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T P Almdal

Publications and source records attributed to T P Almdal.

At least 19 recordsLinked to original sources
PubMed2001

Thyroid-associated orbitopathy developed during hormone replacement therapy.

Thyroid-associated orbitopathy (TAO) developed in relation to estrogen combined with progesterone therapy has not been reported previously. We report a case of a 56-year-old postmenopausal woman who during estrogen/progesterone treatment developed signs and symptoms of orbitopathy. The patient had no previous history of autoimmune- or thyroid disorders. The initial eye symptoms disappeared after withdrawal of hormone replacement therapy. Five years later estrogen/progesterone treatment was re-instituted. The patient had relapse of orbitopathy. The hormones were discontinued and the eye symptoms disappeared again. This suggests that estrogen and/or progesterone could be of some pathogenetic importance in the induction of orbitopathy

Drug Therapy, Combination↗
PubMed1999

Prognostic value of nutritional status in chronic obstructive pulmonary disease.

The association between low body mass index (BMI) and poor prognosis in patients with chronic obstructive pulmonary disease (COPD) is a common clinical observation. We prospectively examined whether BMI is an independent predictor of mortality in subjects with COPD from the Copenhagen City Heart Study. In total, 1,218 men and 914 women, aged 21 to 89 yr, with airway obstruction defined as an FEV(1)-to-FVC ratio of less than 0.7, were included in the analyses. Spirometric values, BMI, smoking habits, and respiratory symptoms were assessed at the time of study enrollment, and mortality from COPD and from all causes during 17 yr of follow-up was analyzed with multivariate Cox regression models. After adjustment for age, ventilatory function, and smoking habits, low BMI was predictive of a poor prognosis (i.e., higher mortality), with relative risks (RRs) in underweight subjects as compared with that in subjects of normal weight of 1.64 (95% confidence interval [CI]: 1.20 to 2.23) in men and 1.42 (95% CI: 1.07 to 1.89) in women. However, the association between BMI and survival differed significantly with stage of COPD. In mild and moderate COPD there was a nonsignificant U-shaped relationship, with the lowest risk occurring in normal-weight to overweight subjects, whereas in severe COPD, mortality continued to decrease with increasing BMI (test for trend: p < 0.001). Similar results were found for COPD-related deaths, with the strongest associations found in severe COPD (RR for low versus high BMI: 7.11 [95% CI: 2.97 to 17.05]). We conclude that low BMI is an independent risk factor for mortality in subjects with COPD, and that the association is strongest in subjects with severe COPD.

Adult↗
PubMed1998

[Interaction between warfarin and coenzyme Q10].

Coenzyme Q10 (Ubidecarenone) is marketed as a dietary supplement. Drug interaction between coenzyme Q10 and warfarin has previously been reported. In the present case, a 72-year-old female treated with warfarin showed less responsiveness to warfarin than previously. It appeared she had taken coenzyme Q10, and when this was stopped, her responsiveness to warfarin was the same as before. Coenzyme Q10 is chemically similar to K-vitamins, which may explain the interaction with warfarin. Patients in treatment with warfarin should be aware of the possible risk of treatment failure when taking coenzyme Q10. The need for questioning patients concerning not only medications but also use of dietary supplements and alternative medications is emphasised.

Aged↗
PubMed1996

[Adverse effects of selective serotonin uptake inhibitors. Hyponatremia caused by Schwartz-Bartter syndrome].

This report describes three cases of hyponatraemia/syndrome of inappropriate secretion of antidiuretic hormone. The cases are most likely caused by treatment/intoxication with three different selective serotonin reuptake inhibitors: Fluoxetine, paroxetine and citalopram. All three patients were elderly women (75-83 years). Serum sodium values returned to normal or near normal after discontinuation of the drug and concomitant fluid restriction. Hyponatraemia has previously been described as an adverse effect to fluoxetine and paroxetine, but not to citalopram.

Aged↗
PubMed1996

[Treatment of obesity in patient groups].

The purpose of this study was to assess the results of group treatment in obesity. Patients referred to a department of endocrinology were on referral given individual diet counselling, and the patients were then seen every second week for control weighing and supplemental counselling either in groups of 10-12, or individually. One hundred and twenty-three (97 female and 26 male) patients who during a two year period, 1991-1993, were referred to the outpatient clinic of the Department of Endocrinology were identified. Ninety-five percent of the patients were markedly obese, body mass index > 30 m2/kg. Seventy percent of the patients continued the treatment and were either followed in the groups or individually. The patients followed in the groups (n = 66) lost 5.2 kg during 127 days (median), and this is not significantly different from those followed individually (n = 22) who lost 4.9 kg during 98 days. In conclusion, only a small weight reduction is seen in obese patients treated either in groups or individually. These results are comparable with previously reported results from a Danish study only using individual counselling.

