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Biomedical subjects

S Møller

Publications and source records attributed to S Møller.

At least 55 records · Page 3Linked to original sources
PubMed1999

Increased arterial compliance in decompensated cirrhosis.

BACKGROUND/AIMS: In patients with cirrhosis, the systemic circulation is hyperdynamic with low arterial blood pressure and reduced systemic vascular resistance. The present study was undertaken to estimate the compliance of the arterial tree in relation to severity of cirrhosis, circulating level of the vasodilator, calcitonin gene-related peptide (CGRP) and mean arterial blood pressure (MAP). METHODS: Arterial compliance (COMPart=deltaV/deltaP) was determined as the stroke volume relative to pulse pressure (i.e. systolic minus diastolic blood pressure) during a haemodynamic evaluation of portal hypertension in patients with biopsy-verified cirrhosis (Child-Turcotte classes A/B/C=10/15/6). RESULTS: COMPart was significantly higher in cirrhotic patients (n=31) than in controls (n=10) (1.44 vs 1.00 x 10(-3) l/mmHg, p<0.01). It increased significantly through the Child-Turcotte classes A, B, and C (1.02, 1.47, and 2.1 x 10(-3) l/mmHg, respectively, p=0.03). The stroke volume did not change significantly with the severity of the disease, but pulse pressure decreased through class A, B, and C (79, 65, and 50 mmHg, respectively, p<0.01). COMPart was slightly, but significantly correlated to the circulating level of CGRP (r=0.34, p<0.05), and a substantial but inverse correlation was present to MAP (r= -0.63, p<0.002). CONCLUSIONS: Elevated arterial compliance in cirrhosis is directly related to the severity of the disease and to the elevated level of circulating vasodilator peptide CGRP, and inversely related to the level of arterial blood pressure. The altered static and dynamic functions of the arterial wall in cirrhosis may have implications for the circulatory and homoeostatic derangement, and potentially for therapy with vasoactive drugs.

Adult↗
PubMed1999

Hepatic and renal extraction of circulating type I procollagen aminopropeptide in patients with normal liver function and in patients with alcoholic cirrhosis.

The circulating level and splanchnic and renal extraction of serum type I procollagen aminoterminal propeptide (PINP) was studied in 20 patients with normal liver function and in 15 patients with alcoholic liver cirrhosis. In patients with alcoholic cirrhosis, the concentration of PINP in the femoral artery blood was significantly higher than in the group of patients with normal liver function (median 145 microg/l, 95% CI 98-195 versus 57 microg/l, 95% CI 42-92, p<0.001). A significant decrease in the concentration of PINP between the femoral artery (median 57 microg/l, 95% CI 42-92) and the hepatic vein (median 45 microg/l, 95% CI 40-70, p<0.001) was found in patients with normal liver function. In this group we also observed a significantly higher concentration of PINP in femoral artery blood (median 60 microg/l, 95% CI 45-87) as compared with that in renal vein (median 50 microg/l, 95% CI 40-65, p<0.001). In contrast, serum-PINP did not differ between arterial and hepatic or venous venous blood in patients with alcoholic cirrhosis. Size-chromatography revealed no significant change in the ratio of the high and low molecular forms of PINP following extraction in liver and kidney. It is concluded that circulating PINP is extracted in the normal liver and kidney, and that the serum concentration of PINP is significantly higher in patients with alcoholic cirrhosis than in patients with normal liver function. Both the hepatic and the renal clearance of PINP are seriously impaired/reduced in patients with alcoholic cirrhosis.

Adult↗
PubMed1999

Elevated carboxy terminal cross linked telopeptide of type I collagen in alcoholic cirrhosis: relation to liver and kidney function and bone metabolism.

