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H Danielsen

Publications and source records attributed to H Danielsen.

At least 19 recordsLinked to original sources
PubMed2001

Abnormal DNA content predicts the occurrence of carcinomas in non-dysplastic oral white patches.

The majority of oral squamous cell carcinomas (OSCCs) are preceded by visible changes in the oral mucosa, most often white patches. Although the histological finding of dysplasia in oral white patches signals increased risk of developing OSCC, this may also occur in non-dysplastic lesions. However, no reliable markers exist to predict the occurrence of OSCC in these patients. From a total of 263 patients diagnosed with oral white patches, biopsies from 45 patients were selected on the criteria that the patients had lesions histologically proven to be non-dysplastic. The lesions were analyzed with respect to their DNA content. The clinical outcome of the patients was known from the Cancer Registry of Norway, and these data were compared to the DNA content of their lesions. Among the 45 patients, five cases (11%) later developed an OSCC. Four of the cases that subsequently developed an OSCC were among the five aneuploid (abnormal) cases (P=0.001). One aneuploid lesion did not develop a carcinoma during a follow-up time of 120 months. The fifth case that subsequently developed an OSCC was diploid (normal), and developed into an OSCC after an observation time of 73 months (P=0.001). In conclusion, aberrant DNA content reliably predicts the occurrence of OSCC in patients that otherwise would be regarded as at very low risk. Normal DNA content indicates low risk.

Adult↗
PubMed2001

Serum hepatocyte growth factor levels in patients with chronic renal disease--effect of GFR and pathogenesis.

UNLABELLED: Hepatocyte growth factor (HGF) is a growth-promoting peptide that appears to act in a renotropic and nephroprotective manner during acute renal damage. Recent studies suggest that HGF is also of importance in chronic renal diseases. The serum HGF level is correlated with serum creatinine, and it has been suggested that glomerular and tubular diseases affect serum HGF differently. In the present study. levels of serum HGF were determined and correlated to glomerular filtration rate (GFR) in 118 patients with various chronic renal diseases. GFR was determined by 99mTc-DTPA clearance, and the GFR values were evenly distributed in the interval 5-155 mL/min/1.73 m2. Serum HGF levels increased slightly with decreasing GFR: the Pearson correlation coefficient being 0.49 (p<0.0001). In 21 additional patients with end-stage renal disease treated with continuous ambulatory peritoneal dialysis, there was a more marked increase in the serum levels of HGF. The effect of glomerular and tubular diseases on serum HGF was examined by comparing the HGF levels in two groups of patients with similar GFR values: 57 patients with mainly glomerular disorders (diabetic nephropathy with micro- or macroalbuminuria or glomerulonephritis) and 14 patients with mainly tubular disorders (polycystic kidney disease). There was no significant difference between the HGF levels of the two groups (p=0.30). IN CONCLUSION: Serum HGF levels are correlated with GFR (for GFR > or = 5 mL/min/1.73 m2) in patients with chronic renal diseases, and glomerular and tubular disorders seem to affect the HGF level similarly.

Adult↗
PubMed2001

Fourth updated ESACP consensus report on diagnostic DNA image cytometry.

A task force of experts in the field of diagnostic DNA image cytometry, invited by the ESACP, and further scientists or physicians revealing experience in that diagnostic procedure (names are given in Addendum A), agreed upon the following 4th updated Consensus Report on Standardised Diagnostic DNA Image Cytometry during the 7th International Congress of that society in Caen, 2001. This report is based on the three preceding ones [6,14,17]. It deals with the following items:- Critical review and update of the definitions given in the 1997 Consensus Update;- Review and detailed description of basic terms, principles and algorithms for diagnostic interpretation;- Recommendations concerning diagnostic or prognostic applications in specific fields of tumour pathology. This update is not aimed to substitute the 1997 consensus, but to make necessary addenda and give more detailed descriptions of those items not unequivocally to interpret by potential users of the methodology.

Algorithms↗
PubMed2000

Serum cystatin C as an endogenous parameter of the renal function in patients with normal to moderately impaired kidney function.