Adult↗
PubMed1994

Control of non-insulin-dependent diabetes mellitus partially normalizes the increase in hepatic efficacy for urea synthesis.

The relation of urea synthesis rate to blood alanine concentration was assessed in seven healthy controls and eight patients with non-insulin-dependent diabetes mellitus (NIDDM) before (hemoglobin A1c [HbA1c] = 9.9% +/- 1.9%, mean +/- SD) and after (HbA1c = 7.9% +/- 0.8%) improvement of metabolic control. Following an overnight fast, alanine was infused at a rate of 2 mmol/(h.kg body weight [BW]). The hourly rate of urea synthesis was determined as the urinary excretion of urea corrected for accumulation of urea in total body water (TBW) and intestinal hydrolysis. The functional hepatic nitrogen clearance (FHNC) was calculated as the slope of the linear relation of urea synthesis rate to blood alanine concentration. The glucagon level was increased by twofold at the first investigation, but was not increased at the second. The insulin level was moderately increased at both investigations. In controls FHNC was 21.8 +/- 4.4 L/h, in poorly controlled patients it was increased to 36.6 +/- 4.3 L/h (P < .01), and following improvement of metabolic control it was not different from control levels at 28.6 +/- 4.3 L/h. By correlation analyses, FHNC was found only to be related to the fasting glucose value, albeit weakly (R2 = .39). In conclusion, hepatic kinetics of urea synthesis in poorly controlled NIDDM patients are changed in favor of increased conversion of alanine N to urea N at any amino acid concentration. This perturbation is partially normalized by improved metabolic control.

Adult↗
PubMed1992

Glucagon immunoneutralization in diabetic rats normalizes urea synthesis and decreases nitrogen wasting.

To study the effect of glucagon neutralization on urea synthesis in diabetic rats, animals with newly induced (75 mg/kg streptozocin) experimental diabetes mellitus were divided into two groups. One group was given one weekly injection of nonimmune rabbit serum (n = 6), and the other group was given one weekly injection of a specific high-titer antibody against pancreatic glucagon (n = 6). Four weeks later, serum-treated diabetic rats had fasting glucagon concentrations 2-3 times higher than nondiabetic controls given one weekly injection of saline (control). Plasma glucagon binding capacity of diabetic rats given glucagon antibodies was 10-15 times higher than the glucagon concentration. A second group of nondiabetic controls were given nonimmune serum. Blood glucose concentration and urinary glucose output were identical in both groups of diabetic animals. Food intake doubled in both groups of diabetic rats. In control rats, the accumulated nitrogen balance, determined weekly for 4 wk, was positive at 81 +/- 3.1 mmol/96 h; in serum-treated diabetic rats, the accumulated nitrogen balance was negative, -8.3 +/- 2.4 mmol/96 h throughout the 4 wk, whereas it was higher at 4.7 +/- 2.3 mmol/96 h in the glucagon antibody-treated diabetic rats (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗
PubMed1991

Pharmacokinetics of paroxetine in patients with cirrhosis.

In a 14-day multiple-dose study the pharmacokinetics of paroxetine was investigated in 12 patients with alcoholic cirrhosis and in 6 subjects without liver disease. The dose of 20-30 mg paroxetine daily was adjusted to the reduction in liver function, as assessed by the galactose elimination capacity. Accordingly, all but two of the cirrhotic patients received 20 mg, while all six control subjects received 30 mg. Dose-corrected, trough drug concentration at steady state (CSSmin) and dose-corrected AUC24h were significantly higher in the patients with liver diseases than in the control subjects [3.4 vs 1.5 ng.ml-1 per mg paroxetine and 89 vs 43 h (ng).ml-1 per mg paroxetine]. The elimination t1/2 was prolonged [83 vs 36 h], but the difference was not statistically significant, and the cirrhotic patients were still able to clear almost all the paroxetine by metabolism. All but two patients with cirrhosis experienced nausea during the first two or three days after the first dose, while none of the controls had this symptom. The study showed slower elimination of paroxetine and consequently higher plasma levels in patients with cirrhosis, suggesting that in the latter the dose of paroxetine should be in the lower end of the therapeutic range.

