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Biomedical subjects

H G Tiselius

Publications and source records attributed to H G Tiselius.

At least 127 records · Page 7Linked to original sources
PubMed1983

Effects of calcium, aluminium, magnesium and cholestyramine on hyperoxaluria in patients with jejunoileal bypass.

The urinary excretion of oxalate, calcium, magnesium and citrate as well as the inhibition of calcium oxalate crystal growth in diluted urine was studied in seven patients with hyperoxaluria following jejunoileal bypass. The study was performed on an outpatient basis before and during daily administration of 38 or 113 mmol calcium, 28 mmol of aluminum, 20 mmol of magnesium or 16 g of cholestyramine. Each substance was administered for seven days with a free interval of at least seven days. The mean urinary oxalate excretion was not reduced with any of these regimens. Administration of 38 mmol of calcium per day resulted in increased oxalate and magnesium excretion. Increased excretion of both calcium and citrate was observed during administration of 113 mmol of calcium per day. Calcium and magnesium excretion was increased with aluminium. An increased magnesium excretion was also observed during administration of magnesium, resulting in a decreased calcium/ magnesium ratio. Cholestyramine resulted in increased oxalate and decreased citrate excretion.

Adult↗
PubMed1982

An improved method for the routine biochemical evaluation of patients with recurrent calcium oxalate stone disease.

By means of a computerized calculation program, a simplified estimate of the ion-activity product of calcium oxalate was derived (AP(CaOx)-index), based on the 24-h urinary excretion of calcium (Ca), oxalate (Ox), magnesium (Mg), citrate (Cit) and the urine volume (V): (formula: see text) With urinary electrolyte values within the normal range, there was a good correlation between the AP(CaOx)-index and the more laboriously obtained ion-activity product (r = 0.997). To express the biochemical risk of CaOx stone formation a CaOx-risk index was designed, which also includes the inhibition of calcium oxalate crystal growth (I) and with all variables related to urinary creatinine (Cr): (formula: see text) The mean CaOx-risk index (+/-SEM) in urine from 100 normal men and 156 male stone formers were 648 +/- 27 and 1019 +/- 38 respectively (p less than 0.001). A risk index without inhibition index, had the corresponding values 366 +/- 14 and 527 +/- 17 (p less than 0.001).

Calcium Oxalate↗
PubMed1981

Metabolic effects of bendroflumethiazide in patients with recurrent calcium oxalate stone disease.

Two groups of patients with urolithiasis were treated with 2.5 mg. (group A) and 5.0 mg. (group B) bendroflumethiazide daily. There were 14 men and 3 women in group A, and 14 men and 2 women in group B in whom metabolic effects were followed during 1 year of treatment. Serum calcium was significantly increased in group B after 1 month but later returned to the pretreatment level. A significant decrease in serum magnesium was recorded in group B after 6 and 10 months. No significant effect on serum calcium or magnesium was observed in group A. Serum potassium decreased in both groups but serum urate remained at the pre-treatment level. An increased alkalinity was noted in both groups. Urinary calcium was decreased significantly only in group B. Although significantly increased excretion of magnesium was observed after 1 and 6 months in group A this was not encountered in group B, and after 12 months urinary magnesium was at the pre-treatment level in both groups. Urinary excretion of oxalate, urate and citrate appeared to be unaffected by the treatment. The inhibition of calcium oxalate crystal growth and urine volume did not change. The calcium/magnesium quotient decreased in both groups as did the calcium times oxalate/ magnesium quotient. The main metabolic effect of bendroflumethiazide, with respect to its stone prophylactic property, appears to be a decrease in the calcium/magnesium quotient and a dose of 5 mg. per day probably is more satisfactory than a 2.5 mg. dose.

Adult↗
PubMed1981

The effect of pH on the urinary inhibition of calcium oxalate crystal growth.

Urinary inhibition of calcium oxalate crystal growth was measured in metastable solutions of sodium oxalate and calcium chloride at different pH. Inhibition of calcium oxalate crystal growth in urine from patients with calcium oxalate stone disease increased with increasing pH. The increase was most pronounced between pH 5.5 and 7.0. Sodium pyrophosphate in a similar way inhibited calcium oxalate crystal growth in this pH interval, and between pH 6.0 and 7.5 there was also a slight increase in the inhibiting activity by chondroitin sulphate and citrate. Approximative correction factors were calculated in order to obtain a more appropriate value of the inhibition index when urine pH was different from 6.0, and a reasonably good correlation was obtained between inhibition indices calculated by means of the correction factor and inhibition indices derived from direct measurements of the crystal growth rate in solutions with different pH.