BACKGROUND: The carboxy terminal cross linked telopeptide of type I collagen (ICTP) has been put forward as a marker of bone resorption. Patients with alcoholic liver disease may have osteodystrophy. AIMS: To assess circulating and regional concentrations of ICTP in relation to liver dysfunction, bone metabolism, and fibrosis. METHODS: In 15 patients with alcoholic cirrhosis and 20 controls, hepatic venous, renal venous, and femoral arterial concentrations of ICTP, and bone mass and metabolism were measured. RESULTS: Circulating ICTP was higher in patients with cirrhosis than in controls. No overall significant hepatic disposal or production was found in the patient or control groups but slightly increased production was found in a subset of patients with advanced disease. Significant renal extraction was observed in the controls, whereas only a borderline significant extraction was observed in the patients. Measurements of bone mass and metabolism indicated only a mild degree of osteodystrophy in the patients with cirrhosis. ICTP correlated significantly in the cirrhotic patients with hepatic and renal dysfunction and fibrosis, but not with measurements of bone mass or metabolism. CONCLUSIONS: ICTP is highly elevated in patients with cirrhosis, with no detectable hepatic net production or disposal. No relation between ICTP and markers of bone metabolism was identified, but there was a relation to indicators of liver dysfunction and fibrosis. As the cirrhotic patients conceivably only had mild osteopenia, the elevated ICTP in cirrhosis may therefore primarily reflect liver failure and hepatic fibrosis.

Adult↗
PubMed1998

[Decompensation].

Fluid and sodium retention with peripheral oedema and ascites are often seen in decompensated patients with diseases of the liver, kidney and heart and in malignancies. Despite a careful clinical examination including relevant biochemical tests, decompensation is associated with diagnostic challenges. Two cases are presented where a haemodynamic investigation of the splanchnic and systemic circulation contributed to the establishment of a correct diagnosis, and the advantages of this diagnostic tool are discussed.

Ascites↗
PubMed1998

The organ extraction and splanchnic haemodynamic effects of octreotide in cirrhotic patients.

BACKGROUND: Intravenous octreotide is an established treatment of oesophageal variceal haemorrhage in the cirrhotic patient. AIM: To examine the organ extraction and splanchnic haemodynamic effects of octreotide in cirrhotic patients with portal hypertension. METHODS: Thirteen patients with cirrhosis had hepatic venous catheterization performed. Hepatic venous pressure gradient (HVPG), indocyanine green (ICG) clearance and hepatic blood flow (HBF) were determined in the basal state and during 60 min of octreotide infusion by bolus injection (0.75 microg/kg) followed by continuous infusion of 0.75 microg/kg x h. Blood samples were simultaneously drawn from the femoral artery and the hepatic and renal veins. RESULTS: The extraction fraction of octreotide in the liver was 0.05 (-0.01 - 0.14) (median (interquartile range)) and in the kidneys 0.16 (-0.06 - 0.35). The extraction fraction ratio (E(liver)/E(kidney)) was 0.69 (-0.20 - 1.06). Hepatic clearance was 47 mL/min (3-88) (n = 11). No correlations were found between liver biochemistry or galactose elimination capacity (GEC; a metabolic measure of liver function) and renal extraction fraction or liver clearance. Octreotide had no effect on HVPG or wedged hepatic venous pressure although free hepatic venous pressure increased during octreotide infusion: 6 mmHg (5-9) vs. 7 mmHg (6-10) (P = 0.02). No effect on HBF was observed while ICG clearance decreased significantly. CONCLUSIONS: Octreotide is extracted in cirrhotic patients by both the liver and the kidney, the latter being the most important organ of elimination. Octreotide decreases liver metabolic activity determined by the ICG clearance technique, but no significant effects of octreotide on HVPG or HBF could be demonstrated.

Adult↗
PubMed1998

Calcipotriol cream with or without concurrent topical corticosteroid in psoriasis: tolerability and efficacy.

