Intestinal permeability in children with Crohn's disease and coeliac disease.

Mannitol and lactulose were used as probe molecules to measure intestinal permeability in children with active small-bowel Crohn''s disease and with untreated coeliac disease. Mannitol and lactulose were administered by mouth in a moderately hypertonic solution (580 mmol (mosmol)/l), and results were expressed as the ratio of the molecules excreted in urine over five hours. Patients with Crohn''s disease had a sixfold increase in permeability (due to increased lactulose permeability) and those with coeliac disease a fivefold increase (due to decreased mannitol permeability). From these results the test offers potential as a noninvasive investigation in children with small-bowel disease.     

Plasma ghrelin levels in patients with end-stage renal disease

Ghrelin is an acylated peptide stimulating secretion of the growth hormone (GH). It was originally isolated from the rat stomach as an endogenous ligand for the growth hormone secretagogue receptor. Although being predominantly produced by endocrine cells of the gastric fundus, its secretion has been found in various tissues including the kidney. To study the influence of renal failure on plasma ghrelin levels we examined 16 patients with end-stage renal disease (ESRD) receiving hemodialysis (8 men and 8 women) and 19 controls (10 men and 9 women). Both groups were comparable in age and BMI. In all subjects we assessed plasma levels of ghrelin, leptin, soluble leptin receptor, insulin, IGF-I, IGFBP-1, IGFBP-3 and IGFBP-6. Ghrelin levels were significantly higher in the group of dialyzed patients (4.49+/-0.74 vs. 1.79+/-0.15 ng/ml; p<0.001). These patients had significantly higher levels of GH, IGFBP-1, IGFBP-6, leptin and percentage of body fat (p<0.05). In the group of patients with ESRD plasma ghrelin levels positively correlated with IGFBP-1 (p<0.01). In the control group, ghrelin positively correlated with GH concentrations (p<0.01) and negatively correlated with the levels of insulin and creatinine (p<0.05). In conclusion, patients with ESRD have higher ghrelin concentrations, which might be caused by a decreased excretion/metabolism of ghrelin in the kidney during renal failure.     

Prevalence of coeliac disease in patients with thyroid autoimmunity.

The occurrence of autoimmune thyroid disorders among patients with coeliac disease (CD) is well documented, but the exact prevalence of CD among patients with autoimmune thyroid diseases (ATD) is as yet unclear. We screened 150 newly diagnosed patients with ATD by serum endomysial antibody detection (EmA). In 5 subjects (3.3%) EmA positivity was found; all underwent jejunal biopsy. On gluten-free diet an excellent clinical and histological response was recorded with an improvement of hypothyroidism and reduction of the thyroxine dosage. Our data suggest a significant high prevalence (3.3%) of CD in patients with ATD, in particular with Hashimoto's thyroiditis.     

Acetylation phenotype and serum levels of T3 and T4 in patients with hypertension treated with propranolol

The acetylation phenotype has been investigated in 76 patients with untreated hyperthyroidism. In 65 of these patients including 23 with fast and 42 with slow acetylation phenotype, the blood serum concentrations of thyroxine and triiodothyronine were determined before and after propranolol therapy involving propranolol administration of a dose of 160 mg per day for 6 days. The occurrence of the fast acetylation phenotype among the patients with hyperthyroidism was similar to that found in the healthy population. Propranolol therapy caused a significant decrease in the blood serum concentration of triiodothyronine only in the patients with the slow acetylation phenotype.     

Detection of continuing gluten ingestion in treated coeliac patients.

To assess the incidence and effects of continuing gluten ingestion in coeliac disease 51 adult coeliac patients were studied after four to 132 (mean 63) months on a prescribed gluten-free diet. Each patient completed a prospective dietary questionnaire, underwent a repeat jejunal biopsy, and gave serum for gluten antibody estimation. Altogether 65% of patients were still ingesting gluten, often inadvertently. Direct questioning on dietary habits had failed to uncover most of this consumption. The gluten antibody test proved a useful screening test for detecting continuing gluten ingestion and patients with both persistent subtotal villous atrophy and gluten antibodies were almost certain to be taking large amounts ( more than 2 g/day). The presence of persistent partial villous atrophy was found, however, to be an unreliable guide to gluten intake.     

Plasma immunoassayable ACTH levels during and after hydrocortisone infusion in patients with Cushing's disease.

The plasma ACTH responses to hydrocortisone infusion were compared in patients with Cushing's disease and primary adrenocortical insufficiency. In 4 patients with primary adrenocortical insufficiency, plasma ACTH levels were suppressed exponentially after administration of a relatively large dose of hydrocortisone (1.0 mg/kg/1.5 hr-3.0 mg/kg/2 hr). In patients with post-adrenalectomized Cushing's disease (4, bilateral; 1, unilateral), plasma ACTH suppression was delayed. Plasma ACTH levels, expressed as a percentage of the basal concentrations, were significantly less suppressed in patients with Cushing's disease than in patients with primary adrenocortical insufficiency 90 (p less than 0.05) and 120 (p less than 0.05) min after the beginning of infusion. When 0.5 mg/kg hydrocortisone was infused over a period of 1.5 hr, suppression was also delayed in Cushing's disease, and plasma ACTH levels were less suppressed in 4 patients with Cushing's disease than in 4 patients with primary adrenocortical insufficiency at 30 (p greater than 0.05), 45 (p greater than 0.05) 60 (p less than 0.05) min.     

Plasma corticotrophin levels in addison-schilder's disease.

Raised plasma immunoreactive corticotrophin (ACTH) levels were found in five boys with the sex-linked disorder progressive leucodystrophy associated with adrenal insufficiency (Addison-Schilder''s disease) and in a symptom-free brother of one of them. Similar ACTH concentrations were found using two antisera, one against the N-terminal part of the ACTH molecule and the other against the C-terminal part. In one patient the circulating ACTH had normal biological activity as measured using the cytochemical ACTH bioassay. Immunoreactive beta/-melanocyte-stimulating hormone was also determined in one patient and found to be raised.