BACKGROUND: Cystatin C is a proteinase inhibitor with a low molecular weight. The serum levels of cystatin C are mainly dependent on glomerular filtration rate (GFR) making cystatin C an endogenous parameter of GFR. The aim of the study was to elucidate the applicability of serum cystatin C as a parameter of GFR in patients with normal to moderately impaired kidney function and to estimate a reference interval for serum cystatin C. PATIENTS AND METHODS: Forty-six patients (25 males and 21 females) aged 22 to 83 years with various kidney diseases and 250 blood donors (164 males and 86 females) aged 19 to 64 years were included. Cystatin C was measured by an automated particle-enhanced nephelometric immunoassay, serum creatinine by an enzymatic and by Jaffé method, urine creatinine by an enzymatic method, and GFR by 99mTc-DTPA clearance. RESULTS: Serum levels ofcystatin C and creatinine showed increments with decreasing values of 99mTc-DTPA clearance and a linear relationship was found between 99mTc-DTPA clearance and l/serum cystatin C, l/serum creatinine (enzymatic method), and creatinine clearance. Comparison of the non-parametric receiver-operating characteristic (ROC) plots for serum cystatin C (area under the curve (AUC) = 0.996; SE = 0.005), serum creatinine (enzymatic method) (AUC = 0.899; SE = 0.044), serum creatinine (Jaffé method) (AUC = 0.870; SE = 0.051), measured creatinine clearance (AUC = 0.959; SE = 0.025), and estimated creatinine clearance (0.950; SE = 0.029) revealed significant differences for serum cystatin C and serum creatinine (enzymatic and Jaffé method) (p values: 0.03 and 0.01). No significant differences were demonstrated between serum cystatin C and measured and estimated creatinine clearance (p value: 0.14 and 0.12). The non-parametric reference interval for serum cystatin C was calculated to be 0.51-1.02 mg/l (median: 0.79 mg/l; range: 0.33 - 1.07 mg/l). CONCLUSION: Serum cystatin C seems to be a better parameter of GFR than serum creatinine in adults with various types of kidney disease with normal to moderately impaired kidney function.

Adult↗
PubMed1998

Serum cystatin C as a marker of the renal function.

The protease inhibitor cystatin C is a non-glycosylated low molecular weight protein (Mr=13359) which is produced by all nucleated cells at a constant rate, freely filtered by the renal glomeruli, and catabolized in the tubuli. The aim of the study was to elucidate the applicability of serum cystatin C as a marker of glomerular filtration rate (GFR) in patients with various kidney diseases with a wide range of renal function and in dialysis patients. Seventy-six patients with various kidney diseases (aged 20 to 79 years) and 61 dialysis patients (aged 21 to 82 years) were included. Serum cystatin C was measured by automated particle-enhanced immunoturbidimetry, serum and urine creatinine by an enzymatic method, and GFR by 99mTc-DTPA-clearance using a single plasma sample method. Serum cystatin C in patients with various kidney diseases was 1.90+/-0.98 mg/L (mean+/-SD) and in dialysis patients 7.14+/-1.91 mg/L. In the non-dialysis patients a linear relationship was found between 99mTc-DTPA-clearance and 1/serum cystatin C (r=0.91, p-value<0.0001), 1/serum creatinine (r=0.89, p-value<0.0001), and creatinine-clearance (r=0.88, p-value<0.0001). Comparison of the non-parametric ROC plots for serum cystatin C (area under the curve (AUC)=0.9665; SE=0.0169), serum creatinine (AUC=0.9554; SE=0.0205), and creatinine-clearance (AUC=0.9731; SE=0.0160) revealed no significant differences (p-values: 0.50, 0.78, and 0.49). In conclusion, cystatin C may be a likewise good marker of the GFR as serum creatinine and creatinine-clearance, cystatin C having the advantage being independent of gender and muscle mass.

Adult↗
PubMed1998

Atraumatic loss of a kidney in a patient with alpha1-antitrypsin deficiency.

Alpha1-Antitrypsin (alpha1AT) deficiency is characterized by a high risk of developing pulmonary emphysema and liver disease. Arteriopathy may be associated with alpha1AT deficiency. We present a patient with only one kidney and alpha1AT deficiency, but only mild pulmonary symptoms and no signs of liver disease, and atraumatic loss of the remaining kidney. Histological examination of the renal artery showed desposits of a mucoid ground substance in the arterial media, as has been demonstrated in other patients with alpha1AT deficiency. After dialysis treatment for 15 months, the patient underwent an uneventful kidney transplantation. The case draws attention to the awareness of complications of alpha1AT deficiency even in cases with only mild pulmonary manifestations of the disorder. To our knowledge, atraumatic loss of a kidney in a patient with alpha1AT deficiency has not previously been reported.

Hemorrhage↗
PubMed1997

Uremia and HbA1c.

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Biomarkers↗
PubMed1994

Caveats in the use of archival cell material for DNA ploidy analysis by image cytometry.

Monolayer preparation from paraffin-embedded tissue from archival biopsy specimens older than 10 years was shown in this study to be more difficult to deal with than recent biopsies. We have studied the disseminative effect of several enzymes on archival biopsies from laryngeal epithelium, as well as mechanical dissemination. Thirty minutes incubation in protease 0.5% in 37 degrees C without syringing provided the best cell yield. Hydrolysis and Schiff staining conditions were also studied. Cell loss was calculated by stereological methods and found to be high in most cases. Cell loss during various steps in monolayer production was examined and we found no proof of selective cell loss. Large variations in Feulgen-Schiff staining intensities were observed, especially in biopsy specimens older than 10 years. The use of reliable internal (intrinsic) control cells is advocated since interspecimen variations in the diploid integrated optical density (IOD) can be expected. Although DNA measurements on archival biopsy material should be treated with caution, we demonstrate that meticulous studies of the preparation procedures will make it possible to obtain reliable histograms from old, archival biopsies.

