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Biomedical subjects

J Faber

Publications and source records attributed to J Faber.

At least 145 records · Page 8Linked to original sources

Prevalence of postenteritis cow's milk protein intolerance.

The object of this study was to ascertain the frequency of postinfectious cow's milk protein hypersensitivity (CMPH). Twenty-four infants less than 3 months old were included in the study. Following hospitalization for acute gastroenteritis, the infants were given a protein hydrolysate formula for a period of 6 weeks, after which an intestinal biopsy was performed. Thereafter, a milk challenge was given. The existence of CMPH was defined as a postchallenge reduction of one or more of the mucosal disaccharidases below the normal levels for our laboratory. A bacterial etiology of the gastroenteritis was found in 10. Nineteen infants had no adverse reaction to cow's milk after 6 weeks on a hypoallergenic formula. Only two could be confidently diagnosed as having developed secondary CMPH; both had been infected by Escherichia coli 0 111. One infant had primary CMPH and one extra-intestinal CMPH. The incidence of secondary CMPH with gastrointestinal manifestations in this series was considerably less than described elsewhere.

Animals↗

Rheumatic fever in a 2-year-old child.

A 2-year-old boy with rheumatic fever is described. The patient presented with fever, flitting polyarthritis and an elevated erythrocyte sedimentation rate. Treatment with aspirin was successful. Rheumatic fever in this age-group is very rare, but it is important to consider this diagnosis even in children under 3 years of age.

Age Factors↗

Renal handling of iodothyronines in acromegaly.

Measurement of the free serum concentration, the 24-h urinary excretion and the renal clearance of T4, T3, 3,3',5'-tri-iodothyronine (rT3), 3',5'-diiodothyronine (3',5'-T2) and 3,3'-di-iodothyronine (3,3'-T2) was performed in 13 patients with active acromegaly and in 18 healthy controls. The acromegalic patients had normal serum levels of the free iodothyronines, whereas the urinary excretion of T4 and T3 was increased approximately two-fold in the patients with acromegaly. The creatinine clearance, reflecting the glomerular filtration rate (GFR), was increased in the acromegalic patients, in median 133 ml/min versus 87 ml/min (p less than 0.01) in the controls. Compared to the creatinine clearance the clearance of T3 and 3,3'-T2 was higher (p less than 0.01) in acromegalics as well as in controls. The patients with acromegaly had higher renal clearance of T4 and T3 than controls, in median 81 ml/min versus 33 ml/min, and 269 ml/min versus 137 ml/min, respectively (p less than 0.01). These differences were not due to changes in creatinine clearance. The renal clearance of 3',5'-T2 tended to be enhanced in acromegalic patients (8.2 ml/min versus 3.9 ml/min, p less than 0.10), both before and after correction for creatinine clearance. The data suggest that in acromegaly, as in normal condition, iodothyronines are subject to both glomerular filtration and active tubular transport mechanisms. Further, active acromegaly results not only in increased GFR, but also in changes of the net tubular transport in favour of secretion of at least T4 and T3, and possibly also of 3',5'-T2.

Acromegaly↗

Influence of free thyroid hormone levels on the TSH response to TRH in endogenous depression.

The TSH response to TRH (delta max TSH) and the serum concentrations of free thyroxine (FT4), 3,5,3'-, and 3,3',5'-triiodothyronine (FT3 and FrT3) were studied in two groups of patients with endogenous depression before and after clinical recovery following electroconvulsive treatment (ECT). Before ECT, the patients from group 1 (n = 17) had a reduced delta max TSH (p less than 0.01), which after ECT rose to values not different from those found in controls. FT4 levels were elevated before ECT (p less than 0.01), and they decreased after ECT (p less than 0.05) to levels similar to those found in controls. FT3 and FrT3 levels were not different from the control values, but FrT3 decreased during ECT (p less than 0.01). In group 2 (n = 19), delta max TSH was reduced both before (p less than 0.02) and after (p less than 0.01) ECT. FT4 levels were increased both before and after ECT (p less than 0.02). Both parameters were unaffected by ECT. The data are compatible with the assumption that the decreased TSH response to TRH found in patients with endogenous depression is secondary to an increase in circulating FT4.

