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Biomedical subjects

H Schouten

Publications and source records attributed to H Schouten.

At least 37 records · Page 2Linked to original sources
PubMed1989

Anorectal function: defecographic measurement in asymptomatic subjects.

A study of anorectal function during fluoroscopically monitored defecation was conducted in 32 asymptomatic subjects. Two observers independently measured various parameters on defecograms and reviewed video recordings during the subjects' squeezing, rest, and straining. There was a wide range of measurements for the anorectal angle, the position of the anorectal junction, perineal motility, and anal canal width. Interobserver variation of these measurements was large. In 17 subjects, both observers agreed that rectal emptying was incomplete. In 10 patients, there was agreement on the presence of rectal wall changes such as intussusception, rectocele, and mucosal prolapse. Defecographic measurements should be interpreted with caution and should not be used as the only criteria for treatment. Anatomic changes of the anorectal region during straining at defecation do not necessarily cause symptoms but may be a precursor of clinical disorders. Defecography is useful in the detection of these abnormalities.

Adult↗
PubMed1983

The influence of indomethacin on renal acidification in normal subjects and in patients with sickle cell anemia.

Patients with sickle cell nephropathy have been shown to have a distal type of incomplete renal tubular acidosis. We evaluated renal tubular acidification before and after indomethacin administration because prostaglandins have been shown to inhibit the transepithelial potential difference in the collecting tubule and since we previously found indirect evidence of increased prostaglandin synthesis in patients with sickle cell nephropathy. Indomethacin did not change urine pH in the sickle cell anemia (SCA) patients or in the control subjects. It induced, however, an increase in titratable acid excretion particularly in the SCA patients. Ammonium excretion decreased after indomethacin in the SCA patients while it did not change significantly in the control subjects. In the SCA patients, net acid excretion did not rise after indomethacin. In contrast there was an increase in net acid excretion after indomethacin administration in the control subjects. We conclude from our study that the inability of patients with SCA to lower urine pH to a normal extent after ammonium chloride loading is not improved by indomethacin. The decrease in ammonium excretion after indomethacin administration in SCA might be due to an effect of the prostaglandin synthesis inhibitor indomethacin on ammoniagenesis.

Acidosis↗
PubMed1982

The influence of indomethacin on renal concentrating and diluting capacity in sickle cell nephropathy.

1. The effects of indomethacin on water excretion during both vasopressin stimulation and inhibition were studied in control subjects and in patients with sickle cell anaemia. 2. In the control group as well as in the group of patients with sickle cell anaemia sodium and urea retention occurred after indomethacin in the water-depleted state. During water loading, indomethacin induced sodium retention without urea reabsorption. 3. In healthy volunteers indomethacin increased urinary osmolality during water deprivation, but not after water loading. In contrast, in patients with sickle cell anaemia indomethacin caused a rise in urinary osmolality during water loading, but not after deprivation. 4. The findings support the view that indomethacin promotes solute reabsorption in the distal tubule. 5. From our observations we conclude that renal prostaglandins are not involved in the urinary concentrating defect of patients with sickle cell anaemia. On the other hand, the normal diluting capacity in sickle cell anaemia appears to depend on renal prostaglandins.

Adolescent↗
PubMed1981

Beta-2-microglobulin in sickle cell anaemia. Evidence of increased tubular reabsorption.

Sickle cell nephropathy is characterized by severe defects in renal medullary functions. In contrast, both proximal tubular secretion and reabsorption are found to be elevated. Since proximal tubular cells are involved in reabsorption and catabolism of beta 2-microglobulin (beta 2-m), we studied serum concentration and urinary excretion of this low molecular weight protein in sickle cell nephropathy. Serum beta 2-m concentration was higher in sickle cell anaemia (SCA) patients compared to control persons. beta 2-m excretion, however, was normal and beta 2-m clearance was not significantly decreased. Fractional beta 2-m excretion was significantly lower and therefore tubular reabsorption of beta 2-m was increased in the SCA patients. There was no correlation between serum beta 2-m concentration and the tubular reabsorption of beta 2-m and phosphate. These findings are further evidence of a particular function of the proximal tubule in sickle cell nephropathy.

Adolescent↗
PubMed1980

The influence of indomethacin on renal haemodynamics in sickle cell anaemia.

1. Glomerular filtration rate and effective renal blood-flow were normal in a series of patients with sickle cell anaemia. Fractional creatinine excretion and fractional urea excretion were increased. 2. During indomethacin administration there were significant falls in glomerular filtration rate, effective renal blood-flow, creatinine clearance and urea clearance in the patients with sickle cell anaemia; fractional urea excretion also fell markedly. In control subjects none of these variables changed after indomethacin. 3. Serum concentration of urea rose markedly during indomethacin administration in sickle cell anaemia, owing to both the decrease in glomerular filtration rate and the increase in fractional urea reabsorption. 4. We conclude that prostaglandins have an important role in maintaining a normal glomerular filtration rate and effective renal blood-flow in sickle cell anaemia. The abnormal urea handling in patients with this disease remains to be elucidated.

Adolescent↗