Diabetic ketoacidosis and compliance.
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Biomedical subjects
Publications and source records attributed to J H Christensen.
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BACKGROUND: Uraemia and chronical haemodialysis are associated with an abnormal growth hormone (GH)-insulin-like growth factor (IGF) axis which may contribute to malnutrition and renal bone disease. Short-term studies have shown a beneficial effect of treatment with recombinant human growth hormone (rhGH) on nutritional status in patients on haemodialysis. In the present study, we evaluated the effect of rhGH on bone and mineral metabolism. METHODS: Twenty chronic malnourished patients on haemodialysis took part in a double-blind, placebo controlled trial with subcutaneous injections of rhGH (4 IU/m2/day) or placebo for 6 months. RESULTS: During rhGH treatment, serum IGF-1 increased 264 +/- 52% (mean +/- SEM) (P < 0.008). There were no significant changes in biochemical markers of mineral metabolism (serum ionized calcium, phosphate and parathyroid hormone). Among markers of bone metabolism, there was a significant increase in serum procollagen type I C-terminal propeptide (maximum 155 +/- 8%, P < 0.001) and no significant changes in serum alkaline phosphatase. Bone densitometry showed a significant decrease in whole body bone mineral content (95.7 +/- 1.2%) after 6 months treatment. The effects on the proximal femur were not significant. CONCLUSION: The effects of 6 months treatment with rhGH seen in this study are best explained by a GH- or IGF-1-induced increased bone turnover. Long-term treatment in larger cohorts followed by bone densitometry and, preferentially, bone histomorphometry are needed to evaluate whether this is a beneficial effect in haemodialysis patients.
Lignin is an integral cell wall component of all vascular plants. Peroxidases are widely believed to catalyze the last enzymatic step in the biosynthesis of lignin, the dehydrogenation of the p-coumaryl alcohols. As the first stage in identifying lignin-specific peroxidase isoenzymes, the classical anionic peroxidases found in the xylem of poplar (Populus trichocarpa Trichobel) were purified and characterized. Five different poplar xylem peroxidases (PXP 1, PXP 2, PXP 3-4, PXP 5, and PXP 6) were isolated. All five peroxidases were strongly glycosylated (3.6% to 4.9% N-glucosamine), with apparent molecular masses between 46 and 54 kD and pI values between pH 3.1 and 3.8. Two of the five isolated peroxidases (PXP 3-4 and PXP 5) could oxidize the lignin monomer analog syringaldazine, an activity previously correlated with lignification in poplar. Because these isoenzymes were specifically or preferentially expressed in xylem, PXP 3-4 and PXP 5 are suggested to be involved in lignin polymerization.
Patients with chronic renal failure (CRF) often have autonomic cardiac dysfunction, which can be assessed by measuring heart rate variability (HRV). This dysfunction prediposes the patients to sudden cardiac death. This study describes 24-hour HRV in patients with CRF compared to HRV in patients with a previous myocardial infarction (MI). Furthermore, associations between HRV in patients with CRF and the content of n-3 polyunsaturated fatty acids (PUFA) in cell membranes were examined, because n-3 PUFA may improve HRV. Twenty-nine patients with CRF treated with dialysis were enrolled. A 24-hour Holter recording was obtained at baseline and the HRV variables, RR (= mean of all normal RR intervals during the 24-hour recording) and SDNN (= standard deviation of all normal RR intervals in the entire 24-hour recording) were analyzed. Also, granulocyte fatty acid composition was determined. The patients were allocated to dietary supplementation with either 5.2 g of n-3 PUFA or a placebo oil (olive oil) daily for 12 weeks in a double-blind design. At the end of the supplementation period the Holter recording and blood sampling were repeated. At baseline the CRF patients' mean SDNN ws 86 ms compared to 118 ms (p < 0.01) in patients with a previous MI. After supplementation with either n-3 PUFA or placebo a highly significant correlation was observed between the content of n-3 PUFA in cell membranes and HRV (r = 0.71, p < 0.01). Furthermore, when the patients were dichotomized according to their mean SDNN, it was found, that those with the highest SDNN had a higher content of n-3 PUFA in cell membranes compared to those with the lowest SDNN (7.8% vs 4.2%, p < 0.05). In conclusion, HRV was decreased in CRF patients indicating a cardiovascular autonomic dysfunction. The positive correlation between the n-3 PUFA content in cell membranes and HRV suggests that the effects of an increased intake of n-3 PUFA in CRF patients should be further studied.