Aged↗

Intestinal mast cells in different stages of celiac disease.

A study of mast cell content of the small intestinal mucosa in children with celiac disease is presented. Twenty patients with true celiac disease were studied and compared with 7 patients with transient gluten intolerance and 20 normal control patients. In healthy children we found (mean +/- SE) 142.5 +/- 16.4 mast cells/mm2. In children with active celiac disease, only 40.1 +/- 19.5 cells were found. This difference was highly significant (P less than 0.001). On a gluten-free diet for 1.5 years, the number of mast cells was 82.2 +/- 27.2/mm2 and still remained significantly depressed (P less than 0.001). Upon gluten challenge in celiac disease, the numbers fell to 58.3 +/- 32.6/mm2, while in transient gluten intolerance the numbers of mast cells attained were 102.5 +/- 22.5/mm2, near normal values. These findings indicate that during the untreated phase of celiac disease the number of mast cells is depressed. On a gluten-free diet, the number rises but does not reach normal control levels even after prolonged remission. It is suggested that even during remission of celiac disease the mast cells continue to be damaged by unidentified toxic agents.

Biopsy↗

Obstructive hypertrophic adenoids and tonsils as a cause of infantile failure to thrive: reversed by tonsillectomy and adenoidectomy.

Isolated failure to thrive in an infant caused by chronic hypoventilation due to hypertrophic adenoids and tonsils, has not been previously described. A 9 month-old infant presented with weight loss and mild clinical respiratory signs. Hypoxemia and CO2 retention, however, were documented by transcutaneous gas measurement, and ENT examination revealed enlarged tonsils and adenoids. Adenoidectomy and tonsillectomy at 9 1/2 months of age completely reversed the patient's hypoventilation and growth pattern. While the exact mechanism of failure to thrive secondary to upper airway obstruction in infancy is not clear, we conclude that routine ENT evaluation should be a regular part of the workup of infants under one year who suffer from failure to thrive.

Adenoidectomy↗

Urinary excretion of unconjugated and conjugated 3,5-diiodothyronine.

A radioimmunoassay for the estimation of 3,5-diiodothyronine (3,5-T2) in human urine has been established. The urinary excretion of both glucuronide and sulfate conjugates of 3,5-T2 were estimated after enzymatic deconjugation. In 19 healthy controls the median excretion of unconjugated 3,5-T2 was 276 pmol/d, whereas the median excretion of glucuronidated and sulfated 3,5-T2 in 7 healthy subjects was 448 and 451 pmol/d, respectively. The median excretion of 154 pmol/d in 9 hypothyroid patients did not differ from that found in controls. In contrast 12 patients with hyperthyroidism had an enhanced excretion, 1312 pmol/d (P less than 0.01). Compared with previous data on the daily degradation of 3,5-T2, it is concluded that approximately one-sixth of degradated 3,5-T2 is excreted in the urine.

Adult↗

The effects of phenytoin (diphenylhydantoin) on the extrathyroidal turnover of thyroxine, 3,5,3'-triiodothyronine, 3,3',5'-triiodothyronine, and 3',5'-diiodothyronine in man.

