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Biomedical subjects

L S Eriksson

Publications and source records attributed to L S Eriksson.

At least 37 records · Page 2Linked to original sources
PubMed1992

Hepatotoxicity due to repeated intake of low doses of paracetamol.

The cases of two patients with fulminant hepatic failure after intake of therapeutic doses (4-8 g) of paracetamol, and who were admitted to hospital for assessment for liver transplantation, are described. In both patients starvation, due to abdominal pain, nausea and vomiting or diarrhoea, was probably contributing to the toxic effect of the drug. One of the patients also had an excessive alcohol intake. Paracetamol should not be prescribed for patients with alcoholism or with low food intake.

Acetaminophen↗
PubMed1992

Decreased in vitro production of tumor necrosis factor in primary biliary cirrhosis patients.

Primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) are characterized by immunoregulatory disturbances and fibrosis. Several cytokines may be of importance for the inflammatory response and the development of fibrosis. In the present study the capacity to produce tumor necrosis factor (TNF) and interleukin-1 (IL-1) was determined in 11 patients with PSC, 10 patients with PBC, and 20 healthy control subjects. As compared with the controls, in vitro cultured mononuclear cells from PBC patients showed a lower spontaneous TNF production (median, 16,499 cpm; range, 7181-41,907; p less than 0.02), whereas the TNF production of PSC patients was similar to that of the controls. Lipopolysaccharide (LPS)-stimulated TNF production was also lower in the PBC group (median, 40,564 cpm; range, 23,493-69,452) than in PSC patients (median, 58,898 cpm; range, 37,997-91,485; p less than 0.03). The spontaneous and LPS-stimulated IL-1 production did not differ in patients and healthy controls. The cytokine production in patients with PBC and PSC did not correlate to histologic activity, associated diseases such as ulcerative colitis and bilirubin, or to Child-Pugh classification. Thus, in contrast to hepatocellular diseases, in which cytokine production is reported to be increased, PBC and PSC are accompanied by low or normal TNF and IL-1 production.

Cells, Cultured↗
PubMed1992

Influence of beta blockade on branched chain amino acid concentrations in cirrhosis.

Cirrhosis of the liver is typically accompanied by low plasma levels of the three branched chain amino acids (BCAA). These patients also demonstrate increased concentrations of several hormones such as insulin, glucagon and catecholamines. Catecholamines have been shown to influence the plasma levels of amino acids in healthy subjects and diabetics. In the present study, amino acid concentrations were investigated before and up to 3 hours after beta blockade (Inderal, 40-80 mg, n = 10) or fasting (n = 8) in cirrhotic patients. In the basal state the patients had low levels of all three BCAA, as compared with healthy subjects. Norepinephrine was more than 3 times as high in the patients (3.65 +/- 0.6 vs. 0.84 +/- 0.08 nmol/l, p < 0.01) while epinephrine was only slightly raised (0.43 +/- 0.1 vs. 0.25 +/- 0.06 nmol/l, NS). Significant correlations were observed between the concentrations of norepinephrine and individual as well as the sum of the three BCAA (r = 0.43-0.62, p < 0.05-0.001), while no correlation was observed between the BCAAs and epinephrine or insulin. Three hours after beta blockade the concentrations of leucine (basal: 74 +/- 6, 180 min: 89 +/- 6 mumol/l, p < 0.05) and valine (basal: 110 +/- 10, 180 min: 132 +/- 11 mumol/l, p < 0.01) had increased significantly. A similar tendency was observed for isoleucine. No changes were observed after prolonged fasting. The results suggest that catecholamines, primarily norepinephrine, might contribute to the low levels of BCAA in cirrhotics.

Adult↗
PubMed1991

Introduction.

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Editorial↗
PubMed1991

Ventilation-perfusion inequality in patients with non-alcoholic liver cirrhosis.

Ventilation-perfusion relationships were studied in patients with non-alcoholic liver cirrhosis. Spirometry was essentially normal but the transfer factor of the lung (DLCO) was reduced by an average 34% of predicted. Arterial oxygen tension (PaO2) ranged from normal down to 6.9 kPa. Varying degrees of ventilation-perfusion (VA/Q) abnormalities (multiple inert gas elimination technique) were observed with increased dispersion of the perfusion distribution (log SDQ, 0.90; range 0.32-1.71; upper normal limit, 0.60) and the presence of both regions of low VA/Q ratios (between 0.1 and 0.005) (mean 4.1%; range 0-18.8%) and shunt (VA/Q ratios below 0.005) (mean 3.9%; range 0.19.8%). There was a close similarity between measured and calculated PaO2 in normoxaemic patients, but calculated values exceeded measured PaO2 in hypoxaemic patients. The difference between calculated and measured PaO2 correlated inversely to DLCO (r = 0.65, p less than 0.05). An inverse correlation was also noted between DLCO and the sum of shunt and low VA/Q regions (r = 0.87, p less than 0.001). It is concluded that hypoxaemia in non-alcoholic liver cirrhosis patients can be accounted for by intrapulmonary shunting and VA/Q mismatch, and possibly a "diffusion-perfusion" defect in patients with more severe gas exchange impairment.

Adult↗
PubMed1990

Normalization of ventilation/perfusion relationships after liver transplantation in patients with decompensated cirrhosis: evidence for a hepatopulmonary syndrome.