The objectives of the study were to determine whether concurrent treatment with calcipotriol (50 microg/g) and either clobetasone 17-butyrate cream (0.5 mg/g) (moderate potency) or betamethasone 17-valerate cream (1 mg/g) (potent) or placebo (vehicle of calcipotriol) was more effective and/or caused less skin irritation than calcipotriol cream (50 microg/g) used twice daily. It was a multicentre, double-blind, parallel group study. Patients applied calcipotriol cream in the morning and either vehicle (n = 174), calcipotriol (n = 174), clobetasone (n = 175) or betamethasone creams (n = 176) in the evening for up to 8 weeks. Adverse events led to withdrawal in 20 patients (2.9%). The mean percentage change in PASI (psoriasis area and severity index) was -40.6 in the calcipotriol/vehicle group, -48.3 in the calcipotriol/calcipotriol group, -53.7 in the calcipotriol/clobetasone 17-butyrate group and -57.5 in the calcipotriol/betamethasone 17-valerate group. A statistically significant difference was seen between the four treatment groups (P = 0.006) with calcipotriol/vehicle being less effective than the other treatments. A statistically significant difference in favour of calcipotriol/betamethasone 17-valerate was seen between the calcipotriol/calcipotriol group and the calcipotriol/betamethasone 17-valerate group. The majority of adverse events were skin irritations, which were reported for 31.2% of patients treated with calcipotriol/vehicle, 34.3% of patients treated with calcipotriol twice daily and 23.8% vs. 17.1% of patients treated with calcipotriol/clobetasone 17-butyrate and calcipotriol/betamethasone 17-valerate, respectively. Skin irritation was seen statistically significantly less frequently in patients treated with calcipotriol/ clobetasone 17-butyrate or calcipotriol/betamethasone 17-valerate (P = 0.001), whereas no difference was seen between the other groups. In conclusion, calcipotriol applied twice daily was as effective as calcipotriol/clobetasone 17-butyrate, but slightly less effective than calcipotriol/betamethasone 17-valerate. The incidence of skin irritation was less for patients using concurrent corticosteroids, whereas treatment with calcipotriol/vehicle did not reduce the incidence of skin irritation when compared with calcipotriol twice daily.

Adult↗
PubMed1998

Neurohumoral fluid regulation in chronic liver disease.

Impaired homeostasis of the blood volume, with increased fluid and sodium retention, is a prevailing element in the deranged systemic and splanchnic haemodynamics in patients with liver disease. In this review, some basic elements of the circulatory changes that take place and of neurohumoral fluid regulation are outlined in order to provide an update of recent investigations on the neuroendocrine compensation of circulatory and volume dysfunction in chronic liver disease. The underlying pathophysiology is a systemic vasodilatation in which newly described potent vasoactive substances such as nitric oxide and vasodilating peptides seem to play an important role. The development of central hypovolaemia and activation of potent vasoconstricting systems such as the renin-angiotensin-aldosterone system and the sympathetic nervous system lead to a hyperdynamic circulation with increased heart rate and cardiac output. Moreover, patients exhibit an autonomic dys- and hyperfunction with vascular hyporeactivity to pressor stimuli. The circulatory dysfunction may be part of a multiorgan failure with disturbed haemodynamics of various vascular beds, including those of the splanchnic system, kidneys, brain and lungs. It is still an enigma why patients with chronic liver disease are at the same time overloaded and functional hypovolaemic with a hyperdynamic, hyporeactive circulation. Further research is needed to find the solution to this apparent haemodynamic conflict concerning the abnormal neurohumoral fluid regulation in chronic liver disease.

Adrenomedullin↗
PubMed1998

In situ gene expression in mixed-culture biofilms: evidence of metabolic interactions between community members.

Microbial communities growing in laboratory-based flow chambers were investigated in order to study compartmentalization of specific gene expression. Among the community members studied, the focus was in particular on Pseudomonas putida and a strain of an Acinetobacter sp., and the genes studied are involved in the biodegradation of toluene and related aromatic compounds. The upper-pathway promoter (Pu) and the meta-pathway promoter (Pm) from the TOL plasmid were fused independently to the gene coding for the green fluorescent protein (GFP), and expression from these promoters was studied in P. putida, which was a dominant community member. Biofilms were cultured in flow chambers, which in combination with scanning confocal laser microscopy allowed direct monitoring of promoter activity with single-cell spatial resolution. Expression from the Pu promoter was homogeneously induced by benzyl alcohol in both community and pure-culture biofilms, while the Pm promoter was induced in the mixed community but not in a pure-culture biofilm. By sequentially adding community members, induction of Pm was shown to be a consequence of direct metabolic interactions between an Acinetobacter species and P. putida. Furthermore, in fixed biofilm samples organism identity was determined and gene expression was visualized at the same time by combining GFP expression with in situ hybridization with fluorescence-labeled 16S rRNA targeting probes. This combination of techniques is a powerful approach for investigating structure-function relationships in microbial communities.

Acinetobacter↗
PubMed1998

Arterial hypoxaemia in cirrhosis: fact or fiction?

