bluuebunny/crossref_metadata_2025 huggingface dataset:
Macroamylasaemia after treatment with hydroxyethyl starch
Authors: KOHLER H. , KIRCH W. , WEIHRAUCH T. R. , PRELLWITZ W. , HORSTMANN H. J.
Published: March 2008

Abstract. After infusion of 500 ml of 6% hydroxyethyl starch into fifty‐four patients an increase of serum amylase was observed which in fifty‐one cases exceeded the upper limit of normal (190 U/l). In most cases serum amylase reached twice the basal value. Renal function influenced the duration of the increase in serum amylase, but not the maximum increase (201±15 U/l; mean±SEM). In patients with advanced renal failure (glomerular filtration rate (GFR) = 2–10 ml/min) serum amylase was still markedly elevated after 72 h (298±24 U/l; mean±SEM). In patients with normal renal function (GFR>90 ml/min) serum amylase decreased to 183±40 U/l (mean±SEM) within 72 h without reaching basal values. After infusion of HES no changes were observed in serum lipase or in amylase or lipase activities in duodenal secretion. Amylase excretion in the urine decreased. The assumption of a macroamylasaemia caused by formation of an HES‐amylase complex was confirmed by gel filtration. The elimination from plasma of this high molecular enzyme‐substrate complex is slow and causes hyperamylasaemia. In no case was the macroamylasaemia associated with signs or symptoms. An awareness of this causal relationship seems to be important, to avoid the erroneous diagnosis of a pancreatic disease.
Serum 25‐hydroxyvitamin D in patients with chronic renal disease
Authors: PIETREK J. , KOKOT F.
Published: March 2008

Abstract. Serum 25‐hydroxyvitamin D (25‐OH‐D) was measured by means of a sensitive competitive protein binding assay in forty‐five patients with conservatively treated renal disease and in fifteen patients on chronic dialysis. The mean concentration of 25‐hydroxyvitamin D in twenty‐five normal subjects was 41.4 nmol/l with a range from 19.2 to 90 nmol/l. Fourteen patients with chronic pyelonephritis (creatinine clearance over 25 ml/min) had normal serum 25‐OH‐D. Low values were found in twelve patients with nephrotic syndrome (mean 11.2 nmol/l, range 1–19 nmol/l) and in these subjects the serum 25‐OH‐D levels were inversely correlated with the 24 h urinary protein loss. In thirteen conservatively treated uraemic subjects without significant proteinuria, the mean 25‐OH‐D was 29.4 nmol/l (range 18.2–41.4 nmol/l), whereas in six uraemics losing more than 3 g protein in 24 h urine the mean was 14.2 nmol/l, range 5.2–23.2 nmol/l.

Fifteen patients on chronic dialysis were routinely given a multi‐vitamin preparation providing 125 nmol (2000 i.u.) vitamin D3 daily, and their mean 25‐OH‐D concentration in March 1975 was 51.4 nmol/l. In August 1975, 25‐OH‐D averaged 89.1 nmol/l suggesting seasonal variation and possible role of endogenous vitamin D production in the prevention of clinical signs of renal osteodystrophy.
Vitamin A stimulation of parathyroid hormone: interactions with calcium, hydrocortisone, and vitamin E in bovine parathyroid tissues and effects of vitamin A in man
Authors: CHERTOW B. S. , WILLIAMS G. A. , NORRIS R. M. , BAKER G. R. , HARGIS G. K.
Published: March 2008

Abstract. The effect of vitamin A, a membrane surface‐active agent, on parathyroid hormone secretion was studied in vitro, using bovine parathyroid tissue, and in vivo in man. Parathyroid tissues were incubated with vitamin A (retinol), retinoic acid, and calcium, and with hydrocortisone and vitamin E, agents that antagonize the membrane effects of vitamin A. The stimulation of parathyroid hormone release by vitamin A, 10‐6 to 10‐9 mol/l in vitro, was dose and time dependent. Retinoic acid did not stimulate secretion. High calcium concentration, hydrocortisone, 10‐5 mol/l and 10‐6 mol/l, and vitamin E, 10‐5 mol/l, antagonized vitamin A‐induced parathyroid hormone secretion. Vitamin A increased the lysosomal cathepsin D activity of parathyroid tissues.

In human studies, eleven healthy men received two intramuscular injections of vitamin A palmitate, 25 000 units each, within 24 h. In every subject, serum parathyroid hormone increased after vitamin A administration.

Our studies indicate that: (1) vitamin A stimulates parathyroid hormone secretion in vitro, possibly through modification of the cell or secretion granule membrane, or through stimulation of lysosomal proteolytic activity, and (2) vitamin A increases serum parathyroid hormone in vivo, and this effect may be important in clinical states of vitamin A excess.
Serum gastrin response to acute and chronic hypercalcaemia in man: studies on the value of calcium stimulated serum gastrin levels in the diagnosis of Zollinger‐Ellison syndrome
Authors: LAMERS C. B. H. , TONGEREN J. H. M. VAN
Published: March 2008

Abstract. In this study the effect of calcium infusion over 3 h without gastric aspiration on serum gastrin was determined in fifteen normal subjects, ten patients with duodenal ulcer, nine with stomal ulcer, five with total gastrectomy, six with achlorhydria and sixteen with proved or presumed Zollinger‐Ellison (ZE) syndrome. Serum gastrin only rose significantly in the patients with ZE‐syndrome or achlorhydria. An increase of above or below 50% of basal value seems to be a valuable criterion by which to differentiate between patients with and without ZE‐syndrome. Serum gastrin levels in forty‐four patients with chronic hypercalcaemia (72±24 pg/ml, mean± SD) were not significantly different from the levels in 100 normal subjects (66±18 pg/ml; p>0.10). However, in one patient with ZE‐syndrome and in two patients with achlorhydria serum gastrin values were markedly higher during chronic hypercalcaemia than during normocalcaemia.

