma fibronectin. Raised plasma fibronectin concentration in obesity may more readily be explained by an increased fibronectin formation by lipocytes.
Literature on liver morphology in untreated obesity reveals varying prevalences of various pathological findings. The purpose of this literature study was to summarize and evaluate the published observations and to discuss discrepant findings. A complete search was aimed at utilizing bibliographic methods including a computerized survey. Forty-one original articles were included, comprising information on liver morphology in 1515 morbidly obese patients. Liver biopsy was considered normal in 12 per cent of the cases. The most frequent abnormality reported was fatty change, present in 80 per cent of the biopsies. Portal inflammation was also common (33 per cent). Fibrosis, mainly portal or periportal, was observed in 29 per cent. Cirrhosis, however, involved only 3 per cent. Study of relationships between the degree of liver change and certain possible pathogenetic factors (eg degree and duration of obesity, age, sex, alcohol consumption, diabetes mellitus) does not point towards a single causal factor. Co-influence of additional pathogenetic factors are likely in the development of liver changes in morbid obesity.
In gastroplasty and gastric bypass procedures for obesity much importance has been attached to obtaining a small fundic pouch combined with a narrow outlet, factors considered to determine weight loss. The present study is a prospective investigation of the influence of these stomach dimensions on the clinical outcome. With a standardized radiological procedure 72 examinations were carried out in 27 patients during the first 18 months after gastroplasty by the method of Gomez. Median pouch volume and stoma diameter were unaltered through the observation period. Early pouch volumes ranged from 51 to 244 ml, and stoma size ranged from 6 to 24 mm after 6 months. Within these limits pouch and stoma size were not significantly correlated to the weight loss obtained. Other factors seem to be of major importance for the weight-reducing effect of gastroplasty.
Calcium homeostasis in morbidly obese subjects has attracted little attention. Prompted by reports of elevated serum levels of parathyroid hormone in such patients, calcium homeostasis was investigated in 36 patients with morbid obesity and in 44 normal weight controls. Concerning serum immunoreactive parathyroid hormone (C-terminal), serum ionized calcium (Ca++) and serum albumin corrected magnesium no significant differences between the groups were detected. When albumin corrected, serum total calcium turned out to be significantly elevated (p less than 0.0001) in the obese subjects. Also, serum alkaline phosphatase activity was significantly raised in the obese state. The results demonstrate that calcium homeostasis, as expressed by the metabolically active serum Ca++, is normal in morbid obesity. But the results also point towards an abnormal calcium binding due to either an increased calcium binding to albumin or to calcium complexing small anions.
Liver morphology and biochemistry were investigated in 61 morbidly obese subjects selected by defined criteria. Median overweight was 82 per cent (range 61 to 170 per cent), and median duration of overweight was 20 years (range two to 45 years). No patient had more than a moderate alcohol consumption and only one was diabetic. Four biopsies (7 per cent) showed normal liver tissue, while fatty change was the main diagnosis in most cases (85 per cent). Increasing degrees of fatty change was significantly (P less than 0.02) associated with presence of lipogranulomas (found in 54 per cent of the biopsies), focal necroses (found in 28 per cent), slight parenchymal inflammation (found in 33 per cent), and Kupffer cell proliferation (found in 49 per cent). Slight portal inflammation was seen in 23 per cent but portal fibrosis in only 2 per cent of the biopsies. No case of cirrhosis was registered. Patients with moderate or severe fatty change, lipogranulomas , focal necroses or with parenchymal inflammation were significantly more obese than patients without these changes (P less than 0.05). Even in absence of fatty change, obese subjects showed a markedly decreased serum albumin concentration and an elevated serum alkaline phosphatase activity (P less than 0.0001) compared with non-obese controls. Serum lactate dehydrogenase and aspartate aminotransferase were significantly raised only in patients with fatty change. With respect to serum bilirubin and plasma cholesterol concentrations no significant differences were detected between patient subgroups and controls.(ABSTRACT TRUNCATED AT 250 WORDS)