Enhanced Access and Parents' Preferred Contact for a Child's Chronic Condition.

OBJECTIVES: To assess whether the perception of enhanced access by parents in their child's primary care and main specialty practices is associated with preference for contacting either practice when problems arise with a child's chronic condition. STUDY DESIGN: In this cross-sectional survey study of parents whose children use both primary and specialty practices, we assessed perceptions of 3 components of enhanced access: (1) appointment availability when needed, (2) electronic communication with practices, and (3) other staff that help manage a child's health care needs. Parents also indicated which practice they would contact for an exacerbation of the main chronic condition for which the child receives specialty care. We used logistic regression to examine relationships of enhanced access components in both practices with parents' indicated practice. RESULTS: Among 609 parents, 244 (40%) would contact primary care and 365 (60%) the main specialty practice for a chronic condition exacerbation. Although parents perceived enhanced access components with similar frequency in both settings, enhanced access was associated only with preference for contacting the main specialty practice: e-mail communication (aOR for preferring the specialty practice 2.0 [1.3, 3.2]) and staff that coordinate a child's care needs (aOR 2.8 [1.4, 5.9]). CONCLUSIONS: Enhanced access is associated with preference for addressing chronic condition exacerbations in specialty but not primary care. Future study should further identify factors important to parents in deciding when and how to contact practices and should seek to develop family-centered communication within medical homes that integrate primary and specialty care.

Estimated savings from paid telephone consultations between subspecialists and primary care physicians.

OBJECTIVES: Pediatric subspecialists are not routinely reimbursed by Medicaid or insurance payers for telephone consultations. Generally, access to pediatric subspecialists is limited because of the small number of providers, their concentration in academic medical centers, and increasing demand for their services. Little is known about the nature of such consults, the time required to provide them, or whether there is a positive economic impact for payers. METHODS: Between March and October of 2007, pediatric subspecialists from 6 academic medical centers in North Carolina completed consultation reimbursement-request forms to prospectively track their telephone consultations with primary care physicians for the care of Medicaid patients<22 years of age. Data collected included the amount of time required per consult and consult outcomes in terms of service use and quality of care. Medicaid claims records and primary care physician surveys were used to validate the pediatric subspecialist consultation outcomes. RESULTS: A total of 47 pediatric subspecialists provided 306 consults regarding the care of 292 Medicaid-insured children over the 8 study months. Telephone consults were generally <15 minutes in length and exceeded 30 minutes in <7% of calls. Pediatric subspecialists reported that telephone consults led to avoidance of specialist visits (n=98), hospital transfers (n=35), hospital admissions (n=14), and emergency department visits (n=14). Medicaid claims data supported these reports; matched primary care physician surveys suggested even higher levels of service avoidance. After adjusting for the reimbursed costs of providing telephone consults, an estimated $477274 was saved ($39 per dollar spent). CONCLUSIONS: Telephone consultations with pediatric subspecialists provide a valuable service to primary care physicians providing medical homes to Medicaid patients. Rewarding physicians for telephone consults seems to be cost-effective because of reduced use of costly services and reported improvements in quality of care.

A medical home for children with insulin-dependent diabetes: comanagement by primary and subspecialty physicians--convergence and divergence of opinions.