It is concluded that acute or chronic hypercalcaemia without gastric aspiration does not lead to hypergastrinaemia in the absence of ZE‐syndrome or achlorhydria.
Effect of exercise and of prolonged oral administration of propranolol on haemodynamic variables, plasma renin concentration, plasma aldosterone and c‐AMP
Authors: BONELLI J. , WALDHÄUSL W. , MAGOMETSCHNIGG D. , SCHWARZMEIER J. , KORN A. , HITZENBERGER G.
Published: March 2008

Abstract. The effect of submaximal exercise upon haemodynamic and biochemical variables was investigated in healthy male subjects, aged 17–27 years, before and at the end of 2 weeks treatment with propranolol (40 mg p.o., q.i.d.).

Propranolol reduced the resting blood pressure in normal subjects significantly. This effect was due to reduction of cardiac output and of systemic vascular resistance. No effect of propranolol on BP was seen during maximal exercise, since a reduced cardiac output was accompanied by an increased peripheral resistance.

The reduction of cardiac output during exercise can be compensated in part by an increase in stroke volume.

The sympathetic activity induced by physical exercise in normotensives increased plasma renin concentration (PRC) and plasma aldosterone (PA), and suppressed urinary excretion of c‐AMP. PRC returned to basal levels after 45 min. No increase of PRC was observed after exercise in subjects treated with propranolol. Yet the increase of PA was not completely suppressed. No direct relation was demonstrated between PRC and the haemodynamic variables before or during the administration of propranolol.
Effects of a large dose of oestradiol on antithrombin III metabolism in male and female dogs
Authors: KOBAYASHI N. , TAKEDA Y.
Published: March 2008

Abstract. Canine antithrombin III (AT) metabolism was studied in twenty healthy dogs of both sexes first under control conditions, using 125I‐AT as a tracer, then, in the same dogs after 20 mg oestradiol intramuscularly and another 20 mg 7 days later. Under control conditions the plasma AT concentration and the amount of plasma AT (x̄) were greater in males than females. The plasma half‐lives of 125I‐AT averaged 2.14 ± 0.09(SD) days in males and 1.97 ± 0.05(SD) days in females and were significantly different. The fractional catabolic rate of plasma AT (j3p) was lower in males than in females, but the amount of plasma AT catabolized (j3pX̄) (synthesis rate) was not significantly different (averaging 20 ± 3.7 (SD) in males and 18 ± 2.2(SD) mg/kg/day in females). The total body AT (x̄+ȳ) was greater in males than in females; average values 55 ± 7.5(SD) and 46 ± 5.2(SD) mg/kg, respectively. Under the influence of oestradiol, the plasma AT concentration and AT(x̄) decreased in both sexes, but the plasma half‐lives of 125I‐AT showed no appreciable changes. The values of AT(j3p) and AT(j3pX̄) were significantly decreased in both sexes; average values of the latter being 14 ± 1.5(SD) in males and 12 ± 2.2(SD) mg/kg/day in females. AT(x̄+ȳ) averaged 43 ± 3.8(SD) in males and 33 ± 6.3(SD) mg/kg in females and were significantly decreased. These results indicate that the decreased values in plasma AT concentration, x̄ and x̄+ȳ following oestradiol administration are due to the decreased synthesis rate of AT and not to an increased catabolic rate.
Biocompatibility of coated and uncoated charcoal during haemoperfusion in healthy dogs
Authors: WESTON M. J. , HANID A. , RUBIN M. H. , LANGLEY P. G. , MELLON P. J. , WILLIAMS ROGER
Published: March 2008

Abstract. The biocompatibility of two commercially available charcoal columns, one containing coated and the other uncoated but immobilized charcoal, was compared during four haemoperfusions with each in eight healthy greyhounds. Reductions in arterial levels of platelets (49% and 42% respectively) and leucocytes (both 21%) were similar. Microaggregates, detected by the Swank screen filtration pressure technique, were found in blood leaving the columns during three of the four perfusions with each column.

Another twelve perfusions with the uncoated column were carried out with the addition of one or other of the following three agents which inhibit platelet aggregation: sulfinpyrazone, dipyridamole, or citrate‐phosphate‐dextrose. With none of these were platelet losses less as compared with the four perfusions in which heparin only was used. However, rises in screen filtration pressure were less pronounced. In other perfusions, where its dosage was varied, heparin was shown to reverse, and in large doses delay, the appearance of micro‐aggregates.

Thrombus in the column itself may be a source of microaggregates, but platelet aggregation in the absence of thrombus deposition may be responsible.

The relation of these findings to micro‐aggregate formation, which has constituted a clinical problem during charcoal haemoperfusion in humans with fulminant hepatic failure, is considered.
Consequences of myocardial reperfusion following temporary coronary occlusion in pigs: effects on morphologic, biochemical and haemodynamic findings
Authors: ALTHAUS U. , GURTNER H. P. , BAUR H. , HAMBURGER S. , ROOS B.
Published: March 2008

Abstract. The effects of myocardial reperfusion have been examined following a I h coronary occlusion and compared to a permanent coronary ligation in pigs. Haemodynamic investigations were carried out through‐out the surgical intervention and repeated after 7 days. Cellular injury was estimated by serial serum enzyme determinations (creatin phosphokinase, α‐hydroxybutyric dehydrogenase, aspartate aminotransferase, lactic dehydrogenase) during the first 5 postoperative days; infarct size was assessed morphometrically by a histo‐chemical staining procedure I week after the temporary or permanent coronary occlusion. A linear correlation was found between the logarithmically plotted peak serum activity of AST, HBDH, CPK and the morphometrically determined infarct size. Based upon enzyme and morphometrical studies no significant difference could be detected between the two experimental groups. In the animals subjected to transient coronary occlusion, however, the development of a ventricular aneurysm had been prevented by early and sustained reperfusion. Early re‐establishment of coronary circulation appears to accelerate the proliferation of a more resistant granulation tissue into the infarcted area. Cardiac performance was not improved by myocardial reperfusion.
Secondary hypertriglyceridaemia in patients with parenchymal liver disease
Authors: KLOSE G. , WINDELBAND J. , WEIZEL A. , GRETEN H.
Published: March 2008

Abstract. Hypertriglyceridaemia occurring in patients with liver disease has been studied by measuring hepatic triglyceride lipase (H‐TGL) and plasma lipoprotein lipase (LPL) by selective precipitation of H‐TGL with specific antibodies. Lipid analysis, determination of lecithincholesterol‐acyltransferase (LCAT) activity, and liver function tests were performed in parallel in fifty patients with acute hepatitis, twenty patients with chronic active or persistent hepatitis and fifty with cirrhosis of the liver.

