PubMed Health⌕ Search

Biomedical subjects

C De Giacomo

Publications and source records attributed to C De Giacomo.

At least 19 recordsLinked to original sources

The use of ciclosporin in paediatric inflammatory bowel disease: an Italian experience.

AIM: To asses the efficacy and safety of ciclosporin in a paediatric population with inflammatory bowel disease. PATIENTS AND METHODS: Twenty-three Italian children treated with ciclosporin were studied retrospectively. The indications for treatment were severe unresponsive colitis, chronic active colitis or severe fistulizing Crohn's disease. The treatment duration, follow-up and causes of drug discontinuation were assessed. RESULTS: Sixteen patients were treated intravenously for a mean time of 10 +/- 7 days (1-24 days) and 19 orally for a mean time of 133 days (17-660 days). The mean follow-up of all patients was 13.2 months. Ciclosporin was totally ineffective, being discontinued for surgery, in nine of 23 patients (39%); it was discontinued for partial response in three patients (13%). During treatment, clinical remission was achieved in eight children (35%) and maintained after drug withdrawal in four (17%). In severe unresponsive colitis, urgent colectomy was avoided in 12 (85%) of 14 patients who tolerated the drug. Side-effects appeared in six of 23 patients (26%), and three (13%) required ciclosporin to be discontinued due to neurotoxicity. CONCLUSIONS: Ciclosporin shows disappointing long-term results in the treatment of refractory inflammatory bowel disease, but can play an important role in preventing urgent surgery in unresponsive severe colitis. Severe side-effects can occur.

Adolescent↗

Celiac disease in children with autoimmune thyroid disease.

Ninety children and adolescents with autoimmune thyroid disease were screened for celiac disease. All 90 patients were typed for HLA antigen class I and II and for HLA-DQA1 and DQB1 heterodimers. Celiac disease and DQA1*0501, DQB1*02 were found in 7 (7.8%) patients. The prevalence of celiac disease was 1 of 13. Screening for celiac disease is recommended in children with autoimmune thyroid disease.

Adolescent↗

Effect of a water-soluble fiber (galactomannans)-enriched formula on gastric emptying time of regurgitating infants evaluated using an ultrasound technique.

BACKGROUND: Milk formulas enriched with water-soluble fibers are a first-line measure for infants with gastroesophageal reflux. However, it has been reported that these compounds could affect gastric emptying. The aim of this study was to evaluate the effects of these thickeners on gastric emptying time in infants with frequent regurgitation or vomiting. METHODS: Forty-seven infants, aged 1 to 12 months, with uncomplicated gastroesophageal reflux underwent two ultrasound evaluations of gastric emptying time after receiving either a standard formula or a formula enriched with 0.4 g galactomannan per 100 ml diluted milk. Gastric emptying time was calculated by measuring the antrum area at baseline and at defined intervals over the next 3 hours. RESULTS: The gastric emptying time (mean +/- SD) for the standard and the thickened formula was 136 +/- 33 and 133 +/- 34 minutes, respectively. There was no significant difference in the gastric emptying patterns of the two formulas. Gastric emptying time was longer after the standard formula in 15 of the 47 subjects, shorter in 15 of the 47, and the same in 17 of the 47. CONCLUSIONS: The ingestion of a water-soluble fiber-enriched formula does not have any significant influence on the gastric emptying time of infants with frequent regurgitation or vomiting.

Dietary Fiber↗

Validation of the 13C-urea breath test for the diagnosis of Helicobacter pylori infection in children: a multicenter study.

OBJECTIVE: The 13C-urea breath test (13C-UBT) is a safe, noninvasive, and accurate test for the detection of Helicobacter pylori (H. pylori) infection in adults. The aim of this study was to evaluate sensitivity and specificity of 13C-UBT in children using different types of test meal, doses of 13C-urea and breath sampling intervals. As yet, a validated, standardized 13C-UBT protocol for children has not been formulated. METHODS: 13C-UBT was performed in 115 children and repeated within 3 days, modifying the test meal or the dose of 13C-urea. H. pylori status was assessed by histology and rapid urease test. 13C-UBT was performed using 100 mg or 50 mg of 13C-urea and a fatty test meal (100 FA; 50 FA), 50 mg of 13C-urea, and a carbohydrate test meal (50 CA). Breath samples were collected every 10 min for 60 min. RESULTS: The 13C-UBT in children was highly sensitive and specific with all three protocols used. The best combination of sensitivity (97.92%) and specificity (97.96%) was obtained with Protocol 50 FA at 30 min with a cut-off of 3.5 per mil. CONCLUSIONS: The 13C-UBT is an accurate test for the detection of H. pylori infection also in children. Administration of 50 mg of 13C-urea, a fatty test meal, and breath sampling at 30 min appears to be the most convenient protocol.