BACKGROUND: Epidural analgesia before limb amputation is commonly used to reduce postamputation pain. But there have been no controlled studies with large numbers of patients to prove such a pre-emptive effect. We investigated whether postamputation stump and phantom pain in the first year is reduced by preoperative epidural blockade with bupivacaine and morphine. METHODS: In a randomised, double-blind trial, 60 patients scheduled for lower-limb amputation were randomly assigned epidural bupivacaine (0.25% 4-7 mL/h) and morphine (0.16-0.28 mg/h) for 18 h before and during the operation (29 patients; blockade group) or epidural saline (4-7 mL/h) and oral or intramuscular morphine (31 patients; control group). All patients had general anaesthesia for the amputation and were asked about stump and phantom pain after 1 week and then after 3, 6, and 12 months by two independent examiners. Study endpoints were rate of stump and phantom pain, intensity of stump and phantom pain, and consumption of opioids. FINDINGS: Two patients in each group were withdrawn before amputation. The groups were well matched in baseline characteristics. Median duration of preoperative saline treatment was 18.5 h (IQR 17-20). Median duration of preoperative epidural blockade in the blockade group was 18 h (15-20.3). The combined median duration of postoperative epidural pain treatment in both groups was 166 h (89.3-308.3). After 1 week, 14 (52%) patients in the blockade group and 15 (56%) in the control group had phantom pain (95% CI - 30.6 to 22.7, p = 0.9). The figures for blockade versus control group were: 14 (82%) vs ten (50%; 4.0 to 60.8, p = 0.09) at 3 months; 13 (81%) vs 11 (55%; -2.7 to 55.3, p = 0.2) at 6 months; and nine (75%) vs 11 (69%; -27.0 to 39.6, p = 1.0) at 12 months. Intensity of stump and phantom pain and consumption of opioids were similar in both groups at all four postoperative interviews. INTERPRETATION: Perioperative epidural blockade started a median of 18 h (15-20.3) before the amputation and continued into the postoperative period does not prevent phantom or stump pain.
There is evidence for an antiarrhythmic effect of n-3 polyunsaturated fatty acids (n-3 PUFA) in animals. The aim of the present study was to investigate the effect of dietary n-3 PUFA on ventricular arrhythmias and heart rate variability (HRV) in patients with a previous myocardial infarction. Fifty-five patients were randomized to receive either 5.2 g of n-3 PUFA daily for 12 weeks or placebo in a double blind, placebo-controlled study. Prior to randomization a 24-hour Holter recording was obtained, and this was repeated at the end of the study. The major end-points were the number of ventricular extrasystoles (VE)/24 hours and the 24-hour HRV. A non-significant decrease in VE/24 hours was found in both the n-3 PUFA group and among controls after dietary supplementation, whereas HRV significantly increased after n-3 PUFA compared to both baseline values (p = 0.04) and to controls (p = 0.01). The present study therefore supports the hypothesis that n-3 PUFA may have an anti-arrhythmic effect in humans.
To elucidate a possible antiarrhythmic effect of long-chained n-3 polyunsaturated fatty acids, heart rate variability was assessed in 52 patients with a previous myocardial infarction and left ventricular dysfunction. The content of n-3 polyunsaturated fatty acids in platelets was closely associated with the patient's fish-consuming habits, and a significant positive correlation was observed between the n-3 fatty acid docosahexaenoic acid and heart rate variability.