Adult↗
PubMed1991

Blockade of glucocorticoid receptors prevents the increase in urea synthesis after hysterectomy in rats.

The postoperative increase in hepatic conversion of amino nitrogen to urea nitrogen seems to be a primary cause of post-surgical catabolism. The importance of glucocorticosteroids for the spontaneous urea nitrogen synthesis rate (UNSR) and for the maximally amino acid-stimulated capacity of urea nitrogen synthesis (CUNS) was investigated 3 and 24 h postoperatively, respectively, in hysterectomized rats. Corticosteroid effects were neutralized by glucocorticoid receptor blockade by the pharmacological analogue RU486. Hysterectomy doubled UNSR from 3.16 +/- 0.20 to 6.12 +/- 0.27 mumol (per min per 100 g body weight) after 3 h (P less than 0.01) and increased CUNS by 40% from 7.47 +/- 0.30 to 10.29 +/- 0.41 mumol (per min per 100 g body weight) after 24 h (P less than 0.01). These changes were both normalized by the receptor blockade. Hysterectomy decreased total blood alpha-amino nitrogen concentration by 25% from 3.4 +/- 0.2 to 2.6 +/- 0.2 mmol l-1 (P less than 0.05) 3 h after surgery, which was normalized by glucocorticoid receptor blockade. Hysterectomized rats lost 10 +/- 1 g the first 24 h after surgery. The blockade reduced the weight loss to 6 +/- 1 g body weight (P less than 0.05) without changing food intake. The results indicate that glucocorticoid action plays a major role in the postoperative increase in hepatic amino nitrogen conversion.

Amino Acids↗
PubMed1991

Acute in vivo effects of low ethanol concentration on the capacity of urea synthesis in rats.

We studied the effect of acute exposure, by constant intravenous infusion, to a low blood ethanol concentration (range 8-14 mmol/l) on the in vivo capacity of urea-N synthesis (CUNS), alanine elimination, and the nitrogen retention in fed and fasted rats. Alanine was infused to obtain a constant blood concentration of alpha-amino nitrogen between 7.3 and 11.7 mmol/l, at which concentrations urea synthesis is at maximum. CUNS was calculated after nephrectomy as accumulation of urea in body water, elimination of alanine as alanine infusion rate corrected for accumulation, and nitrogen retention as the difference. In the fed state ethanol decreased CUNS from 7.84 +/- 0.32 mumol N/(min 100 g body weight (BW] (mean +/- SEM) (n = 7) to 6.30 +/- 0.58 (n = 6) (p less than 0.001) and in the fasted state from 8.25 +/- 0.27 mumol N/(min 100 g BW) (n = 10) to 6.90 +/- 0.25 (n = 10) (p less than 0.001). In the fed state ethanol increased the elimination of alanine from 6.49 +/- 0.28 mumol/(min 100 g BW) (n = 7) to 6.95 +/- 0.25 (n = 6) (p less than 0.01), and in the fasted state decreased it from 6.25 +/- 0.12 mumol/(min 100 g BW) (n = 10) to 5.67 +/- 0.20 (n = 10) (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholic Intoxication↗
PubMed1991

Incidence of parenchymal liver diseases in Denmark, 1981 to 1985: analysis of hospitalization registry data. The Danish Association for the Study of the Liver.

The sex-specific and age-specific incidence rates of the major parenchymal liver diseases in a North European population were estimated using a computerized registry of all admissions to somatic hospitals in Denmark. The incidence was calculated by counting all incident cases of these diseases reported to the registry in the 5-yr period 1981 to 1985 and dividing the number of cases by the number of person-years at risk in this period. The incidence rates (per million person-years) were for men and women, respectively: infectious hepatitis, 109 and 71; toxic hepatitis, 19 and 22; chronic hepatitis, 27 and 29; alcoholic cirrhosis, 190 and 85; nonalcoholic nonbiliary cirrhosis, 110 and 82; primary biliary cirrhosis, 4 and 14. The pattern of the age-specific incidence rates was similar in men and women in infectious hepatitis, alcoholic cirrhosis, nonalcoholic nonbiliary cirrhosis and primary biliary cirrhosis. Toxic and chronic hepatitis had a higher incidence in women than in men only in older age groups. The incidence of idiopathic hemochromatosis, Wilson's disease, secondary biliary cirrhosis, portal vein thrombosis and Budd-Chiari's syndrome were less than four in both sexes.