The extrathyroidal metabolism of T4, T3, rT3, and 3',5'-diiodothyronine (3',5'-T2) was studied before and after treatment with 350 mg phenytoin (DPH) daily for 14 days in six hypothyroid patients receiving constant L-T4 replacement. The total and free serum concentrations of the four iodothyronines were reduced by approximately 30% during DPH treatment, whereas the free fractions in serum were unaltered. Concomitantly, serum TSH increased 137% (P less than 0.02). The production rate (PR) of T4 decreased 16% (P less than 0.005), indicating decreased intestinal absorption (bioavailability) of oral L-T4 during DPH treatment. The fractional rate of 5'-deiodination of T4 to T3 increased from 27% to 31% (P less than 0.05), whereas the rate of 5-deiodination of T4 to rT3 decreased from 45% to 25% (P less than 0.05). The urinary excretion of free and conjugated T4 was 2.3% of the T4 PR and was unaffected by DPH. Thus, the amount of T4 metabolized through nondeiodinative pathways apart from urinary excretion increased from 25% to 44% (P less than 0.05). The apparent distribution volume (Vd) of T4 increased (P less than 0.05), whereas the pool size was unchanged. The PR of T3 did not change during DPH treatment, nor did the mean transit time or the cellular clearance. The rT3 PR was reduced by 54% (P less than 0.02) during DPH treatment. Concomitantly, the transit time increased 10-fold (P less than 0.05), whereas Vd and pool size increased 5-fold (P less than 0.01 and P less than 0.05, respectively). The turnover of 3',5'-T2, in contrast to that of the other iodothyronines, did not change significantly during DPH treatment. T3 formation from T4 was measured in liver microsomal fractions from rats treated for 8 days with DPH and was almost identical to that in untreated animals. The data demonstrate that DPH in therapeutic concentrations did not affect serum protein binding of the iodothyronines. DPH reduced the intestinal absorption of T4 and increased the nondeiodinative metabolism of T4. The resulting decrease in total and free serum T4 and T3 was associated with an increase in serum TSH, demonstrating reduced negative feedback on the pituitary. Our data do not support the assumption that DPH induces increased hepatic deiodinating enzyme activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗

The bioavailability of thyroxine and 3,5,3'-triiodothyronine in normal subjects and in hyper- and hypothyroid patients.

A new method for the estimation of the bioavailability of thyroxine (T4) and 3,5,3'-triiodothyronine (T3) is described based on gel separation followed by antibody extraction of labelled T4 and T3 from serum, and using the area under the curve of disappearance of the tracer (AUC) for the calculations. The peak serum concentrations of radioactive labelled T4 and T3 were reached approximately 90 min after oral administration of both tracers. The relative difference of duplicate estimations was below 10% (n = 3). The bioavailability of T4 in 6 euthyroid controls was in median 65% (range 64-75%), and it was significantly increased both in hyperthyroidism (88% (75-99%), n = 6, P less than 0.01) and hypothyroidism (84% (67-100%), n = 6, P less than 0.02). The bioavailability of T3 in 6 euthyroid controls was in median 78% (69-99%) and significantly greater than that of T4 (P less than 0.02). The bioavailability was unaffected by hyperthyroidism (79% (61-98%), n = 9) and hypothyroidism (77% (66-97%), n = 7). No significant difference between T4 and T3 bioavailabilities was found in hyper- or hypothyroidism. The clinical implication of the present study is that the bioavailability of T4 and T3 is almost identical and approximately 80% in patients with severe hypothyroidism.

Adult↗

Lymphocyte response to a bovine milk protein in ulcerative colitis.

A recently described in vitro test for cow's milk protein hypersensitivity was applied to adult patients with ulcerative colitis. The test system involved the culture of their peripheral blood lymphocytes with and without beta-lactoglobulin, and the results were expressed as a stimulation index. Stimulation with beta-lactoglobulin was significantly higher (P less than 0.02) in patients with active disease than in those with inactive disease or in healthy controls. beta-Lactoglobulin was the only one of four cow's milk proteins that showed this effect. It is concluded that the cow's milk protein beta-lactoglobulin has a specific blastogenic effect on the lymphocytes of patients with active ulcerative colitis, and, therefore, may serve as a marker of disease activity.

Adolescent↗

Left ventricular size, output, and structure during guinea pig pregnancy.

