Reduced levels of growth hormone, insulin-like growth factor-I and binding protein-3 in patients with shunted hydrocephalus

OBJECTIVE: Children with hydrocephalus are characterised by slow linear growth in prepuberty, accelerated physical maturation during puberty, and reduced final height. We aimed to study the possible roles of growth hormone, insulin-like growth factor-I (IGF-I), and IGF binding protein-3 (IGFBP-3) in this growth pattern. STUDY DESIGN: One hundred and fourteen patients with shunted hydrocephalus (62 males) aged 5 to 20 years, of whom 17 had spina bifida (six males), and 73 healthy controls (38 males) were studied. Anthropometric measures, body mass index, and body fat mass were assessed and the stage of puberty was determined. Serum growth hormone and plasma IGF-I and IGFBP-3 concentrations were measured. RESULTS: The patients comprised 44 (26 males) who were prepubertal and 70 (36 males) pubertal or postpubertal, while 32 of the controls (19 males) were prepubertal and 41 (19 males) pubertal or postpubertal. The prepubertal children with hydrocephalus had lower IGF-I (p = 0.002) and IGFBP-3 concentrations (p < 0.001) than the controls, and the pubertal children had four times lower basal growth hormone concentrations (p < 0.001). There was a correlation between height SD score and IGF-I levels in the total patient population (r = 0.23; p = 0.01). Peripheral IGF-I concentrations peaked at pubertal stages 2-3 in the female patients and at stage 4 in the controls. The prepubertal patients on antiepileptic treatment, carbamazepine in most cases (73%), had higher IGF-I (p = 0.01) and IGFBP-3 concentrations (p = 0.03) than those who had never been treated with antiepileptic drugs, but still lower IGFBP-3 levels than the controls (p = 0.01). CONCLUSION: Based on these findings, it can be concluded that reduced growth hormone secretion may contribute to the pattern of slow linear growth and reduced final height observed in these patients.     

Increasing breastfeeding rates to reduce infant illness at the community level

OBJECTIVE: Although breastfeeding is associated with lower rates of a variety of infant illnesses, skeptics have suggested that much of the association is attributable to confounding, even after appropriate statistical adjustment. This article utilizes a novel design to investigate changes in infant illness at the community level after a successful breastfeeding promotion program. METHODS: In this population-based cohort study, the medical records of all infants born in one Navajo community the year before a breastfeeding promotion program (n = 977) and the year during the intervention (n = 858) were reviewed. Outcomes assessed include changes after the intervention in: proportion breastfeeding and/or breastfeeding exclusively; incidence of common infant illnesses in the first year of life; and feeding-group specific incidence of illness. RESULTS: The proportion of women breastfeeding exclusively for any period of time increased from 16.4% to 54.6% after the intervention. The percent of children having pneumonia and gastroenteritis declined 32. 2% and 14.6%, respectively, after the intervention. Feeding-group specific rates of these illnesses were unchanged, indicating that the decline observed was attributable to the increased proportion of infants breastfeeding. In contrast, rates of croup and bronchiolitis increased after the intervention among those fed formula from birth, suggesting a viral epidemic which was limited to those never exclusively breastfed. Finally, sepsis declined in both formula-fed and breastfed infants after the intervention, suggesting that other factors affected this illness outcome after the intervention. CONCLUSIONS: Increasing the proportion of exclusively breastfed infants seems to be an effective means of reducing infant illness at the community level. The experimental design suggests that the increased incidence of illness among minimally breastfed infants is causally related to lack of breast milk, rather than being attributable to confounding.     

Interleukin-3, GM-CSF, and TPA induce distinct phosphorylation events in an interleukin 3-dependent multipotential cell line