Adult↗
PubMed1991

Importance of glucagon for nitrogen loss in diabetes--via an accelerated hepatic conversion of amino nitrogen to urea nitrogen.

In diabetes mellitus amino nitrogen is lost from organs and excreted as urea. Traditionally it has been assumed that the only explanation of this phenomenon was lack of insulin. The blood amino acid concentration in diabetic patients is, however, reduced, which suggests that the hepatic uptake of amino acids is accelerated. Glucagon accelerates the hepatic uptake and conversion of amino nitrogen into urea nitrogen, and hyperglucagonaemia is present in diabetes. This survey describes the significance of hyperglucagonaemia in the abnormal diabetic nitrogen metabolism. Rats with experimental diabetes and hyperglucagonaemia, given the same amount of food as controls, double the urinary excretion of urea-N within 4 days. This increase can be completely normalized by an intensive insulin treatment regimen, which normalises the hyperglucagonaemia as well. Selective hyperglucagonaemia in otherwise optimally insulin treated diabetic rats raises the urinary urea-N excretion by one third, also within 4 days. The kinetics of urea synthesis in experimental diabetes is changed towards an increased maximum rate, but only after 14 days, so this alone cannot explain the increased urea excretion. Constant hyperglucagonaemia increases the spontaneous rate of urea synthesis within 2 days. In uncontrolled diabetes nitrogen is lost from most organs, and most is lost from muscles. Selective hyperglucagonaemia in insulin treated diabetic rats leads to a loss of muscle nitrogen of about one third of that seen in uncontrolled diabetes. It is suggested that he glucagon induced loss of muscle nitrogen is due to an increased flux of amino nitrogen from muscle to liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Glucagon increases hepatic efficacy for urea synthesis.

The effect of glucagon on the relation between urea synthesis and blood amino acid concentration was studied in seven healthy volunteers. Alanine was given as prime-continuous infusions and, after 1 hr for equilibration, the urea nitrogen synthesis rate was measured in two periods of about 2 hrs as urinary excretion corrected for accumulation and intestinal hydrolysis. During one of the periods, glucagon was infused to obtain a constant concentration of 200-1200 ng/l. The spontaneous urea synthesis during the alanine infusion was 86-141 mmol/hr and linearly related to the alanine concentrations of 1.33-2.99 mmol/l. The hepatic clearance of alanine-nitrogen to urea-nitrogen, assessed by the ratio between the increase in the urea synthesis rate and alanine concentration, was 23 +/- 4 l/hr (mean +/- S.D.). Glucagon increased the rate of urea synthesis by 35 +/- 11 mmol/hr (p less than 0.02) and decreased the alanine concentration by 0.22 +/- 0.06 mmol/l (p less than 0.01). Glucagon increased the hepatic nitrogen clearance to an average of 42 +/- 13 l/hr (p less than 0.01). The difference between infusion of amino-nitrogen and appearance of urea-nitrogen was +15 +/- 10 mmol/hr during alanine infusion alone and -11 +/- 25 mmol/hr during exogenous glucagon. The loss of nitrogen could be accounted for by depletion of non-alanine amino acids from the blood. Glucagon increases the efficacy of urea synthesis, which may be of importance for catabolism by changing the hepatic contribution to nitrogen homeostasis.

Adult↗
PubMed1990

No effect of bicarbonate-induced alkalosis on urea synthesis in normal man.

The effect of metabolic alkalosis was studied in 10 healthy volunteers. In each person urea synthesis was determined in two periods of 2 h as urinary excretion corrected for accumulation in body water and for intestinal hydrolysis. Infusion of bicarbonate (115 mmol/h) increased pH of the venous blood by 0.10 units. In four subjects fasting urea synthesis was 24 mmol N/h at normal pH and unaffected by alkalosis (mean difference +/- SED was 1.04 +/- 4.1). In six subjects alanine was infused so as to increase blood alanine concentration from 0.4 to 2.5 mmol/l and urea synthesis to 107 mmol N/h. Alkalosis did not change urea synthesis (mean difference +/- SED was 1.5 +/- 7.4 mmol N/h). The results favour the view that urea synthesis mainly serves to eliminate nitrogen, but do not support the hypothesis that urea synthesis is an important immediate and direct regulatory process in acute acid-base disturbances.

Adult↗
PubMed1990

Increased hepatic efficacy of urea synthesis from alanine in insulin-dependent diabetes mellitus.