BACKGROUND: Although low arterial oxygen tension (Po2) has been claimed to occur in one to two thirds of patients with cirrhosis, hypoxaemia appears to be rare in clinical practice. AIMS: To assess the frequency of arterial hypoxaemia in cirrhosis in relation to clinical and haemodynamic characteristics. PATIENTS: One hundred and forty two patients with cirrhosis without significant hepatic encephalopathy (grades 0-I) (41 patients in Child class A, 57 in class B, and 44 in class C) and 21 patients with hepatic encephalopathy. RESULTS: Mean Po2 in kPa was 11.3 in Child class A, 10.8 in class B, 10.6 in class C, and 10.6 in patients with encephalopathy (p < 0.05). The fraction of patients with Po2 below the lower normal limit of 9.6 kPa was 10%, 28%, 25%, and 43%, respectively in class A, B, C, and in patients with encephalopathy (p < 0.05). Oxygen saturation (So2) in these groups was respectively: 96%, 96%, 96%, and 93% (NS). So2 was below the lower limit of 92% in 0%, 9%, 7%, and 24% (p < 0.05). In patients without hepatic encephalopathy, a multivariate regression analysis revealed that independent determinants of a low Po2 were a high arterial carbon dioxide tension, a low systemic vascular resistance, and a low indocyanine green clearance (p < 0.0001). CONCLUSION: The prevalence of arterial hypoxaemia in cirrhosis is about 22% in patients without encephalopathy, but it varies from 10-40% depending on the degree of hepatic dysfunction. Arterial hypoxaemia in patients with cirrhosis of differing severity seems lower than previously reported, and patients with severe arterial hypoxaemia are rare.

Adult↗
PubMed1998

The acid-labile subunit of human ternary insulin-like growth factor binding protein complex in serum: hepatosplanchnic release, diurnal variation, circulating concentrations in healthy subjects, and diagnostic use in patients with growth hormone deficiency.

Circulating insulin-like growth factor-I (IGF-I) is predominantly bound in the trimeric complex comprised of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS). Circulating concentrations of IGF-I, IGFBP-3 and ALS are believed to reflect the GH secretory status, but the clinical use of ALS determination is not known. We therefore, determined the: 1) hepatosplanchnic release of ALS by liver vein catheterization (n=30); 2) 24-h diurnal variation of ALS (n=8); 3) normal age-related ranges of circulating ALS (n=1158); 4) diagnostic value of ALS in 108 patients with childhood-onset GH deficiency (GHD). We found: 1) no significant arteriovenous gradient over the liver ofALS, IGF-I, and IGFBP-3; 2) the diurnal variation of ALS was 12% (mean coefficient of variation percent); 3) ALS levels increased throughout childhood with maximal levels in puberty, with a subsequent decrease with age in adults; and 4) ALS levels were below -2 SD in 57 of 79 GHD patients (sensitivity 72%) and above 2 SD in 22 of 29 patients with normal GH response (specificity 76%), which was similar, compared with the diagnostic utility of IGF-I and IGFBP-3. Finally, our findings indicate that hepatic ALS production is not measurable by this approach or, alternatively, that the liver is not the primary source of circulating ALS, IGF-I, or IGFBP-3 in humans. In conclusion, we have provided extensive normal data for a novel ALS assay and found that circulating ALS levels exhibit minor diurnal variation. We suggest that ALS determination may be used in future classification of adults suspected of GHD.

Adolescent↗
PubMed1998

Haemodynamics and fluid retention in liver disease.

Patients with cirrhosis and portal hypertension exhibit characteristic haemodynamic changes with a hyperkinetic systemic circulation, an abnormal distribution of the blood volume and neurohumoral dysregulation. Their plasma and noncentral blood volumes are increased, but the central and arterial blood volume and systemic vascular resistance are decreased. A systemic and splanchnic vasodilatation is of pathogenic importance to the low systemic vascular resistance and abnormal volume distribution. These are important elements in the development of the low arterial blood pressure and hyperkinetic circulation in cirrhosis. Various vasodilators such as nitric oxide, calcitonin gene-related peptide, and adrenomedullin are among potential candidates in the vasodilatation in cirrhosis. Besides reflex induced enhanced sympathetic nervous activity, activation of the renin-angiotensin-aldosterone system, and elevated circulation vasopressin, endothelin-1 may also be implicated in the haemodynamic counter-regulation in cirrhosis. Recent research has focused on the assertion that the haemodynamic and neurohumoral abnormalities in cirrhosis are part of a general circulatory dysfunction, influencing the course of the disease with reduction of kidney function and sodium-water retention as the outcome.