The significance of preamputation pain for the development of postamputation stump and phantom pain has been discussed over the years and is still a matter of dispute. It has been argued that preamputation pain increases the risk of phantom pain and that phantom pain is a revivification of pain experienced before the amputation. The purpose of this prospective study was to clarify the relation between preamputation pain and phantom pain. Fifty-six patients scheduled for amputation of a lower limb were interviewed the day before the amputation about preamputation pain and about stump and phantom pain 1 week, 3 and 6 months after the amputation. Pain was quantitated and described using a visual analogue scale (VAS), 10 different word descriptors, the McGill Pain Questionnaire (MPQ) and the patients' own words. If phantom pain was present patients were asked if the pain was similar to any pain experienced before the amputation. At each postoperative interview patients were asked to recall preamputation pain intensity. Location of pain and analgesic requirements were registered. Preamputation pain significantly increased the incidence of stump pain (P = 0.04) and phantom pain (P = 0.04) after 1 week and the incidence of phantom pain after 3 months (P = 0.03). About 42% of the patients reported that their phantom pain resembled the pain they had experienced at the time of the amputation. However, there was no relation between the patients' own opinion about similarity between preamputation pain and phantom pain and the actual similarity found when comparing pre- and postoperative recordings of pain. Patients significantly overestimated preamputation pain intensity after 6 months.
Lightning injuries occur sporadically and are rarely seen in emergency departments, during the years 1991-1993 there have been 12 admissions due to this cause in Denmark. The special mechanisms of damage in lightning accidents are illustrated by review of the literature. The clinical findings are described, especially the transient neurological damage characterises lightning accidents. Contrary to what one would expect, the victim often survives a lightning accident. This is surprising considering the tremendous powers of nature involved and the serious clinical manifestations. Prevention is important, this is the reason why the population should be taught the appropriate behaviour if there is a thunderstorm. Resuscitation should be started immediately and continued even though the victim seems lifeless and might have dilated pupils not reacting to light. Good results have been reported even after prolonged resuscitation.
During the years 1991-1993, the emergency department of Arhus Kommune Hospital received four victims of lightning accidents. Two of these were admitted to the intensive care unit for further treatment and observation. This case report brings their histories including clinical findings. Possible mechanisms of damage are discussed and the importance of immediate and continued resuscitation of the presumably lifeless victim of a lightning accident is confirmed. All four patients recovered without serious physical sequelae.
In order to assess the impact of thrombolytic therapy on return to work 18 months after a first myocardial infarction 32 patients treated with streptokinase were compared to 30 patients not treated with streptokinase. The study was designed as a historical cohort study. The patients in both groups had continuous chest pain of less than six hours prior to admission and electrocardiographic changes consistent with acute myocardial infarction. The two groups were comparable with respect to medical variables related to their myocardial infarction and to educational level. A total of 17 patients (53%) in the streptokinase group and 16 (53%) among controls had stopped working 18 months after their MI. An association between the treatment and the working status could not be found (relative risk = 1.0) nor could it be found if the figures were corrected for deaths and retirements because of age. In conclusion, this study could not demonstrate any beneficial effect of thrombolytic therapy on the return to work 18 months after an initial myocardial infarction.
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In order to assess the impact of thrombolytic therapy on return to work eighteen months after a first myocardial infarction, 32 patients treated with streptokinase were compared with 30 patients not treated with streptokinase. The study was designed as a historical cohort study. The patients in both groups had continuous chest pain of less than six hours prior to admission and electrocardiographic changes consistent with acute myocardial infarction (MI). The two groups were comparable with respect to medical variables related to their myocardial infarction and to educational level. A total of 17 patients (53%) in the streptokinase group and 16 (53%) among controls had stopped working eighteen months after their MI. An association between the treatment and the working status could not be found (relative risk = 1.0) nor could it be found if the figures were corrected for deaths and retirements because of age. In conclusion, this study could not demonstrate any beneficial effect of thrombolytic therapy on the return to work eighteen months after an initial myocardial infarction.
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We studied cardiovascular and catecholamine responses for 3 days in three groups of patients undergoing abdominal hysterectomy. The night before surgery and again 2 h before induction of anaesthesia, patients received the ACE inhibitor, ramipril, the beta 1 blocker, metoprolol, or placebo. In the actively treated groups, mean diastolic pressure was reduced during surgery and increases in heart rate and arterial pressure after surgical incision were attenuated. During operation, stroke volume (SV) and cardiac output (CO) were significantly higher in the ramipril group. In contrast, beta 1, adrenergic block caused no significant changes in SV or CO. The concentration of noradrenaline in plasma and urine indicated that ACE inhibition caused attenuated release of noradrenaline. The results support the concept that angiotensin II facilitates release of noradrenaline from sympathetic nerves and that ACE inhibition inhibits this release.