We investigated left ventricular (LV) hemodynamics, pressure-volume relations, and morphometry to determine what cardiac changes characterize pregnancy in the guinea pig. Time-bred virgin guinea pigs were paired by weight with unbred controls. Hemodynamic studies and LV pressure-volume relations were obtained on days 59-68 of the 68-day gestation. Weight of control sows increased from 817 to 902 g (P less than 0.01) and pregnant sows from 810 to 1,251 g (P less than 0.01). LV weights were not different. When indexed for maternal weight minus uterus and contents, pregnancy produced increases in O2 consumption, +48% (P less than 0.01); cardiac output, +32% (P less than 0.05); and stroke volume, +46% (P less than 0.025). Passive LV pressure-volume curves (dP/dV) were shifted to the right (P less than 0.025), but dP/dV at constant pressure was unchanged. Using a thin-walled spherical model, elastic modulus at constant stress was not different. The percent LV inter- and intracellular volumes and myocyte myofibril and organelle volumes were unchanged during pregnancy. In the guinea pig, pregnancy increases LV output, stroke volume, and size without changes in LV mass, morphometry, or elastic modulus.

Animals↗

Splanchnic extraction of 3,3'-diiodothyronine and 3',5'-diiodothyronine in hyperthyroidism.

The splanchnic extraction of 3,3'-diiodothyronine (3,3'-T2) and 3',5'-diiodothyronine (3',5'-T2) was studied in 7 hyperthyroid patients and 20 normal subjects employing the hepatic venous catheterization technique. A significant net uptake by splanchnic tissues was found for both diiodothyronines . The fractional splanchnic extraction calculated as the arterio-hepatic venous plasma concentration difference divided by the arterial concentration was unaffected by hyperthyroidism as compared to normal values. There was a close positive correlation between the arterio-hepatic venous concentration difference and arterial concentration, 3,3'-T2: r = 0.988, and 3',5'-T2: r = 0.932 (P less than 0.001). The splanchnic extraction was nonsaturable at endogenous plasma concentrations of 3,3'-T2 up to at least 17.0 ng/dl and of 3',5'-T2 up to at least 15.2 ng/dl. The data suggest that the splanchnic extraction of 3,3'-T2 and 3',5'-T2 obeys first order kinetics, the fractional extraction being unaffected by hyperthyroidism. Furthermore, changes in the net splanchnic extraction of 3,3'-T2 and 3',5'-T2 do not seem to contribute to changes in circulating levels of these iodothyronines. It is suggested that tissues other than the liver contribute significantly to the deiodination process both in normal and in hyperthyroid man.

Adolescent↗

The effect of D,L-4-hydroxypropranolol on the thyroxine to 3,5,3'-triiodothyronine conversion in rat renal and liver microsomes.

The in vitro effect of D,L-4-hydroxypropranolol, a major pharmacological active metabolite of the beta adrenoceptor blocking drug D,L-propranolol, on the thyroxine (T4) to 3,5,3'-triiodothyronine (T3) conversion has been studied using rat renal and liver microsomal fractions. The results showed, that primarily the metabolite, but also the parent drug inhibits the T3-production in a dose dependent manner. The potency, expressed as the 50% inhibition of the T3-production, was reached using 65 +/- 12 (SD) microM D,L-4-OH-propranolol and 1000 +/- 22 (SD) microM D,L-propranolol, respectively in both tissues. The efficacy of 4-OH-propranolol corresponded to a maximal inhibition of 86 +/- 7% while it for D,L-propranolol corresponded to 58 +/- 6% (P less than 0.001). The beta adrenoceptor agonist isoprenaline itself did not effect the T4 to T3 conversion but considerably opposed the inhibitory effect of D,L-4-OH-propranolol but not of D,L-propranolol. The D-isomer form of propranolol, which is without beta receptor blocking activity inhibited the T3-production in the same degree as D,L-propranolol. Evaluation of the enzyme kinetic data suggested that 4-OH-propranolol caused a competitive inhibition of both T4 and DTT. It is concluded, that the metabolite D,L-4-OH-propranolol is a much more potent and efficacious inhibitor of the T4-5'-deiodination than D,L-propranolol.

Animals↗