Total post‐heparin lipolytic activity (PHLA) decreased with the severity of liver dysfunction. This decrease was due to low H‐TGL and only to some degree to low LPL activity. With improvement over several weeks of hospitalization, hypertriglyceridaemia disappeared with a concomitant increase of H‐TGL and LPL. It is concluded that impaired triglyceride metabolism in liver disease is at least partly caused by diminished plasma hepatic TGL activity.
High density lipoprotein infusion and partial plasma exchange in Tangier disease
Authors: ASSMANN G. , SMOOTZ E.
Published: March 2008

Abstract. High density lipoprotein (HDL) infusion and partial plasma exchange were undertaken in two patients homozygous for Tangier disease. Serum samples and ultracentrifugally isolated serum fractions were analysed over a period of 7 days post infusion by agarose electro‐phoresis, two‐dimensional immunoelectrophoresis (employing antibodies to HDL, HDL3, Apoprotein A‐I, and Apoprotein A‐II), Apoprotein A radioimmuno‐assay, and analytical polyacrylamide electrophoresis. The following observations were made: (a) immediately after HDL substitution the broad‐βband, normally visible upon agarose electrophoresis of Tangier plasma, resolved into a distinct β and pre‐β band; (b) as HDL was cata‐bolized, an abnormal a‐migrating lipoprotein was generated which contained Apoprotein A‐II as protein constituent; and (c) there was a proferential loss of Apoprotein A‐I from HDL and the plasma compartment in the course of HDL catabolism.

The results suggest that the defect in Tangier disease resides with enhanced catabolism or defective synthesis of Apoprotein A‐I.
Initial potassium loss and hypokalaemia during chlorthalidone administration in patients with essential hypertension: the influence of dietary sodium restriction
Authors: LANDMANN‐SUTER R. , STRUWENBERG A.
Published: March 2008

Abstract. To investigate the initial potassium loss and development of hypokalaemia during the administration of an oral diuretic, metabolic balance studies were performed in ten patients with essential hypertension who had shown hypokalaemia under prior oral diuretic treatment. Chlorthalidone (50 mg daily) was given for 14 days. Six patients received a normal‐sodium diet and four a low‐sodium (17 mmol/day) diet. All patients had a normal initial total body potassium (40K). The electrolyte balances, weight, bromide space, plasma renin activity, and aldosterone secretion rate were measured. In both groups a potassium deficit developed, with proportionally larger losses from the extracellular than from the intracellular compartment. In the normal‐sodium group the highest mean potassium deficit was 176 mmol on day 9, after which some potassium was regained; in the low‐sodium group the highest deficit was 276 mmol on day 13. The normal‐sodium group showed an immediate but temporary rise of the renin and aldosterone levels; in the low‐sodium group renin and aldosterone increased more slowly but remained elevated. It is concluded that dietary sodium restriction increases diuretic‐induced potassium loss, presumably by an increased activity of the renin‐angiotensin‐aldo‐sterone system, while sodium delivery to the distal renal tubules remains sufficiently high to allow increased potassium secretion.
Plasma phenylethanolamine in hepatic encephalopathy
Authors: CANGIANO C. , ROSSI‐FANELLI F. , BOZZI A. , CALCATERRA V. , CASCINO A. , CAPOCACCIA L.
Published: March 2008

Abstract. It has been suggested that mines other than octopamine may be involved in the pathogenesis of hepatic encephalopathy. Plasma phenylethanolamine has been determined by a radioenzymatic method in twenty‐six biopsy‐proven cirrhotics with or without encephalopathy and in seven normal adults. Phenylethanolamine plasma levels correlated statistically with the presence of liver cirrhosis and severe coma. These results are consistent with the false neurotransmitter hypothesis of hepatic encephalopathy.
A comparison between naturally occurring macroamylasaemia and macroamylasaemia induced by hydroxyethyl‐starch
Authors: DÜRR H. K. , BODE CHRISTIANE , KRUPINSKI R. , BODE J. CH.
Published: March 2008

Abstract. Macroamylasaemia was produced in vitro by incubation of hydroxyethylstarch with serum, and in vivo by intravenous infusion of hydroxyethylstarch. Gel filtration on Sephadex G‐100 revealed distinct differences in molecular size distribution between such hydroxyethylstarch‐induced macroamylase and the usual form of naturally occurring macroamylase which was observed in a few patients from our hospital. Further studies demonstrated that the gel filtration elution pattern of amylase activity in serum containing hydroxyethylstarch‐induced macroamylase is significantly altered with time in vitro and in vivo, probably because of an enzymatic degradation of the hydroxyethylstarch components of the macromolecular complexes.