Calcium Oxalate↗
PubMed1981

Biochemical evaluation of patients with urolithiasis.

Inhibition of calcium oxalate crystal growth was analyzed in 84 male and 30 female patients with urolithiasis and in 27 normal men and 7 normal women. No significant difference in inhibition index was found between stone formers and normal subjects or between male and female stone formers. The quotient, calcium X oxalate/magnesium X inhibition index, was significantly higher in urine from male stone formers (p less than 0.01) and the same was found for the quotient, calcium X oxalate/magnesium X citrate X inhibition index (p less than 0.005).

Calcium Oxalate↗
PubMed1981

Renal stone disease in a Swedish district during one year.

In a Swedish district served by only one hospital the annual incidence of urinary stone colic was estimated to 1.4 per 1000 inhabitants. Sixty-two per cent of the patients were treated entirely as out patients whereas 9% required some form of surgery during the study. Thirty-seven per cent of the patients were recurrent stone formers. No significant seasonal variation in stone incidence was noted. A definite reason for stone formation could be established in 6%, and among 56 patients with recurrent stone disease run through a biochemical investigation, abnormal findings were recorded in 70%.

Adolescent↗
PubMed1981

[14C]Oxalate absorption by normal persons, calcium oxalate stone formers, and patients with surgically disturbed intestinal function.

Intestinal absorption of oxalate can be judged from the urinary excretion of orally administered [14C]oxalate. Fifteen normal subjects, 21 patients with "idiopathic" calcium oxalate stone disease and a high oxalate excretion, four patients operated with ileocecal resection, and seven patients operated with jejunoileal bypass were so investigated. We saw no significant difference in the amount of isotope excreted by normal subjects and idiopathic stone formers; 13.6% (SD 5.9%) and 14.4% (SD 6.5%), respectively, of the administered dose was accounted for in the urine. The patients with resection or bypass showed a quite different pattern of isotope excretion, and 18.3% (SD 7.0%) and 36.8% (SD 14.0%), respectively, of the isotope was accounted for in the urine.

Calcium Oxalate↗
PubMed1981

Evaluation of a routine method for determination of calcium oxalate crystal growth inhibition in diluted urine samples.

We have evaluated a routine method for determination of the inhibition of calcium oxalate crystal growth in diluted urine samples. A crystallization inhibition index is calculated from the decrease in [14C]oxalate concentration in a metastable solution of calcium chloride and sodium oxalate after addition of seed crystals of calcium oxalate. The coefficient of variation between different determinations on the same sample is less than 1.5%, and there is good correspondence between indices obtained by this method and by a more laborious older method. We also studied the influence of different urinary constituents on the crystal growth rate in the system; whereas there was significant inhibition with citrate, chondritin sulfate, and pyrophosphate, no effects were observed with ordinary urinary concentrations of calcium, magnesium, and oxalate. The mean inhibition index was lower in a group of male patients with calcium oxalate stone disease than in a control group of normal men.

Calcium Oxalate↗
PubMed1980

Urine composition in patients with urolithiasis during treatment with magnesium oxide.

Fifteen patients with recurrent renal stone formation were treated with 400 mg magnesium oxide daily. Urine composition was analyzed before the start of treatment and after 6-12 months. The urinary excretion of magnesium before and during treatment was 321 +/- 120 (mean +/- SD) and 409 +/- 140 mmol per mol creatinine respectively, a difference that was not statistically significant. Urinary calcium increased from 473 +/- 186 to 662 +/- 213 mmol per mol creatinine (p less than 0.05). All patients who increased their excretion of magnesium also increased the urinary output of calcium and, as a result of this, the calcium/magnesium-quotients were unaffected by the treatment. No significant effect was observed on urine oxalate excretion. Serum concentrations of calcium, magnesium and urate all remained at the pre-treatment level. From the results obtained in this study, magnesium oxide in this dosage cannot be recommended for use in treatment of patients with urolithiasis.