Adolescent↗

MR imaging of CNS involvement in children affected by chronic liver disease.

BACKGROUND AND PURPOSE: MR imaging sheds new light on CNS involvement in the course of acquired chronic liver disease; however, the exact pathogenetic mechanisms of hepatic encephalopathy and associated MR abnormalities remain unclear. Our purpose was to relate MR signal intensity abnormalities of the CNS to clinical, biochemical, and pathologic features of childhood-onset chronic liver disease. METHODS: Twenty-one patients (12 male and nine female patients) were included in the study; two had Crigler-Najjar disease type 2, 17 had chronic liver disease of different causes, and two had idiopathic copper toxicosis. Twelve patients had histologically proved liver cirrhosis, with a median disease duration of 175 months at the time of MR study. None had clinical symptoms of hepatic encephalopathy. MR imaging was performed using spin-echo T1- and T2-weighted sequences. RESULTS: Eleven patients had abnormal MR imaging findings of the brain revealed by T1-weighted MR sequences; two of the 11 had idiopathic copper toxicosis. The affected sites were the hypothalamus and globus pallidus, presenting symmetrical and bilateral high signal intensities, or the pituitary gland, which appeared homogeneously hyperintense, or both findings. Eight of the 12 patients with cirrhosis had abnormal MR signals of the brain. In these, the median cirrhosis duration was shorter (169 months) than in the remaining four patients with normal MR signals (177 months). A significant correlation was found between abnormal MR signals of the brain and cirrhosis (P = .008) and factor V activity (P = .008). CONCLUSION: MR imaging confirms the presence of abnormal brain signals in the globus pallidus, hypothalamus, and pituitary gland in patients with childhood-onset liver disease in the absence of clinical symptoms of encephalopathy. Signal intensity abnormalities are likely caused by an as yet unidentified metabolic process partially correlated with the severity of liver disease.

Adolescent↗

Failure to increase insulin-like growth factor-I synthesis is involved in the mechanisms of growth retardation of children with inherited liver disorders.

OBJECTIVE: Growth retardation is a prominent secondary feature of chronic liver disease. We investigated the hypothalamic-pituitary-liver axis in six patients with inherited liver disease and growth failure. The objectives were to determine (1) whether there were any abnormalities in the GH/IGF-I/IGFBPs/GH binding protein (GHBP) axis, (2) whether any abnormalities were nutrition-dependent, and (3) whether recombinant human (rh) GH could be efficaciously and safely administered. MEASUREMENTS: The evaluation included two standard GH provocative tests, GHRH test, night-time GH secretion, GHBP; and IGF-I, IGFBP-3 and IGFBP-1 before and after 0.1 and 0.3 U/kg/day of rhGH given i.m., for 4 days. Two patients were enrolled for rhGH treatment. RESULTS: Quantitative nutritional assessment showed the patients' calorie and protein intake to be compatible with the recommended daily allowance in liver disease. The mean baseline GH level was higher in patients than in controls (8.4 +/- 3.8 vs 2.6 +/- 2.0 mU/l, P < 0.005) and the GH response to stimuli was normal; spontaneous GH secretion was apparently normal. The mean baseline IGF-I value in the patients was significantly below the mean of controls (31.6 +/- 16.4 vs 260 +/- 35.2 micrograms/l, P = 0.00001) and similar to that of children with GH-deficiency (40.8 +/- 18.4 micrograms/l). The mean peak IGF-I response after 0.1 U/kg/day of rhGH increased (84.9 +/- 28.2 micrograms/l, P = 0.009) but remained lower than the mean IGF-I response in GH-deficient patients and in controls (P = 0.00001). The mean peak IGF-I response after 0.3 U/kg/day (113.3 +/- 52.3 micrograms/l) was significantly higher than that after 0.1 U/kg/day (P = 0.002). The mean standard deviation score (SDS) peak for IGF-I response to 0.1 and 0.3 U/kg/day of rhGH decreased significantly from -1.7 to -1.0 (P = 0.02) and from -1.9 to -0.9 (P = 0.005), respectively. There was no difference between patients and controls in serum GHBP activity or in mean baseline IGFBP-3 and IGFBP-1 levels. IGFBP-3 levels did not change significantly in response to rhGH at either 0.1 or 0.3 U/kg/day, while IGFBP-1 significantly decreased after 0.3 U/kg/day (56.3 +/- 35.6 vs 45.9 +/- 33.1 micrograms/l, P = 0.04). A significant positive correlation was present between albumin and peak IGF-I responses to rhGH at the dose of 0.1 and 0.3 U/kg/day (R = 0.83, P = 0.03; R = 0.78, P = 0.03 respectively), as well as between height SDS and baseline or stimulated IGF-I after rhGH 0.1 U/kg/day (R = 0.81, P = 0.04; R = 0.88, P = 0.01 respectively). In the two patients treated with rhGH at 22-25 U/m2/week, the growth rate doubled in one and trebled in the other during the first year of treatment, and in both was maintained in the second year without acceleration of bone maturation or evidence of adverse effects. CONCLUSIONS: The underlying cause of growth retardation in patients with inherited liver disease seems to be a progressive failure to increase IGF-I synthesis (at the conventional rhGH dose) and the consequent lack of its growth-promoting effect. The moderate increase in baseline GH values, the greater IGF-I response to the higher rhGH dose and the improvement in growth rate following rhGH administration suggest at least a degree of sensitivity to rhGH which could be of therapeutic value.