In a healthy volunteer the serum amylase activity was elevated to a maximum of 797 u/l and the renal clearance rate of amylase was diminished to a minimum of 0.3 ml/ min after infusion of 500 ml of a 6% solution of hydroxyethylstarch, as compared to 300 u/l, and 0.95 ml/min, respectively, during the pre‐infusion period.
Pituitary‐testicular function in patients with chronic alcoholism
Authors: LINDHOLM J. , FABRICIUS‐BJERRE N. , BAHNSEN M. , BOIESEN P. , BANGSTRUP L. , PEDERSEN M. LAU , HAGEN C.
Published: March 2008

Abstract. Testis and liver histology, and pituitary—testicular function were studied in thirty chronic alcoholics. Severe reduction of spermatogenesis was found in 30% and in these patients serum follicle stimulating hormone and prolactin concentrations were significantly higher. There was no correlation between abnormalities in the liver and testis. The serum testosterone was normal in most cases. Sexual dysfunction and testicular atrophy occurred in more than half of the patients and were not related to liver disease. Testicular disorder in chronic alcoholism may be independent of liver disease.
Intestinal and renal handling of calcium in human diabetes mellitus: influence of acute oral glucose loading and diabetic control
Authors: MONNIER L. , COLETTE C. , AGUIRRE L. , SANY C. , MIROUZE J.
Published: March 2008

Abstract. The intestinal absorption and the urinary excretion of calcium were compared in two groups of diabetic patients during periods of satisfactory and poor control. In a first group of ten patients, periods of isolated high glycosuria were obtained by giving an oral glucose load. The second group consisted often patients with a severe endogenous insulin deficiency. The subjects of this latter group were investigated before and after a few days of insulin therapy. In group I, the oral glucose load induced a significant increase in the intestinal calcium absorption and had a tendency to lower the urinary calcium excretion. Furthermore, an inverse relationship was found between the changes in the intestinal calcium absorption and the variations of the urinary calcium excretion. In group II, both intestinal absorption and urinary excretion of calcium fell significantly after recovery of satisfactory metabolic control by insulin therapy. From the results as obtained in group I one can conclude that glucose enhances the calcium transfer from the luminal to the serosal pole of both intestinal and renal tubular cells. During severe ketosis as observed in group II, calcium metabolism is considerably accelerated and the increase in the intestinal calcium absorption rate may be interpreted as a compensatory mechanism for the high urinary loss of calcium.
Is thallium‐201 of use in the measurement of total exchangeable potassium in man?
Authors: MACKAY ALISTAIR , DAVIES D. L. , HORTON P. W.
Published: March 2008

Abstract. Simultaneous measurements of exchangeable potassium were made in seven normal male subjects using potassium‐43 and thallium‐201. Exchangeable potassium values obtained using the ‘thallium‐201 space’ were unreliable.
Effect of muscle spasms on blood gases and acid‐base status in tetanus patients
Authors: ELEGBELEYE O. O.
Published: March 2008

Abstract. Blood gas tensions and acid‐base status were determined in six patients with tetanus before and after the onset of severe muscle spasms. Hypoxaemia and metabolic acidosis present in all the patients, were worsened by muscle spasms. It is suggested that frequent measurements of blood gases should be carried out where such facilities are available.
Anticlotting properties of fragments D from human fibrinogen and fibrin
Authors: HAVERKATE F. , TIMAN G. , NIEUWENHUIZEN W.
Published: March 2008

Abstract. It appeared from our previous studies that Ca2+ concentrations comparable to those occurring in blood protect the C‐terminal part of the γ‐chain remnants of fibrin(ogen) fragments D against further plasmin attack. This study shows that purified fibrin(ogen) fragments D formed in the presence of Ca2+ ions have anticlotting activity in vitro, whereas shortening of the γ‐chain remnants leads to loss of such activity.
Lipid and carbohydrate metabolism in uraemia
Authors: ATTMAN PER‐OLA , GUSTAFSON ANDERS
Published: March 2008

Abstract.Lipid and carbohydrate metabolism variables were studied in twenty‐eight patients with chronic renal failure (mean GFR 7.7 ± 2.5 ml/min) and uraemic symptoms.

71% of the patients had hypertriglyceridaemia (≥ 2.2 mmol/l). Total serum cholesterol was normal while VLDL cholesterol was high and α‐lipoprotein cholesterol was low. The fractional elimination rate of Intralipid was low and inversely correlated to serum triglyceride levels.

Intravenous glucose tolerance was reduced with normal or slightly increased fasting blood glucose and insulin values before and during the test.

Serum triglycerides were correlated to plasma insulin but not to residual renal function or serum urea levels.

The cause of hypertriglyceridaemia and lowering of α‐Lp cholesterol is not unequivocally clear. Present evidence indicate that retarded catabolism of triglyceride‐rich lipoproteins is important but accentuated release of triglyceride‐rich lipoproteins may have occurred in a number of cases. The commonly used treatment with β‐blocking agents for hypertension in chronic renal failure may accentuate certain of the metabolic responses in uraemia.
Renin‐activation by kallikrein: evidence for alkaline‐activation of plasma renin
Authors: HUMMERICH W. , FELTKAMP H. , KONRADS A. , AHLMANN P. , BORNHOFEN H.
Published: March 2008

Abstract. Porcine pancreatic kallikrein leads to a significant activation of human plasma renin when incubated at pH 8·2. ‘Endogenous’ activation of plasma renin can be seen by incubation of plasmas at the same pH. Both ‘endogenous’ alkaline‐ and kallikrein‐activation of plasma renin can be inhibited by aprotinin. Both, kallikrein‐ and ‘endogenous’ alkaline activation of plasma renin are significantly correlated to cryo‐ and acid‐activation. We suggest that kallikrein‐ and ‘endogenous’ alkaline‐activation come close to the in vivo activation process.
Free insulin, bound insulin, C‐peptide and the metabolic control in juvenile onset diabetics: comparison of C‐peptide secretors and non‐secretors during 24 hours conventional insulin therapy
Authors: GERBITZ K.‐D. , KEMMLER W. , EDELMANN A. , SUMMER J. , MEHNERT H. , WIELAND O.H.
Published: March 2008

Abstract. In two groups of juvenile onset diabetics similar in age, weight, diet and daily insulin dosage (eight without C‐peptide, group I; eight with C‐peptide, group II) the serum levels of free and antibody bound insulin, C‐peptide, glucose, lactate, alanine and FFA were determined over 24 h. In addition the affinity and binding capacity of the insulin antibodies were determined in vitro.