The relation of urea synthesis rate to blood alanine concentration was assessed in seven healthy controls and in 18 patients with insulin-dependent diabetes mellitus (HbAlc = 8.4 +/- 1.0% (mean +/- SD)). Following an overnight fast alanine was infused at 2 mmol h-1 kg-1 body weight. The hourly rate of urea synthesis was determined as the urinary excretion of urea corrected for accumulation of urea in total body water and intestinal hydrolysis. The functional hepatic nitrogen clearance, i.e. the relation of urea synthesis rate to blood alanine concentration, was calculated as the slope of linear regression of urea synthesis rates on blood alanine concentrations. Fasting glucagon concentrations were 85 +/- 26 ng l-1 in controls and 161 +/- 35 ng l-1 (P less than 0.01) in patients. The functional hepatic nitrogen clearances were 21.8 +/- 4.4 l h-1 in controls and 44.7 +/- 12.4 l h-1 (P less than 0.001) in patients. By multiple step-wise linear regression analysis the functional hepatic nitrogen clearance was found to correlate independently to fasting glucagon concentration, duration of diabetes, change in blood glucose and insulin following alanine infusion (r2 = 0.74). In a simple linear regression analysis the functional hepatic nitrogen clearance correlated strongly to fasting glucagon concentration (r2 = 0.54). In conclusion the kinetics of urea synthesis in insulin-dependent diabetes is changed in favour of increased conversion of alanine-N to urea-N at any blood amino acid concentration. The increased FHNC correlates strongly with hyperglucagonaemia.

Adult↗
PubMed1990

Increased amino acid clearance and urea synthesis in a patient with glucagonoma.

Fasting concentrations, clearance of exogenous infused amino acids, and lean body mass were studied in a patient with glucagonoma syndrome (fasting glucagon = 380 pmol/l, normal range 15-45 pmol). The fasting concentrations of all amino acids were reduced. The clearances of alanine, arginine, glycine, isoleucine, leucine, lysine, methionine, proline, serine, threonine, and tyrosine were increased. The urea synthesis rate during amino acid infusion was 27 mumols/kg per minute (normal range 20-24 mumols/kg per minute). The lean body mass of the patients was reduced to 59% of the expected value. It is suggested that the weight loss of patients with glucagonoma syndrome is partly due to increased hepatic conversion of amino acid nitrogen to urea nitrogen, resulting in decreased blood amino acid concentration, and secondary to this, organ protein catabolism, as shown by the decreased lean body mass.

Adenoma, Islet Cell↗
PubMed1989

Effects of xylitol versus glucose on urea synthesis and alanine metabolism in rats.

The relation between xylitol concentration (1.0 and 5.5 mmol/1), the Capacity of Urea-N Synthesis, and the rate of Alanine Metabolism was investigated in nephrectomized rats of 200 g and compared with the effect of glucose at concentrations between 5.5 and 15.5 mmol/1. The xylitol and glucose concentrations were controlled by "clamp" techniques and the endogenous hormonal effects by somatostatin. The Capacity of Urea-N Synthesis was determined during alanine infusion to constant amino acid concentrations within the interval 7.3-11.6 mmol/1. The rate of alanine metabolism was assessed as alanine infusion rate corrected for changes in alanine concentration. At normal hormonal response, xylitol at 1.0 mmol/1 and 5.5 mmol/1 reduced urea synthesis from 10.3 +/- 1.1 mumol/(min.100 g) in controls to on average 6.2 +/- 0.9 mumol/(min.100 g) (mean +/- SD, n = 2 x 10, p < 1.01). Alanine metabolism was reduced to the same extent. Glucose concentration increased from 5.4 +/- 1.0 mmol/1 in controls to 8.1 +/- 1.4 mmol/1 at both xylitol concentrations. Xylitol reduced plasma glucagon concentration to one third and tripled plasma insulin concentration. During somatostatin and blood glucose maintained above 8 mmol/1, the Capacity of Urea-N Synthesis fell to 6.1 +/- 1.0 mumol/(min.100 g). In that situation, xylitol at 1.0 mmol/1 reduced neither urea synthesis nor alanine metabolism, whereas xylitol at 5.5 mmol/1 further reduced urea synthesis to 3.4 +/- mumol/(min.100 g) (n = 10, p < 0.05) and almost stopped alanine metabolism. Thus xylitol, independently of glucose and hormonal responses, inhibited urea synthesis and alanine metabolism. This may have therapeutic implications at catabolic conditions.

Journal Article↗