OBJECTIVE: The purpose of this work was to examine pediatricians' and endocrinologists' views about management for routine preventive and acute care, diabetes-specific care, and family education and care coordination for children with insulin-dependent diabetes. METHODS: We conducted a mixed-mode survey of all of the pediatricians in 1 medicaid managed care network and all of the pediatric and adult endocrinologists who treat children with diabetes in North Carolina. RESULTS: Of the 201 pediatricians surveyed, 132 responded (65%). Among the 61 endocrinologists who treat children, 59% replied. Nearly all of the respondents agreed that primary care physicians should have responsibility for routine primary care (eg, well-child checkups, treating minor illnesses or injuries, and immunizations). Likewise, large majorities favored endocrinologists as leads for diabetes-specific care (eg, 94% for training in use of an insulin pump and 82% for training in use of a glucometer). Many generalists and subspecialists reported that specific aspects of diabetes care should be comanaged (eg, 31% for tracking of hemoglobin A1c). However, large proportions of pediatricians and endocrinologists expressed differing opinions about the primary responsibility for family education and care coordination and for specific diabetes services. For example, 80% of endocrinologists saw subspecialists as leads for monitoring blood sugar levels, whereas 52% of pediatricians favored comanagement. CONCLUSIONS: An effective medical home model of care depends on establishing clear lines of responsibility between the primary care physician and subspecialist. Our findings suggest that primary care physicians and subspecialists agree on who should lead most aspects of care for patients with insulin-dependent diabetes and that some aspects of care should be comanaged. However, primary care physicians and subspecialists did not agree either between or within disciplines on who should be more responsible for the basic aspect of monitoring of blood sugar levels. Approaches that recognize the appropriate division of care between primary care physicians and subspecialists, facilitate comanagement when it is needed, and reward the collaboration required to provide medical homes for patients should be investigated as models of care.

Human insulin-like growth factor-IA expression in transgenic mice promotes adenomatous hyperplasia but not pulmonary fibrosis.

Insulin-like growth factor-I (IGF-I) has been implicated in postnatal alveolar development, pulmonary fibrosis, and non-small cell lung cancer. To further investigate the role of IGF-I, we created a line of transgenic mice in which alveolar type II epithelial cells express human IGF-IA under the control of the surfactant protein C promoter. We determined the effect of pulmonary overexpression of human IGF-IA on 1) pulmonary inflammation and fibrosis in response to intratracheal instillation of bleomycin, 2) premalignant pulmonary adenomatous hyperplasia, and 3) adenoma formation. Transgenic expression of human IGF-IA had no effect on baseline gross lung pathology, cellularity of bronchoalveolar lavage, or total lung collagen content. In addition, there were no significant differences between transgenic mice and nontransgenic littermate controls in the development of pulmonary inflammation or pulmonary fibrosis in response to intratracheal bleomycin instillation. However, pulmonary expression of human IGF-IA in older mice (>12 mo) significantly increased the incidence of premalignant adenomatous hyperplastic lesions compared with littermate controls without affecting adenoma formation. These findings suggest that increased expression of human IGF-IA in alveolar air spaces does not affect the development of pulmonary fibrosis but promotes premalignant changes in the alveolar epithelium.

Dexamethasone changes the composition of insulin-like growth factor binding proteins in the newborn mouse ileum.

BACKGROUND: Early postnatal glucocorticoid exposure accelerates the maturation of the bowel mucosa but results in bowel wall thinning in the newborn mouse ileum and increases the risk of focal ileal perforation in extremely premature infants. We have previously demonstrated a redistribution of insulin-like growth factor-I (IGF-I) from the submucosa in control animals to the distal villi of those treated with early postnatal dexamethasone, implicating IGF-I as an important mediator of dexamethasone's capacity to alter tissue growth. To investigate the possibility that IGF binding proteins (IGFBPs) might contribute to this process, we characterized the localization and abundance of IGFBP peptides and mRNAs in the same model. METHODS: Newborn mice received daily intraperitoneal injections of dexamethasone (l microg/g) or phosphate-buffered saline and then were euthanized on day 3 of life. Their ileums were harvested and prepared for microscopy. Tissue sections of ileum from both treatment conditions were processed in parallel for immunolocalization of each of the six IGFBP peptides and for in situ hybridization of each of the six IGFBP transcripts. RESULTS: Transcripts for IGFBP-1, -2, and -3 were highly abundant and ubiquitous the ileal mucosa, whereas transcripts for IGFBP-4, -5, and -6 were less abundant in epithelial cells. There were no differences in abundance between control and dexamethasone-treated ileum with regard to mRNA localization or abundance for IGFBP-1, -2, -3, and -6. In contrast, mRNA transcripts for IGFBP-4 and -5 were modestly increased with dexamethasone treatment (although only IGFBP-4 was significant). Strikingly different patterns of IGFBP immunolocalization were observed between control and dexamethasone-treated animals. IGFBP-1, -2, -3, and -5 were not detected in control ileum, whereas IGFBP-4 and -6 were both present in the mucosa. In contrast, dexamethasone treatment resulted in dramatic mucosal increases in IGFBP-2, -3, -4, and -5, paralleling the changing distribution of IGF-I that we previously reported. CONCLUSION: Taken together, these findings further implicate the IGF system as an important participant in dexamethasone-induced maturation in the newborn mouse ileum.