No correlation was found between free or bound insulin and glucose. This holds true for the individual profiles as well as for the averaged profiles of the two groups. Free insulin and lactate or alanine were positively correlated in the C‐peptide secreting group. C‐peptide secretion followed the fluctuations of the glucose level during 24 h in each individual patient.

As a group, C‐peptide secretors were better controlled than non‐secretors with respect to mean blood glucose, M‐value and the lability index and showed higher free insulin levels despite a similar daily insulin dosage. The possible reasons for this fact are discussed.

No correlation was found between the affinity characteristics of the insulin antibodies and the degree of metabolic control or the daily insulin dosage.
Studies on cortisol metabolism during haemodialysis in man
Authors: DECK K. A. , FISCHER B. , HILLEN H.
Published: March 2008

Abstract. Plasma clearance rates and dialysance of labelled cortisol were measured in patients on chronic intermittent dialysis during and after dialysis. Plasma clearance rates during dialysis were 30–63% higher than after dialysis; dialysance was 0.3–0.7 1/h and accounted only for 20–35% of the increase of plasma clearance rates during dialysis. After bolus injection of labelled cortisol, disappearance curves were obtained in two normal subjects and two uraemic subjects on and off dialysis. Biological halftimes of the different segments of the disappearance curves and distribution volumes were calculated. The size of the inner compartment (V1) is greater in uraemia. The disappearance curves flatten after the end of dialysis, indicating an increase of biological halftime after dialysis. Plasma 17‐OHCS‐glucuronides dropped from 2.13 ± 0.62 μmol/l (n= 20) at the beginning to 1.05 ± 0.65 μmol/l at the end of dialysis and increased to 1.51 ± 0.43 μmol/l (n= 12) within 3 h thereafter.

During dialysis cortisol metabolites are removed from the blood. This may decrease inhibition of cortisol metabolism by the end products of cortisol metabolism which might explain the more rapid plasma clearance and the shortened cortisol half‐life during haemodialysis.
Esterification of cholesterol in human small intestine: the importance of acyl‐CoA:cholesterol acyltransferase
Authors: NORUM KAARE R. , LILLJEQVIST ANNE‐CHARLOTTE , HELGERUD PER , NORMANN ELDAR R. , MO ARVE , SELBEKK BODIL
Published: March 2008

Abstract. Human intestinal mucosa contains acyl‐CoA: cholesterol acyltransferase activity. The enzyme has been studied by using oleylcarnitine, CoA and carnitine palmitoyltransferase as an oleyl‐CoA regenerating system. The enzyme was found in the particulate fraction of the cells, it had a pH optimum between 7.2 and 8.2, and was inhibited by taurocholate. The specific enzymic activity in biopsies from intestinal mucosa of normal men was found to be 3.6 ± 1.37 nmol cholesteryl ester formed mg protein‐1 h‐1, an activity which can account for all cholesteryl esters in intestinal lymph. Low enzymic activity was found in biopsies from patients with small intestinal disorders. Two pancreatectomized patients had values within the normal range.
The effects of oral sucrose and of estimated infarct size on plasma free fatty acids, plasma glucose and serum insulin in the early stages of acute myocardial infarction
Authors: TANSEY M. J. B. , OPIE L. H. , KENNELLY B. M.
Published: March 2008

Abstract. Twenty‐two patients with early myocardial infarction were studied to test the effect of oral sucrose as an antilypolytic agent. Without sucrose, plasma free fatty acids rose to a peak (mean 1.48 mM/l 8 h after onset of symptoms) and then fell spontaneously by 32% of the peak level in 2 h. Sucrose had no effect on the peak fatty acid level and did not accelerate the initial rate of fall in the first 2 h. Where the peak free fatty acid was less than 1.5 mM/l, however, it fell to a lower level in patients given sucrose (P < 0.05). A subsequent rebound of free fatty acid values, as seen in starved patients, was delayed for about 6 h in sucrose‐fed patients. The responses of free fatty acid, glucose and insulin varied according to the size of the infarct as estimated by the plasma creatine kinase method. Patients with larger infarcts (>65 creatine kinase gram equivalents) had higher insulin and blood sugar levels on and after admission, and had higher plasma free fatty acid peaks than patients with smaller infarcts (≤65 creatine kinase gram equivalents). When patients with larger infarcts were given oral sucrose, the rise in blood glucose was higher and more sustained than in patients with small infarcts and there was no insulin response. The insulin response to sucrose was normal in those with smaller infarcts. Thus oral sucrose was an effective antilipolytic agent only in patients with smaller infarcts.
Very low density lipoprotein overproduction in genetic forms of hypertriglyceridaemia
Authors: CHAIT ALAN , ALBERS JOHN J. , BRUNZELL JOHN D.
Published: March 2008

Abstract. Very low density lipoprotein kinetic parameters were compared in familial hypertriglyceridaemia and familial combined hyperlipidaemia, two distinct genetic forms of hypertriglyceridaemia. Very low density lipoprotein apoprotein B turnover rate was greater in hypertriglyceridaemic subjects with familial combined hyperlipidaemia (099±0–27 mg/kg/h; n= 5; P < 0005) and also in familial hypertriglyceridaemia (0–74±0–10; n= 6; P < 0–005) than in age and weight matched non‐hyperlipidaemic controls (0–54±0–21; n= 6), suggesting that the hypertriglyceridaemia seen in both genetic disorders was due to very low density lipoprotein overproduction. Very low density lipoprotein apoprotein B turnover rate was greater in familial combined hyperlipidaemia than in familial hypertriglyceridaemia while plasma triglyceride turnover was higher in familial hypertriglyceridaemia. This disparity in the turnover rates of apoprotein B and triglyceride between these disorders was accompanied by a higher very low density lipoprotein triglyceride/apoprotein B ratio in familial hypertriglyceridaemia than in familial combined hyperlipidaemia (P < 0001) and in normals (P < 0–005).