To examine the effect of liver transplantation on the respiratory and cardiovascular functions, ventilation/perfusion relationships were determined by multiple inert gas elimination technique in six patients with end-stage liver disease 1 to 19 mo before and 2 to 6 mo after liver transplantation. Cardiac output and pulmonary vascular pressures were measured after catheterization of the pulmonary artery. All patients had normal spirometry and chest x-ray films before transplantation. PaO2 before transplantation was 78.8 +/- 7.4 mm Hg (range = 51.8 to 102.8 mm Hg). All patients had perfusion of poorly ventilated lung regions (low ventilation/perfusion relationships) varying from 3% to 19% of cardiac output (mean = 8.5% +/- 2.4% of cardiac output) and two patients had intrapulmonary shunting (3% and 20% of cardiac output). Measured and calculated PaO2 agreed closely, indicating absence of pulmonary diffusion abnormality, as well as of extrapulmonary shunting. After transplantation, PaO2 normalized in all patients, and both shunting and low ventilation/perfusion relationships disappeared. Cardiac output decreased from 9.1 +/- 1.4 to 6.6 +/- 0.5 L/min (p less than 0.05), and the pulmonary vascular resistance increased from 0.69 +/- 0.14 to 1.64 +/- 0.43 mm Hg/L/min (p less than 0.05). The systemic vascular resistance also increased (before = 8.7 +/- 1.0; after = 15.3 +/- 1.1 mm Hg/L/min; p less than 0.001). Normalization of respiratory and cardiovascular alterations, after liver transplantation, in patients with end-stage liver disease indicates that these changes have a direct functional relationship to the diseased liver. It is hypothesized that this is part of a "hepatopulmonary syndrome,' which in similarity to the hepatorenal syndrome disappears with improved liver function.

Adult↗
PubMed1990

Anesthesia for liver transplantation in patients with arterial hypoxemia.

Arterial oxygenation during anesthesia and time of postoperative mechanical ventilation were investigated in 17 patients with chronic liver disease who underwent liver transplantation. Six patients had arterial hypoxemia (PaO2 64 +/- 3 mm Hg) and the other 11 patients had normal PaO2 (105 +/- 5 mm Hg) before transplantation. None of the patients were smokers and all had normal preoperative pulmonary X-ray and spirometry. During transplantation, PaO2 increased in both groups, but PaO2 was still approximately 20% lower and PA-aO2 was 40%-60% higher in the hypoxemic group than in the normoxemic patients (P less than 0.05). The median postoperative time on mechanical ventilation was three times longer in the hypoxemic group (56 h) than in the normoxemic patients (18 h; P = NS). Number or severity of postoperative complications and outcome did not differ between the two groups. It is therefore suggested that patients with arterial hypoxemia without overt lung disease should also be accepted for liver transplantation.

Adolescent↗
PubMed1990

Influence of leucine infusion on intracellular amino acids in humans.

A continuous intravenous infusion of L-leucine (300 mumols min-1) was given to 12 healthy females over a 2 1/2 h period. Arterial plasma concentrations of amino acids and the keto acids of the branched-chain amino acids (BCAA) were measured. In six subjects muscle biopsies were taken before and at the end of the infusion for determination of intracellular (i.c.) free amino acid concentrations, and leg exchange of amino acids was measured. During infusion the plasma level of leucine rose sixfold. Approximately 40% of the infused amount was taken up by muscle. Of this, half was accumulated intracellularly, where the free leucine concentration increased from basal 190 +/- 22 to 580 +/- 110 mumols l-1 ICW (intracellular water) at the end of infusion. The concentrations of most other amino acids, above all the other BCAA and the aromatic amino acids, decreased, by 17-48% in the i.c. pool and by 17-79% in plasma. The plasma level of ketoisocaproic acid (KIC), the keto acid of leucine, increased in parallel with that of leucine. The concentration of keto valine, ketoisovaleric acid (KIV), decreased by 75%, whereas the keto acid of isoleucine, ketomethylvaleric acid (KMV), was unchanged. Leg release of alanine decreased significantly, whereas the exchange of other amino acids were unchanged. Taken together, decreased i.c. and plasma concentrations but unchanged leg exchange of tyrosine and phenylalanine suggest i.c. accumulation of protein. It can be calculated that approximately 40% of the leucine taken up by muscle was accumulated in the intracellular free pool, some 20% could have been incorporated into protein and 40% was probably oxidized.

Adult↗
PubMed1990

Gut exchange of glucose and lactate in basal state and after oral glucose ingestion in postoperative patients.

Glucose uptake by the intestine and its conversion into 3-carbon compounds in the human intestine in the basal state and after an oral glucose load are not understood. Consequently, we studied the arterial and portal venous concentration differences (A-PV) for glucose and glucogenic substrates in the basal state and 3 h after the ingestion of a 100-g glucose load with the catheter technique. Five patients were studied 3-11 days after surgery for gallbladder disease or cancer of the colon or liver. A-PV for glucose in the basal state was 0.12 +/- 0.02 mM (P less than 0.01), indicating net glucose uptake by extrahepatic splanchnic tissues. No net exchange of lactate or pyruvate was detected, but there was release of alanine and uptake of glutamine. After glucose ingestion, glucose was released by the gut, reflecting absorption of the load (mean A-PV for glucose -2.10 +/- 0.04 mM, P less than 0.01). The arterial glucose concentration rose gradually from 4.6 +/- 0.1 mM before glucose ingestion to a plateau at 9.5 +/- 0.7 mM from 90 to 180 min. Glucose ingestion was accompanied by net lactate and alanine release (A-PV -0.16 +/- 0.06 mM and -48 +/- 7 microM, respectively), whereas A-PV for pyruvate did not change. We conclude that, in postoperative patients, there is a significant net glucose uptake by the gastrointestinal tract in the basal state. Glucose ingestion is accompanied by a small release of lactate and alanine from the intestine. However, the estimated net gut formation of lactate and alanine can play only a minor role in the disposal of an oral glucose load.

3-Hydroxybutyric Acid↗