Animals↗
PubMed1997

[Prognostic value of insulin-like growth factor I-IGF-I--and its binding protein IGFBP-3 in alcoholic liver disease].

IGF-I is a single polypeptide chain with important anabolic and endocrine activities. The liver is the major source of IGF-I and its binding protein, IGFBP-3. Circulating concentrations of IGF-I and IGFBP-3 are decreased in patients with chronic liver disease and correlate with the severity. The aim of this study was to assess the additional prognostic value of IGF-I and IGFBP-3 in patients entered in a large multicentre study (EMALD). Three hundred and thirty-seven patients with alcoholic liver disease were studied in a randomised placebo-controlled trial of malotilate with a mean follow-up period of 569 days (range: 7-1544). A multivariate Cox regression analysis of pertinent clinical and biochemical variables revealed a significant independent prognostic value of years of alcohol intake, coagulation factors 2, 7, and 10, alkaline phosphatases, serum creatinine, and immunoglobulin M (IGM). When IGF-I or IGFBP-3 were added into this model, a Cox regression analysis showed that either had a significant independent prognostic value. As IGF-I and IGFBP-3 were closely correlated, they contained almost the same prognostic information. Inclusion of IGF-I gave these results: IGF-I (p < 0.03), alcohol intake (p < 0.02), coagulation factors 2, 7, and 10 (p < 0.01), creatinine (p < 0.001), and IgM (p < 0.01) contained independent prognostic information. Inclusion of IGFBP-3 gave these results: IGFBP-3 (p < 0.02), alcohol intake (p < 0.05), coagulation factor 2, 7, and 10 (p < 0.01), creatinine (p < 0.001), and IgM (p < 0.02) were independent predictors of survival. In conclusion IGF-I or IGFBP-3 provides important additional information on survival in patients with alcoholic liver disease.

Adult↗
PubMed1997

[Segmental "portal hypertension". A rare cause of severe tractable variceal bleeding].

We present a 33 year-old man with massive upper gastrointestinal bleeding caused by a rare form of segmental portal hypertension. The patient developed a pancreatic abscess, which caused an isolated thrombosis in the splenic vein and the development of pronounced collaterals and bleeding fundus varices. The patient underwent splenectomy and recovered quickly hereafter. The literature is sparse on severe bleeding complications due to acute pancreatitis. The present case emphasizes the importance of recognition of unusual manifestations of common clinical conditions.

Adult↗
PubMed1997

Carbohydrate deficient transferrin (CDT) in alcoholic cirrhosis: a kinetic study.

BACKGROUND/AIMS: Carbohydrate deficient transferrin has been introduced as a marker of excessive alcohol intake. The present study was undertaken in order to measure the circulating level of carbohydrate deficient transferrin in patients with alcoholic cirrhosis and to assess arteriovenous kinetics of carbohydrate deficient transferrin in liver and kidney. METHODS/RESULTS: The median value of serum carbohydrate deficient transferrin was 16.0 U/l in patients with alcoholic cirrhosis (n = 41), and this value was not significantly different from that of a normal control group (median 17.4 U/l, n = 55, ns). Carbohydrate deficient transferrin was significantly higher in patients with cirrhosis and high current alcohol intake than in abstaining patients (20 vs. 14 U/l, p < 0.05). Similarly, controls with a high current alcohol intake (> 50 g/day) had a significantly higher carbohydrate deficient transferrin concentration than controls with a low alcohol intake (< 10 g/day) (36 vs. 14.9 U/l, p < 0.005). No significant differences were detected between carbohydrate deficient transferrin in artery and liver vein or artery and renal vein, either in patients with alcoholic cirrhosis (n = 11) or in controls (n = 8), which indicates a slow turnover rate of carbohydrate deficient transferrin. Food ingestion did not affect the circulating level of carbohydrate deficient transferrin, and the analysis of carbohydrate deficient transferrin was almost unaffected by the presence of ethanol in plasma within the biological range (ethanol 0-100 mmol/l). CONCLUSIONS: Our results suggest that measurement of carbohydrate deficient transferrin may be used in patients with alcoholic cirrhosis. High current alcohol intake is associated with higher carbohydrate deficient transferrin levels than in those with low alcohol intake, but the overlap is substantial in patients with cirrhosis. Carbohydrate deficient transferrin has a low turnover rate in both patients with cirrhosis and normals.

Adult↗