The findings suggest that the hypertriglyceridaemia of familial combined hyperlipidaemia is due to overproduction of very low density lipoprotein of normal composition, while that of familial hypertriglyceridaemia is due to oversecretion of triglyceride‐enriched very low density lipoprotein.
Evidence for 25‐hydroxyvitamin D deficiency as a factor contributing to osteopenia in diabetic patients with idiopathic haemochromatosis
Authors: MONNIER LOUIS H. , COLETTE CLAUDE , RIBOT CLAUDE , MION CHARLES , MIROUZE JACQUES
Published: March 2008

Abstract. Osteopenia is frequently encountered in the course of idiopathic haemochromatosis. In order to establish the mechanism of this bone disorder, the following parameters were studied in nine diabetic patients with idiopathic haemochromatosis: (i) the intestinal calcium absorption measured by using a double radiotracer technique; (ii) the bone mineral content (BMC, mg/cm2) determined on the forearm by the Cameron's absorptiometry technique, (iii) the plasma 25 hydroxyvitamin D (25‐OH‐D ng/ml) by a competitive protein‐binding radioassay. The results were compared to those obtained in ten controls and in eight diabetics without haemochromatosis. The patients suffering from haemochromatosis had a significant fall in total fractional absorption of calcium and BMC as compared with controls and diabetics without haemochromatosis. Furthermore plasma 25‐OH‐D was significantly lower in haemochromatosis patients (51±0–6 ng/ml) than in controls (16‐4±1–3 ng/ml, P < 001) and in diabetics without haemochromatosis (14‐2±1–4 ng/ml, P < 0–02). These results indicate that haemochromatosis patients exhibit important disturbances in calcium homeostasis, i.e. low concentration of plasma 25‐OH‐D and reduced intestinal absorption of calcium. The latter abnormalities may well be related to the bone rarefaction observed in these patients.
Hepatic vein oxygenation, liver blood flow, and the rate of ethanol metabolism in recently abstinent alcoholic patients
Authors: ITURRIAGA HERNÁN , UGARTE GUILLERMO , ISRAEL YEDI
Published: March 2008

Abstract. To determine whether hepatic hypoxia is associated with hepatocellular necrosis in alcoholics, oxygen tension in the hepatic vein and hepatic blood flow were determined in thirteen patients without overt clinical liver disease. Ethanol metabolic rate was also assayed as an index of liver metabolism. Hepatic blood flow and ethanol metabolic rate were also determined in six normal volunteers. According to liver histology patients were separated into two groups, with and without hepatocellular necrosis. Alcoholics with necrosis showed a higher (P < 0–002) ethanol metabolic rate (405±0–23 mmol/kg/h) than those without necrosis (2–46±0–34). Hepatic blood flow in the total group of alcoholics was not significantly different from controls; in the group with necrosis it was lower (651‐7±44‐6 ml/min/m2) than in the group without necrosis (878‐3±81‐6; P < 0025). Hepatic vein pO2 was lower (P < 001) in patients with hepatocellular necrosis (31‐7±0–68 mmHg) than in patients without necrosis (35‐7±0–99). In the whole group, a significant negative correlation (r= ‐0 76, P < 0–003) was observed between hepatic vein pO2 and ethanol metabolic rate. Acute administration of ethanol (21‐7 mmol/kg) did not alter hepatic blood flow in six normal individuals nor in five alcoholic patients, although an increase in hepatic vein pO2 was observed in the latter. The changes observed in hepatic vein pO2, functional hepatic blood flow, and ethanol metabolic rate which correlate with hepatocellular necrosis, may be of pathogenic importance in alcoholic liver disease.
Glucuronidation of bilirubin and the occurrence of pigment gallstones in patients with chronic haemolytic diseases
Authors: FEVERY J. , VERWILGHEN R. , TAN T. G. , GROOTE J. DE
Published: March 2008

Abstract. A group of thirty‐seven patients with increased haem catabolism has been studied to gain insight in their bilirubin conjugating capacity. Bilirubin UDP‐glucuronyl transferase activity (GlcATa) in the liver and bilirubin monoconjugates in bile were measured and the hepatic bilirubin clearance was calculated from the radio‐chromium‐survival data. In the present group, 41% of the patients clearly had a deficiency in bilirubin conjugation similar to what is classically found in Gilbert's syndrome. The association may facilitate detection of these patients as serum bilirubin levels were higher (65‐8 μM ± 19) (m ± 1 SD) in the fifteen patients with associated Gilbert's syndrome versus thirteen having only haemolysis (43‐6 μ± 15). A fair correlation was found between the percentage of monoconjugates in bile and the GlcATa levels in the liver as well as with the calculated hepatic bilirubin clearance, although some discrepancies exist. Using these determinations, a clearcut separation from normal values was not obtained, suggesting at least in the present group of patients that Gilbert's syndrome represents only one end of a continuum of bilirubin conjugation rates and not a separate entity.
Renal handling of urate in healthy man in hyperuricaemia and renal insufficiency: circadian fluctuation, effect of water diuresis and of uricosuric agents
Authors: LANG F. , GREGER R. , OBERLEITHNER H. , GRISS E. , LANG K. , PASTNER D. , DITTRICH P. , DEETJEN P.
Published: March 2008

