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Biomedical subjects

T Jensen

Publications and source records attributed to T Jensen.

At least 199 records · Page 11Linked to original sources
PubMed1987

Adrenocortical function in children on high-dose steroid aerosol therapy. Results of serum cortisol, ACTH stimulation test and 24 hour urinary free cortical excretion.

The adrenocortical function was investigated in 18 children treated with high-doses of inhaled glucocorticoid aerosol (mean: 1965 micrograms/1.73 m2 body surface a day). Basal serum cortisol was only below the normal range in patients treated with doses exceeding 2500 micrograms/1.73 m2 body surface. 15 of 18 children had normal 24 h urinary free cortisol excretion, compared with 27 normal children matched for age, sex and body surface. Three patients taking more than 2400 micrograms/1.73 m2 body surface showed excretion values below the range for the normal controls. 10 of 12 patients showed a normal response to a short ACTH stimulation test. One patient treated with 3300 micrograms/1.73 m2 body surface showed no response and one patient gave a borderline response to ACTH. We concluded that doses up to 2000 micrograms/1.73 m2 body surface/24 can be administered by pressurized aerosol with little risk of adrenocortical suppression.

Administration, Inhalation↗
PubMed1987

Management of Pseudomonas aeruginosa lung infection in Danish cystic fibrosis patients.

The annual mortality rate of cystic fibrosis patients with chronic Pseudomonas aeruginosa lung infection at the Danish CF-centre ranged from 10 to 20% in the years 1970-1975. In this period the patients received antipseudomonal chemotherapy only during acute exacerbations of infection. From 1976 99 patients acquired chronic P. aeruginosa infection and were given regular and intensive antipseudomonal treatment 3-4 times per year. The patients were followed for 612 patient-years; 7 died and the 10-year survival rate after onset of P. aeruginosa infection was 90% +/- 4%. The annual mortality rate is now 1-2%. Although precipitating antibodies against P. aeruginosa increased significantly, pulmonary function did not deteriorate with duration of infection. Cross-infection between patients caused an increased incidence of chronic P. aeruginosa infection which was reduced by hygienic measures.

Adolescent↗
PubMed1987

Cumulative and acute toxicity of repeated high-dose tobramycin treatment in cystic fibrosis.

Forty-six patients with cystic fibrosis and chronic bronchopulmonary Pseudomonas aeruginosa infection entered a study of tobramycin-related chronic and acute nephro- and acousticovestibular toxicity. The patients (mean age, 15.7 years) had previously received 2-week courses of tobramycin therapy, for a mean cumulative total of 279 days each. The cumulative tobramycin dose ranged from 632 to 7,644 mg/kg. The patients were studied before and at the end of a 2-week course of treatment with tobramycin (10 to 20 mg/kg per day) to discriminate between acute and chronic toxicity. In patients studied at the beginning of the present course of treatment, the glomerular filtration rate, measured as 24-h creatinine clearance, did not correlate with the cumulative dose of tobramycin received during previous courses. Eighteen patients (39%) had a reduced glomerular filtration rate compared with normal values (mean, 12.5% reduction) but normal serum creatinine values. Two patients (5%) had a high-frequency hearing deficit (above 8 kHz), but only one deficit was possibly related to tobramycin. No chronic vestibular toxicity was observed. During the course of treatment, no patients developed acute nephrotoxicity. After 2 weeks of treatment 32% had a slightly reduced hearing threshold (15 to 30 dB) in two or more high frequencies, and 28% had a fall in vestibular response greater than 25% of the initial value but remained within normal limits. Thus, the acute and chronic toxicity of repeated high-dose tobramycin treatment in cystic fibrosis patients seems to be very mild.

Adolescent↗
PubMed1987

Changes in blood pressure and renal function in patients with type I (insulin-dependent) diabetes mellitus prior to clinical diabetic nephropathy.

58 type I (insulin-dependent) diabetic patients who in the period 1975 to 1981 developed clinical diabetic nephropathy (urinary protein excretion greater than 0.5 g/day) (group I) were matched in pairs to 58 patients not developing nephropathy (group II) according to sex (29 males and 29 females), age (33 years (18-46) vs. 33 years (15-48] and diabetes duration (19 years (6-39) vs. 19 years (6-42]. Supine blood pressure measured during hospitalization and weight X 100/serum creatinine were evaluated as to diabetes duration in the periods greater than 10, 10-6, 5-1 years prior to and at the onset of proteinuria. There was no difference in initial blood pressure (124/78 +/- 11/10 mmHg (group I) vs. 125/79 +/- 11/10 mmHg (group II]. Diastolic blood pressure was higher from 10-6 (85 +/- 9 vs. 80 +/- 7 mmHg; p less than 0.05) and systolic blood pressure from 5-1 (138 +/- 17 vs. 129 +/- 17 mmHg; p less than 0.01) years before onset of proteinuria in group I compared with group II. There was no difference in weight X 100/serum creatinine initially (87 +/- 17 kg/mumol/l (group I) vs. 88 +/- 13 kg/mumol/l group II) but from the period 5-1 years prior to the onset proteinuria it was reduced in group I (80 +/- 14 kg/mumol/l vs. group II (86 +/- 14 kg/mumol/l); (p less than 0.05). In conclusion, there was no initial difference in blood pressure and renal function between type I diabetic patients who later developed clinical diabetic nephropathy and those who didn't. Increase in blood pressure starts 5-10 years and renal function impairs 1-5 years before the onset of proteinuria.

Adolescent↗
PubMed1986

Angiotensin II, aldosterone and arginine vasopressin in plasma in congestive heart failure.