Retinoic acid attenuates O2-induced inhibition of lung septation.

Exposure of the newborn lung to hyperoxia is associated with impaired alveolar development. In newborn rats exposed to hyperoxia and studied at day 14 of life, retinoic acid (RA) treatment improved survival and increased lung collagen but did not improve alveolar development. To determine whether RA treatment during exposure to hyperoxia results in late improvement in alveolarization, we treated newborn rats with RA and hyperoxia from day 3 to day 14 and then weaned O2 to room air by day 20, and studied the animals on day 42. O2-exposed animals had larger mean lung volumes, larger alveoli, and decreased gas-exchange tissue relative to air-exposed animals, whereas RA-treated O2-exposed animals were not statistically different from air-exposed controls. Relative to control animals, elastin staining at day 14 was decreased in hyperoxia-exposed lung independent of RA treatment, and, at day 42, elastin staining was similar in all treatment groups. At day 14, elastin gene expression was similar in all treatment groups, whereas at day 42 lung previously exposed to hyperoxia showed increased elastin signal independent of RA treatment. These results indicate that RA treatment during hyperoxia exposure promotes septal formation without evidence of effects on elastin gene expression after 4 wk of recovery.

Pro- and anti-inflammatory cytokines regulate insulin-like growth factor binding protein production by fetal rat lung fibroblasts.

The inflammatory response of the lung to noxious factors contributes to the pathogenesis of chronic lung injury. Inflammatory mediators regulate the insulin-like growth factor (IGF) system, a key modulator of lung fibroblast proliferation. The activity of IGFs is regulated by IGF-binding proteins (IGFBPs) secreted by lung cells. To investigate the regulation of lung fibroblast IGFBPs by cytokines, we exposed 19-d fetal rat lung fibroblasts to various pro- and anti-inflammatory mediators. IGFBP abundance in conditioned medium (CM) was measured by ligand blot and RNA transcript abundance by RNase protection assays. Fetal rat lung fibroblasts exposed to interleukin (IL)-1beta or tumor necrosis factor (TNF)-alpha for 48 h demonstrated increased abundance of CM IGFBP-3 (5.9- and 4.7-fold increases for IL-1beta and TNF-alpha, respectively) and IGFBP-4 (5.7- and 7.4-fold increases for IL-1beta and TNF-alpha, respectively) that was accompanied by a small increase in IGFBP-4 mRNA and a larger increase in IGFBP-3 mRNA abundance. IGFBP-4 specific proteolysis was examined in CM collected from fetal rat lung fibroblasts after incubation with serum-free medium (SFM), IL-1beta, or TNF-alpha for 48 h. Cell-free aliquots of SFM-CM incubated at 37C for 24 h showed a 65% decrease in IGFBP-4 abundance that was inhibited by 1,10-phenanthroline. In contrast, CM from cells exposed to IL-1beta or TNF-alpha incubated at 37 degrees C for 24 h did not show a significant decrease in IGFBP-4 abundance unless IGF-I was present during the cell-free incubation. Addition of IGFBP-3 to aliquots of SFM-CM reversed the IGF-I-mediated acceleration of IGFBP-4 proteolysis. Similarly, addition of IGFBP-3 to cells in culture increased the accumulation of CM IGFBP-4. These results demonstrate that cytokines regulate IGFBP production and clearance by fetal lung cells and suggest a mechanism by which cytokines regulate cell proliferation following lung injury.