Abstract. To differentiate between extrarenal and renal causes of hyperuricaemia and gout, clearances of urate and creatinine were monitored for 31/2 days in fifty‐two individuals (seven with a history of gout) with no gross impairment of renal function (creatinine clearance 52–137 ml/min). Dietary purine intake was kept constant. Monophasic circadian fluctuations of fractional urate excretion (= urate clearance over creatinine clearance) were observed with peak values in the afternoon, about 50% higher than during the night. Circadian fluctuations of urinary flow rate were almost identical. However, enhancement of urinary flow rate due to water diuresis had no effect on urate clearance. Despite wide variation of plasma urate concentrations among different individuals (±30% SD), daily urate excretion varied little (± 4% SD) and did not correlate with plasma urate (r= 0–03). Thus extrarenal factors appear not to account for the occurrence of hyperuricaemia in these patients. In contrast, a clearcut negative correlation was apparent between plasma urate concentration and fractional urate clearance (r= ‐0 72), which could fully account for the variations of plasma urate concentration. To elucidate further the mechanism responsible for antiuricosuria in hyperuricaemic patients, the effects of the uricosuric agents benzbromarone and probenecid were tested. A clearcut correlation was apparent between control fractional urate excretion and uricosuric effect of both benzbromarone and probenecid (r= 0–83 and 0–88, respectively), suggesting that anti‐uricosuria was due to defective secretion. In an additional series, the uricosuric effect of probenecid was tested in ten patients with renal insufficiency. In these patients the uricosuric effect was clearly blunted, indicating that urate reab‐sorption is reduced in renal insufficiency.
Capillary supply and muscle fibre types in patients with intermittent claudication: relationships between morphology and metabolism
Authors: HAMMARSTEN JAN , BYLUND‐FELLENIUS ANN‐CHRISTIN , HOLM JAN , SCHERSTEN TORE , KROTKIEWSKI MARCIN
Published: March 2008

Abstract. There have been previous reports on an increased oxidative capacity in muscle tissue from the diseased legs of patients with intermittent claudication. The present study was designed to correlate metabolic and morphological data and to investigate whether the metabolic adaptive changes in muscle tissue of claudicating legs were also reflected in morphological variables such as capillary supply, fibre type distribution, and fibre area. The activity of cytochro‐me‐c‐oxidase in gastrocnemius muscle was determined and the insulin and glucose uptakes were measured across the leg in the basal state and 10 min following intravenous administration of 25 g glucose. The finding of a reduced relative number of Type II B fibres and a reduced ratio Type II B/II A fibre area, as well as an increased capillary supply to Type II A, indicated that the most extensive morphologic changes in muscle tissue of claudicating legs had occurred in Type II fibres. The increased number of capillaries in contact with Type IIA fibres in muscle tissue from claudicating legs, compared with muscle tissue from control legs, suggested that the most apparent metabolic changes occurred in this fibre type in the adaptation process of these patients. The more pronounced morphologic and metabolic changes in Type II fibres suggest that these fibres are more intensely activated than Type I fibres during physical activity in claudicating legs. The insulin uptake correlated positively with the number of capillaries per fibre, suggesting that the endothelial surface area is one of the determining factors for insulin uptake. The percentage of Type II B fibres reflected to a certain extent the metabolic adaptation in muscle tissue.
Hepatic HMGCoA reductase in human cholelithiasis: effects of chenodeoxycholic and ursodeoxycholic acids*
Authors: MATON PAUL N. , ELLIS H. JULIA , HIGGINS MALCOLM J. P. , DOWLING R. HERMON
Published: March 2008

Abstract. To study further the role of hepatic cholesterol synthesis in patients with gallstones, the activity of the rate‐limiting step in cholesterbgenesis, hydroxy‐methyl glutaryl co‐enzyme A reductase (HMGCoAR), was measured in operative wedge liver biopsies from ten patients with untreated cholesterol gallstones, six with pigment stones and ten controls. Hepatic HMGCoAR was also measured in six patients with cholesterol‐rich gallstones treated for 1–24 months with 14‐6‐18‐6 mg chenodeoxycholic acid (CDCA) kg‐1 day‐1, in two patients with radiolucent pigment stones treated with 17‐3 and 17‐7 mg CDCA kg‐1 day‐1 and in ten other patients with cholesterol‐rich stones given 4–5‐7‐2 mg ursodeoxycholic acid kg‐1 day‐1 for 1–6 months. HMGCoAR activity was also related to the free and esterified cholesterol content of both hepatic homogenates and the microsomal fractions.

Compared with the controls (HMGCoAR activity 14‐6±1 6 (SEM) pmole mg microsomal protein‐1 min‐1), the mean activity in untreated cholesterol cholelithiasis was 32 2 ±2‐0 (P < 0–001), but was near normal in patients with pigment stones (16‐2 + 1 5). In cholesterol gallstone patients, chenodeoxycholic acid treatment reduced the mean enzyme activity by 51% compared with the untreated gallstone group (P < 0001) and in smaller doses, ursodeoxycholic acid therapy lowered it by 40% (P < 0001) but in the two patients with pigment stones, CDCA did not seem to affect HMGCoAR activity. Despite this four‐fold variation in enzyme activity, there were no significant differences in mean free or esterified cholesterol concentrations in whole liver homogenates or in the microsomal fraction from any of the patient groups.

Presented in part at the European Society for Clinical Investigation, Rotterdam, April 1978 (Maton P.N. & Dowling R.H (1978) Eur J Clin Invest 8, 329 (abstract)) and at the V International Bile Acid Meeting, Freiburg, June 1978 (Maton P.N. & Dowling R.H. (1978) in: Biological Effects of Bile Acids (ed. by G. Paumgartner, A. Stiehl and W. Gerok), pp. 91–98. MTP Press, Lancaster).
Purine and pyrimidine metabolism in hereditary orotic aciduria: some unexpected effects of allopurinol
Authors: SIMMONDS H. A. , WEBSTER D. R. , BECROFT D. M. O. , POTTER C. F.
Published: March 2008

Abstract. Purine and pyrimidine metabolism have been investigated in the longest surviving case of hereditary orotic aciduria after 15 years of chronic uridine therapy. Several unusual features were recorded:

1. Although the uridine dosage (0–5 mmol/kg) was adequate to control an otherwise normal clinical status, orotic acid excretion was still excessive (± 7 mmol/24 h). Urinary drug metabolites (uracil and uridine), however, accounted for less than 7% of the daily uridine dose, and no orotidine, or any abnormal pyri‐midines or purines, were identified at any time.