Angiotensin II (AII), aldosterone (Aldo) and arginine vasopressin (AVP) in plasma were determined during basal conditions in seventeen patients with congestive heart failure and in seventeen control subjects. The same parameters were measured before and 1, 2 and 3 h after an oral water load of 20 ml (kg body weight)-1 together with urine volume (V) and free water clearance (CH2O) in seven patients with congestive heart failure and in seven control subjects. AII, Aldo and AVP were significantly higher in heart failure than in control subjects (AII:81 and 12 pmol l(-1) (medians), P less than 0.01; Aldo: 411 and 103 pmol l(-1), P less than 0.01; AVP: 5.3 and 2.0 pmol l)-1), P less than 0.01). AVP was positively correlated to Aldo in both heart failure (p = 0.593, n = 17, P less than 0.02) and control subjects (p = 0.511, n = 17, P less than 0.05), but in neither of the groups to AII. V and CH2O were significantly lower in heart failure when compared to control subjects (maximum increase in CH2O 3.55 and 5.86 ml min-1, P less than 0.02), but did not correlate directly with either A II, Aldo or AVP. Creatinine clearance was reduced in heart failure. It is concluded that the activity of both the renin-angiotensin-aldosterone system and the osmoregulatory system is enhanced in congestive heart failure, presumably as a compensatory phenomenon in order to maintain arterial blood pressure. It is suggested that the decrease in free water clearance may be attributed to both an elevated level of vasopressin and a reduced glomerular filtration rate.

Aged↗
PubMed1986

Does centralized treatment of cystic fibrosis increase the risk of Pseudomonas aeruginosa infection?

Two hundred and forty Danish patients with cystic fibrosis (97% of the total CF population in Denmark) participated in a point-prevalence study of Pseudomonas aeruginosa infection. One hundred and ninety-two patients were treated at the Danish CF centre and 48 patients were treated in other places. The age distribution was significantly different as no patients older than 19 years were found in the non-centre group. Pathogenic bacteria were isolated from the sputum of 96% of the patients. P. aeruginosa was more prevalent in patients from the centre, whereas Staphylococcus aureus was more prevalent in the non-centre group. No difference in serogroup and phage pattern of P. aeruginosa was found. There was a tendency that non-centre treated patients acquired chronic broncho-pulmonary P. aeruginosa infection later, but at the age of 16 years 90% of all patients will be chronically infected. Chronic P. aeruginosa infection was significantly more common in the age group 10-14 years at the centre than outside the centre. It is not possible to prevent chronic P. aeruginosa infection in CF patients treated in small groups and because of the better prognosis of centralized treatment the latter must be recommended.

Adolescent↗
PubMed1986

Effect of exercise on plasma concentrations of arginine vasopressin, angiotensin II and aldosterone in hypertensive and normotensive renal transplant recipients.

Plasma concentrations of angiotensin II (A II), aldosterone (Aldo) and arginine vasopressin (AVP), and serum osmolality (Sosm) were determined before and after gradually increasing exercise loads on a bicycle ergometer in 10 hypertensive (group I) and 10 normotensive renal transplant recipients (group II), and in 15 healthy control subjects (group III). Working capacity was reduced in groups I and II. The A II, Aldo, AVP, Sosm increased in all groups after exercise. The A II was higher in group I than II and the percentage changes were significantly lower in groups I and II than in group III. There were no significant differences in Aldo between the groups either before or after exercise. The AVP was the same in groups I and II, and AVP in these groups was higher than in group III. The Sosm and AVP were significantly correlated in all groups. Neither A II, Aldo nor AVP were significantly correlated to systolic blood pressure (BP). Alterations in AVP, but not in A II or Aldo, were correlated to the degree of exercise load. It can be concluded that the renin-angiotensin-aldosterone system and the osmoregulatory system are stimulated during exercise in renal transplant recipients. The A II is elevated in post-renal transplant hypertension, but the responsiveness is reduced in both hypertensive and normotensive recipients. The alterations in AVP are probably secondary to changes in Sosm, and the higher AVP levels in recipients could be due to a decreased responsiveness of the renal tubules to AVP. Our findings are in good agreement with the hypothesis that hypertension after renal transplantation is angiotensin II-dependent.

Adult↗
PubMed1986

Post-renal-transplant hypertension. Urine volume, free water clearance and plasma concentrations of arginine vasopressin, angiotensin II and aldosterone before and after oral water loading in hypertensive and normotensive renal transplant recipients.

Urine volume (V), free water clearance (CH2O) and plasma concentrations of arginine vasopressin (AVP), angiotensin II (A II) and aldosterone (Aldo) were determined before and three times during the first 5 h after an oral water load of 20 ml/kg body wt in 19 patients with post-renal-transplant hypertension (group I), in 13 normotensive renal transplant recipients (group II) and in 20 control subjects (group III). Both V and CH2O increased significantly in all groups, but considerably less in groups I and II than in group III. When CH2O was related to glomerular filtration rate no differences existed between patients and control subjects. Basal AVP was the same in groups I (3.3 pmol/l, median) and II (3.0 pmol/l), but significantly (p less than 0.01) higher than in group III (1.9 pmol/l). Basal A II was significantly (p less than 0.01) elevated in group I (18 pmol/l) when compared to both groups II (10 pmol/l) and III (11 pmol/l), and the level was independent of the presence of native kidneys. Basal Aldo was the same in all groups. During loading, AVP was reduced in all groups, A II was almost unchanged, and Aldo was increased in groups I and II and reduced in group III depending on alterations in serum potassium. Thus urinary diluting ability is reduced in renal transplant recipients due to a reduced glomerular filtration rate. The enhanced A II in hypertensive renal transplant recipients gives further evidence for the point of view that hypertension is angiotensin-dependent in most of these patients.

Adult↗