Archives↗
PubMed1993

Unchanged noradrenaline reactivity and blood pressure after corrective surgery in primary hyperparathyroidism.

In order to evaluate the role of the hyperparathyroid state for blood pressure and volume homeostasis, eight patients with primary hyperparathyroidism were studied before and after corrective surgery. Neither noradrenaline induced blood pressure changes nor basal blood pressure were affected by the operation, and the values were the same as in an age- and sex-matched control group. Noradrenaline infusion induced an increase in PTH(1-84) values before (72-86 ng l-1, medians, p < 0.02), in contrast to a decrease after (28 to 19 ng l-1, p < 0.05) operation for primary hyperparathyroidism. Basal plasma atrial natriuretic peptide was lower before than after removal of adenomata (3.2 vs. 4.8 pmol l-1, medians, p < 0.02). Cyclic 3'-5'-guanosine monophosphate was not significantly changed (4.7 vs. 5.5 nmol l-1). Aldosterone was higher before than after surgery (139 vs. 71 pmol l-1, p < 0.02), whereas angiotensin II was unaltered (20 vs. 9 pmol l-1). Arginine vasopressin was higher before than after the operation (0.9 vs. 0.7 pmol l-1, p < 0.05), but urinary excretion of prostaglandin E2 was unchanged. In conclusion primary hyperparathyroidism was not associated with changes in noradrenaline reactivity or basal blood pressure despite derangements of hormones adjusting sodium and water homeostasis. It is suggested that the hormonal changes may be secondary to a relative volume depletion.

Adult↗
PubMed1993

Skeletal muscle magnesium content during cyclosporin and azathioprine treatment in renal transplant recipients.

Cyclosporin treatment is often accompanied by hypomagnesaemia and renal magnesium wasting, but it is unknown whether cyclosporin induces tissue magnesium depletion. Magnesium status is best evaluated by measurement of skeletal muscle magnesium content. The purpose of the present study was to evaluate whether skeletal muscle magnesium content was reduced during cyclosporin treatment. In two groups of renal transplant recipients treated with either cyclosporin and prednisolone (group Cy, n = 13) or azathioprine and prednisolone (group Az, n = 17) skeletal muscle content of magnesium, serum magnesium, and urinary excretion of magnesium were determined, and the relationships between skeletal muscle magnesium content, serum magnesium and urinary magnesium were analysed. Skeletal muscle magnesium content did not differ significantly between groups; 7.93 mumol/g wet weight (median) in group Cy versus 8.38 mumol/g wet weight in group Az. Serum magnesium was significantly (P < 0.01) lower in group Cy (0.71 mmol/l) than in group Az (0.82 mmol/l). The urinary excretion of magnesium did not differ between the groups. Skeletal muscle magnesium did not correlate with either serum magnesium or urinary magnesium excretion in group Cy or group Az. Thus the present study indicates that cyclosporin-treated patients are not magnesium depleted, and serum magnesium in these patients does not reflect the skeletal muscle content of magnesium.

Adolescent↗
PubMed1993

Effect of captopril on renal extraction of renin, angiotensin II, atrial natriuretic peptide and vasopressin, and renal vein renin ratio in patients with arterial hypertension and unilateral renal artery disease.

Plasma renin activity (PRA) and plasma concentrations of angiotensin II (AngII), atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) were determined in the abdominal aorta and the renal veins before and 1 h after peroral ingestion of captopril 25 mg in 29 patients with arterial hypertension and unilateral renal artery stenosis or occlusion, in order to study the effect of ACE inhibition on single-kidney extraction ratio (ER) of PRA, AngII, ANP, and AVP, and on renal vein renin ratio (RVRR). PRA was increased, AngII and ANP were reduced, and AVP unchanged after captopril. On the affected side the negative ER or PRA (-1.03) and AngII (-0.28) and the positive ER of ANP (0.25) and AVP (0.14) were not significantly changed by captopril. On the non-affected side ER of AngII and ER of ANP were significantly reduced (ER of AngII, 0.41-0.00, ER of ANP, 0.29-0.17), but ER of PRA and ER of AVP were unchanged. RVRR was not significantly changed by captopril. RVRR was greater than 1.5 in 79% of the patients before captopril, in 82% after captopril, and in 93% either before or after captopril. It is concluded that captopril reduces ER of AngII and ER of ANP on the non-affected side but not on the affected side in unilateral renal artery disease with hypertension, and that the use of RVRR both before and after captopril improves the predictive value of RVRR with regard to the diagnosis of unilateral renal artery disease.