Adolescent↗

Omeprazole for severe reflux esophagitis in children.

BACKGROUND: Severe esophagitis is a rare complication of gastroesophageal reflux in children. In adults, omeprazole therapy of severe erosive esophagitis has become the gold standard short-term treatment of the disease. In children, data on its use are limited, and problems about the dosage are unresolved. The aim of this study was to evaluate the efficacy of a simplified, body-weight-based daily dosage of omeprazole in children with severe esophagitis. METHODS: Ten children (median age 75.6 months; range 25-109 months) with severe esophagitis were prospectively investigated. All patients were evaluated by endoscopy, histology, and 24-h pH-metry study before and after 3 months of omeprazole. The starting dose of omeprazole was 20 mg as a single daily dose in children weighing less than 30 kg, and 40 mg daily for those weighing over 30 kg. RESULTS: A significant improvement in all the children was demonstrated after 3 months of treatment by clinical, endoscopic, and pH-metry assessment. However, histologic study failed to show significant improvement of both inflammatory and hyperplastic findings. Relapse occurred in six of 10 patients after discontinuation of therapy. CONCLUSIONS: Omeprazole is effective in the short-term treatment of severe oesophagitis in children. The daily dose of the drug could be easily based on the body weight. The persistence of histologic features of esophagitis in spite of clinical and endoscopic healing could be an indicator of poor outcome.

Anti-Ulcer Agents↗

Celiac disease.

Explore the source record for details and available documents.

Celiac Disease↗

Clinical aspects of coeliac disease in children with insulin-dependent diabetes mellitus.

Coeliac disease (CD) is heterogeneous in its clinical presentation and pathological expression. Silent, latent and potential forms represent the submerged part of the so-called "coeliac iceberg". The association of insulin-dependent diabetes mellitus (IDDM) and CD has been widely reported. For the screening of CD in diabetic patients, anti-reticulin R1 (ARA-R1) and anti-endomysium (AEA) antibodies are more reliable markers than anti-gliadin (AGA) antibodies. Recent studies have reported an increased prevalence of CD in children with IDDM. In our experience intestinal biopsy confirmed a diagnosis of CD in 6 out of 172 diabetic patients, with a prevalence of 3.5%. Only occasionally does CD precede the onset of IDDM; more often CD is diagnosed shortly or sometimes years after the onset of diabetes. Typical gastrointestinal complaints of CD (such as diarrhoea, abdominal distension) are rare in IDDM patients, while atypical isolated signs or symptoms of CD are more common, in particular sideropenic anemia, short stature, delayed puberty, epilepsy, hypertransaminasemia, dyspeptic symptoms, herpetiform dermatitis, and recurrent aphthous stomatitis. It is recommended that all diabetic children, even those asymptomatic, should be screened yearly for CD, using a combination of AGA plus ARA-R1 and AEA.

Adolescent↗

Lymphocytic gastritis: a positive relationship with celiac disease.

Lymphocytic gastritis is characterized by lymphocytic infiltration of the surface and pit epithelium. Its cause has not been established, but an association with Helicobacter pylori infection or celiac disease has been suggested. We evaluated the histologic features of both gastric and duodenal biopsy specimens from 245 consecutive children and adolescents, and found chronic gastritis in 60 children and celiac disease in 25. Chronic gastritis was associated with H. pylori infection in 36 children and with celiac disease in 15. Lymphocytic gastritis was found in nine children with celiac disease. Children with lymphocytic gastritis had a mean of 40.64 lymphocytes per 100 epithelial cells, compared with a mean of 3.92 lymphocytes per 100 epithelial cells in children with H. pylori-associated gastritis and 5.15 lymphocytes in normal control subjects. Immunohistochemical studies showed that the intraepithelial lymphocytes in lymphocytic gastritis were T cells. No child with lymphocytic gastritis had serologic evidence of past H. pylori infection. We conclude that lymphocytic gastritis in children is associated with celiac disease. Dyspeptic symptoms are frequent; the endoscopic appearance is not characteristic.

Adolescent↗