2. Urinary uric acid excretion was high and plasma uric acid low, resulting in a clearance up to 4 times normal. This was attributed to the uricosuric effect of orotic acid.

3. In direct contrast to previous findings in gouty subjects and healthy male controls we noted: (i) no increase in plasma or urinary uric acid levels, or uric acid clearance, following the change from a low to a high nucleoprotein regime (normally up to two‐fold); (ii) allopurinol reduced both urinary uric acid and total oxypurine levels by more than 50% on the low (normally unaffected) as well as the high (normally reduced 20–50%) nucleoprotein regime; (iii) a substantial (up to 70%) reduction in orotic acid excretion during allopurinol therapy (normally mild orotic aciduria), of similar magnitude and in parallel with the reduction in uric acid levels. Uric acid and orotic acid excretion were closely related throughout.

These findings differ from those of a similar study of hereditary orotic aciduria and suggest there is competitive transport between exogenous (dietary) purines and pyrimidines, as well as an important interdependence between endogenous purine and pyrimidine metabolism, by mechanisms as yet undefined.
Insulin receptors in acute and chronic lymphoid leukaemias
Authors: THOMOPOULOS P. , MARIE J. P.
Published: March 2008

Abstract. Normal lymphocytes lack insulin receptors. The binding of this hormone was studied in twelve patients with acute lymphoblastic leukaemia (ALL) and fourteen patients with chronic lymphocytic leukaemia (CLL). Lymphoblasts from ALL have been found to possess hormone receptors with properties identical to those of the known target cells for insulin: specificity, pH and temperature dependence, and ligand‐induced increase in dissociation rate. All patients with ALL displayed insulin receptors on their lymphoblasts. The null‐type cells possessed higher numbers of binding sites than the T‐type cells, without overlapping of the values. In the fourteen patients with CLL, eight had low levels of insulin receptors on their lymphocytes while six showed a complete lack of such binding sites. Our results suggest that measurement of insulin binding might be a useful non‐immunological marker for the classification of human leukaemias.
The effectiveness of digoxin‐specific F(ab‘)2‐antibody fragments in the treatment of digitoxin poisoning: experimental investigations in the cat
Authors: HESS T. , SCHOLTYSIK G. , RIESEN W.
Published: March 2008

Abstract. In animal experiments heterologous digoxin‐specific F(ab')2 antibod fragments have been found to be effective for the treatment of arrhthmias induced b toxic doses of digoxin. So far the have been successfull emploed in three patients suffering from digoxin poisoning. The present stud was undertaken to test whether these antibodies are also effective in the treatment of digitoxin poisoning.

Ventricular tachcardia, induced in digitalized cats b intravenous injections of digitoxin, was fatal in four out of five controls. However, sinus rhthm was reinstated in all the animals treated with digoxin‐specific F (ab') 2 after onset of the arrhthmia. Cross‐reactivit between the antibodies used and digitoxin, while slight in vitro, is, nevertheless, sufficient to justif their clinical use in cases of digitoxin poisoning.
Effect of indomethacin upon the renin‐angiotensin sstem in patients with Bartter's sndrome
Authors: VIERHAPPER H. , WALDHAUSL W. , Klinik I. Medizinische
Published: March 2008

Abstract This stud reports on the influence of indomethacin upon the renin‐angiotensin sstem in three patients with Bartter's sndrome. An analogue of angiotensin II with weak agonistic properties (suc‐cinam 11 ‐val5‐phenlglcine‐acetate8‐angiotensin II) induced a fall of blood pressure and a rise of plasma renin concentration but no change in plasma aldosterone. Pretreatment with indomethacin (75 mg/da) reversed the hpotensive effect of the analogue of angiotensin II and abolished the increase of plasma renin concentration. It is concluded that elevated levels of endogenous angiotensin II are of major importance for the maintenance of blood pressure in patients with Bartter's sndrome. The inhibition of the snthesis of prostaglandins reversed some, though not all, of the metabolic abnormalities in this sndrome.
Lipoprotein lipase in adipose tissue and plasma triglceride clearance in patients with primar hpertriglceridaemia
Authors: TALOR K. G. , HOLDSWORTH G. , GALTON D. J.
Published: March 2008

Abstract.

The activit of lipoprotein lipase (E.C.3.1.1.3) extracted and released from adipose tissue has been measured in obese subjects with mild or severe hpertriglceridaemia. The Intralipid® tolerance test has been studied as a measure of in vivo clearance of exogenous triglceride from plasma.

Plasma triglceride clearance was reduced in patients with severe hpertriglceridaemia (> 4 mmol/1) and this was associated with reduced activities of extracted lipoprotein lipase in adipose tissue compared to patients with mild hpertriglceridaemia (2–4 mmol/1).

A course of insulin therap (20 u/da) for 1 week increased the extracted, but not the released component of the enzme from adipose tissue of hpertri‐glceridaemic patients.

Serum (25% v/v) potentiated the release of lipoprotein lipase from adipose tissue of normo‐ but not hpertriglceridaemic patients.

The effect of serum on enzme release was abolished if lipoprotein‐deficient serum was used. Addition of ver low densit lipoprotein (VLDL) or high densit liproprotein (HDL) restored the abilit of de‐lipidated serum to augment release of enzme from adipose tissue, but this was not observed with low densit lipoprotein (LDL).

It is suggested that a defect in the release of lipoprotein lipase activit in adipose tissue ma contribute to the development of hpertriglceridaemia in this group of patients.