Adult↗
PubMed1992

Glomerular and tubular antinatriuretic actions of low-dose angiotensin II infusion in man.

OBJECTIVE: The aim was to study the physiological effects of angiotensin II upon the glomerular and tubular handling of sodium. DESIGN: Healthy volunteers were examined before and during infusion with either low-dose angiotensin II (n = 11) or placebo (n = 13). METHODS: Lithium clearance was used to estimate the segmental tubular reabsorption of sodium. RESULTS: During infusion with angiotensin II a sustained and marked fall in renal plasma flow was observed. The glomerular filtration rate (GFR) decreased to a minor extent so that the filtration fraction increased during angiotensin II infusion. Angiotensin II caused an extensive and instantaneous fall in both urinary flow and urinary sodium excretion. Proximal absolute reabsorption of sodium was unchanged despite the fall in GFR, showing that proximal fractional reabsorption was enhanced by angiotensin II. Distal absolute reabsorption was decreased during the entire period of angiotensin II infusion. However, when the distal reabsorption was related to the delivery of sodium from the proximal tubules, distal fractional reabsorption in fact increased after 30 min angiotensin II infusion. None of the measured parameters changed during infusion with placebo. A significant increase in plasma aldosterone was observed 30 min after the start of the angiotensin II infusion. Plasma atrial natriuretic peptide did not change during infusion with either angiotensin II or placebo. CONCLUSIONS: We conclude that physiological increments in angiotensin II affect glomerular haemodynamics and cause a marked antinatriuresis in man. The antinatriuretic effect of angiotensin II is caused initially by a combination of a decrease in the GFR and an increase in proximal fractional sodium reabsorption, and later by the enhanced distal fractional reabsorption of sodium.

Adult↗
PubMed1991

Attenuated renal excretory response to atrial natriuretic peptide in congestive heart failure in man.

The renal and hormonal effects of atrial natriuretic peptide given as a bolus injection (2.0 micrograms/kg) were studied in 12 patients with congestive heart failure before and after treatment with captopril for 4 weeks and in 13 healthy control subjects. Atrial natriuretic peptide caused a rise in urinary excretion of sodium and urinary flow in the controls, whereas no increases were observed in the patients. Both proximal and distal fractional reabsorption of sodium, as evaluated by the lithium clearance technique, decreased less in the patients than in the controls. Basal plasma concentrations of atrial natriuretic peptide and cyclic guanosine monophosphate (cGMP), and the basal urinary excretion of cGMP, were elevated in the patients. The increases in both plasma and urinary cGMP after administration of atrial natriuretic peptide were blunted in heart failure. Basal glomerular filtration rate and renal plasma flow were reduced, and filtration fraction increased, in the patients. A positive correlation (r = 0.958, P less than 0.01) was found between renal plasma flow and the relative increase in urinary excretion of sodium in the patients with heart failure. Treatment with captopril did not improve the natriuretic and diuretic effect of exogenous atrial natriuretic peptide, but resulted in an increase in filtration fraction after administration of atrial natriuretic peptide not present before captopril.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1991

Mechanisms of sodium retention in heart failure: relation to the renin-angiotensin-aldosterone system.

Renal plasma flow (RPF), glomerular filtration rate (GFR), renal proximal tubular delivery of sodium and water evaluated by lithium clearance, and hormonal parameters were measured in 12 patients with congestive heart failure NYHA class II-IV before and after captopril treatment for 4 wk and in 13 healthy control subjects. RPF and GFR were significantly decreased in heart failure, whereas the filtration fraction (FF) was increased. Treatment with captopril increased RPF and decreased FF, whereas GFR was unchanged. Total and fractional urinary excretion of sodium were reduced in the patients compared with the controls, but increased after captopril. Fractional excretion of lithium was normal in heart failure and was increased by captopril. Atrial natriuretic peptide, guanosine 3',5'-cyclic monophosphate, and aldosterone in plasma were significantly elevated in heart failure and were reduced by treatment with captopril. Plasma renin activity was increased in patients, correlated inversely with RPF, and increased further after captopril treatment. It is concluded that the reduced sodium excretion in heart failure was caused by a combination of diminished glomerular filtration and enhanced tubular reabsorption beyond the proximal tubule and that treatment with captopril increased urinary sodium excretion partly due to an attenuated sodium reabsorption in the proximal tubule. The present data in patients with congestive heart failure are consistent with an increased intrarenal angiotensin II generation and an elevated plasma level of aldosterone being involved in the pathogenesis of the glomerular hemodynamic changes and the enhanced distal tubular reabsorption, respectively.

Adult↗