Calcium↗
PubMed1980

Effects of postmenopausal ethinylestradiol treatment on gallbladder bile.

Bile composition was studied in three postmenopausal women without evidence of gallstone disease during administration of 50 micrograms of ethinylestradiol daily. The treatment resulted in an increased fraction of cholesterol in gallbladder bile and a shift in the bile acid composition with decreased relative concentration of chenodeoxycholate and increased fraction of cholate. These changes in bile lipid composition might explain the higher incidence of gallstones in women treated with estrogens.

Bile Acids and Salts↗
PubMed1980

Inhibition of calcium oxalate crystal growth in urine during treatment with allopurinol.

Twelve male patients with urolithiasis were treated with 300 mg allopurinol daily. Urinary urate decreased from 251 +/- 55 to 156 +/- 19 (mean +/- SD) mmol per mol creatinine. The inhibition of calcium oxalate crystal growth was measured in an in vitro system and the inhibition index increased from 0.51 +/- 0.06 to 0.57 +/- 0.08 (mean +/- SD). Urinary citrate excretion was unaffected by the treatment.

Allopurinol↗
PubMed1980

Validity of biochemical findings in the evaluation of patients with urolithiasis.

Urinary excretion of calcium, magnesium and oxalate was studied in 38 patients with urolithiasis on two different occasions, and there appeared to be a good correlation between the biochemical findings in the two samples. All values were expressed per mole of creatinine and it was furthermore demonstrated that the variation in creatinine excretion was considerably less than the variation in urine volume. The calcium/magnesium quotients were calculated in 113 2-hour fasting urine samples and 24-hour urine samples and a good correlation was obtained. Biochemical grouping of the patients was performed by means of the two sets of values and the result obtained was approximately the same in both cases.

Calcium↗
PubMed1980

Altered gallbladder bile composition in gallstone disease. Relation to gallbladder wall permeability.

The possible role of conjugated bile salts in the induction and mediation of acute aseptic cholecystitis has been assessed. Using an experimental model, we determined the passive permeability to fluorescently labelled dextran in the gallbladder wall when exposed to different bile salts, alone or together with lecithin. Both taurocholate (20 mM) and, in particular, taurodeoxycholate (20 mM) markedly increased the transmural passage of dextran, but this effect was inhibited by lecithin (50 mM). Bile from patients with cholesterol gallstones contained relatively more deoxycholates (19.4% +/- 8.6%) and less lecithin (35 +/- 20 mmol/l) than did bile from patients with uncomplicated gastric disease (14.1 +/- 6.0% deoxycholates and 53 +/- 26 mmol lecithin/l). Since deoxycholates are more inflammation-promoting than cholates in several systems, and lecithin is considered necessary for protection against the devastating effects of bile salts, these findings should not be overlooked in current hypotheses on the pathogenesis of acute calculous cholecystitis.

Adult↗
PubMed1980

Urine composition in patients with renal stone disease during treatment with allopurinol.

Thirty-four male and seven female patients with urolithiasis were treated with 300 mg allopurinol daily for one year in order to prevent stone recurrences. The mean serum-urate concentration in all patients, and the urine urate excretion in patients with a pre-treatment urate excretion above 250 mmol per mol creatinine were significantly reduced. The mean urinary excretion of calcium, magnesium and oxalate was unaffected by the treatment, although six of eight patients with a pre-treatment oxalate excretion above 25 mmol per mol creatinine demonstrated lower urine oxalate values during the treatment. No significant differences were obtained concerning the calcium/magnesium or calcium x oxalate/magnesium x creatinine quotients, but lower values of the calcium x oxalate x urate/magnesium x creatinine2 quotient were observed during allopurinol administration.

Allopurinol↗
PubMed1980

Urinary oxalate excretion during anti-androgenic therapy.

We studied urinary oxalate excretion in three groups of patients with prostatic carcinoma who were treated with orchiectomy, estrogen, and cyproterone acetate, respectively. Urinary oxalate and plasma testosterone were analyzed before treatment and after 2 and 8 weeks of treatment. Despite a decrease in plasma testosterone concentration no significant change in oxalate excretion was detected in any group.

Aged↗