The mechanism of action of the hemopoietic growth factor, murine interleukin-3 (mIL-3), was investigated using an mIL-3-dependent multipotential hematopoietic cell line, B6SUtA1. Murine granulocyte- macrophage colony-stimulating factor (mGM-CSF) was as potent as mIL-3 in stimulating these cells. In addition, sodium orthovanadate, an inhibitor of phosphotyrosine phosphatase, and 12-O-tetradecanoyl- phorbol-13-acetate (TPA), a known activator of protein kinase C, also stimulated DNA synthesis in these cells, suggesting that protein phosphorylation might be involved in the mechanism of action of mIL-3 and mGM-CSF. To assess this possibility, intact B6SUtA1 cells exposed for brief periods to mIL-3, mGM-CSF, and TPA were analyzed for changes in phosphorylation patterns using metabolic 32P-labeling and antibodies to phosphotyrosine. Both mIL-3 and mGM-CSF induced the serine-specific phosphorylation of a 68-Kd cytosolic protein, whereas all three agents stimulated the serine-specific phosphorylation of a 68-Kd membrane protein. Furthermore, mIL-3 stimulated tyrosine phosphorylation of the 68-Kd membrane protein, as well as of 140-, 90-, 55, and 40-Kd proteins. The 90-Kd protein was also tyrosine phosphorylated in response to mGM-CSF. These phosphotyrosine containing proteins were not detected in TPA-treated cells. These results indicate that protein phosphorylations on tyrosine and serine residues occur in B6SUtA1 cells following short-term incubation with mIL-3 or mGM-CSF and that most of these phosphorylation events are mediated by kinases other than protein kinase C (PkC).     

Percutaneous intervention in portosystemic shunts in Budd-Chiari syndrome.

Budd-Chiari syndrome is a rare, often fatal illness resulting from hepatic venous outflow obstruction. Surgically created portosystemic shunts are frequently necessary in these patients for portal decompression. Over the past 15 years, 30 patients have been surgically treated for this condition at the Johns Hopkins Hospital. Of the 22 long-term survivors (range, 6 months to 13 years), five (23%) have required further surgical intervention and five (23%) have required percutaneous intervention for shunt complications. Percutaneous procedures included angioplasty (n = 10), atherectomy (n = 1), and urokinase therapy (n = 1). Of the five patients treated percutaneously, one has died of complications from her disease. The remaining four have been followed up for a mean of 16.2 months (range, 5-31 months) and all are in stable condition. None of the five treated with percutaneous interventional procedures have required additional surgical procedures or shunt revisions. Although this series is small, the findings indicate that percutaneous intervention may play a strong adjunctive role to surgery in the treatment of selected patients with portosystemic shunt complications.     

Prevalence of apical periodontitis detected in cone beam CT images of a Brazilian subpopulation

Objectives

The aim of this study was to determine the prevalence of apical periodontitis (AP) detected in cone beam CT (CBCT) images from a database.

Methods

CBCT images of 300 Brazilian patients were assessed. AP images were measured in three dimensions. Age, gender, number and location of total teeth in each patient were considered. AP location was considered according to tooth groups. The extent of AP was determined by the largest diameter in any of the three dimensions. Percentages and the χ² test were used for statistical analysis.

Results

AP was found in 51.4% of the patients and in 3.4% of the teeth. Higher prevalence of AP was found in 60- to 69-year-olds (73.1%) and in mandibular molars (5.9%) (p < 0.05). Inadequate endodontic treatment presented higher prevalence of AP (78.1%).

Conclusions

AP can be frequently found in CBCT examinations. The presence of AP has a significant association with patients'' age, and tooth type and condition. CBCT databases are useful for cross-sectional studies about AP prevalence in a population.     

Limitations of MR imaging in the diagnosis of peripheral tears of the triangular fibrocartilage of the wrist.

OBJECTIVE: The treatment of peripheral tears of the triangular fibrocartilage complex is radically different from the more typical central, degenerative tears. To our knowledge, no reports in the imaging literature specifically evaluate tears of the ulnar attachment of the triangular fibrocartilage complex. We evaluated the accuracy of MR imaging in these patients. MATERIALS AND METHODS: Eighty-six MR imaging examinations of the wrist (41 indirect MR arthrograms and 45 unenhanced MR images) were evaluated: 20 wrists with surgically confirmed peripheral triangular fibrocartilage complex tears and 66 wrists with surgically documented normal ulnar attachment. These cases were evaluated by three experienced musculoskeletal radiologists, who were unaware of the surgical findings, to assess the presence of peripheral triangular fibrocartilage complex tears or fluid signal at the ulnar attachment of the triangular fibrocartilage complex. RESULTS: The sensitivity for evaluation of the peripheral triangular fibrocartilage complex tear was 17%, with a specificity of 79% and an accuracy of 64%. High signal intensity at the ulnar insertion of the triangular fibrocartilage complex as a marker for tear showed a sensitivity of 42%, a specificity of 63%, and an accuracy of 55%. Weighted kappa values revealed only fair agreement among the three observers. CONCLUSION: MR imaging does not adequately reveal the peripheral attachment of the triangular fibrocartilage complex.