Purpose: To review our institutional experience in the surgical treatment of pediatric chronic pancreatitis (CP) and evaluate predictors of long-term pain relief.
Methods: Outcomes of patients ≤21 years surgically treated for CP in a single institution from 1995 to 2014 were evaluated.
Results: Twenty patients underwent surgery for CP at a median of 16.6 years (IQR 10.7-20.6 years). The most common etiology was pancreas divisum (n = 7; 35%). Therapeutic endoscopy was the first-line treatment in 17 cases (85%). Surgical procedures included: longitudinal pancreaticojejunostomy (n = 4, 20%), pancreatectomy (n = 9, 45%), total pancreatectomy with islet autotransplantation (n = 2; 10%), sphincteroplasty (n = 2, 10%) and pseudocyst drainage (n = 3, 15%). At a median follow-up of 5.3 years (IQR 4.2-5.3), twelve patients (63.2%) were pain free and five (26.3%) were insulin dependent. In univariate analysis, previous surgical procedure or >5 endoscopic treatments were associated with a lower likelihood of pain relief (OR 0.06; 95% CI 0.006-0.57; OR 0.07; 95%, CI 0.01-0.89). However, these associations were not present in multivariate analysis.
Conclusion: In children with CP, the step-up practice including a limited trial of endoscopic interventions followed by surgery tailored to anatomical abnormalities and gene mutation status is effective in ensuring long-term pain relief and preserving pancreatic function.
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http://dx.doi.org/10.1007/s00383-016-3999-6 | DOI Listing |
Tissue Eng Regen Med
January 2025
Department of Pediatrics, College of Medicine, Ewha Womans University, Seoul, 07804, South Korea.
Background: Exogenous Cushing's syndrome, which results from prolonged glucocorticoid treatment, is associated with metabolic abnormalities. Previously, we reported the inhibitory effect of tonsil-derived mesenchymal stem cell conditioned medium (T-MSC CM) on glucocorticoid signal transduction. In this study, we investigated the therapeutic efficacy of T-MSCs in a mouse model of exogenous Cushing's syndrome.
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January 2025
Department of Pediatrics, University of California San Diego, 3020 Children's Way MC 5137, San Diego, CA, 92123, USA.
Background: Inadequate treatment of acute rejection (AR) in pediatric kidney transplant recipients (KTR) can contribute to early allograft failure. Serum creatinine is an insensitive marker of allograft function, especially in the pediatric population, and may not detect ongoing rejection after treatment. We evaluated the utility of follow-up biopsies to detect persistent inflammation and future episodes of rejection.
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January 2025
Cardiology Department, Faculty of Medicine (Girls), Al-Azhar University, Cairo, Egypt.
Background: Changes in cardiac function and structure as well as their association with the cardiac autonomic nervous system remain incompletely characterized in children with stage 5 chronic kidney disease (CKD) receiving hemodialysis (HD).
Methods: A prospective observational cohort study was conducted on 40 Egyptian children with CKD on regular HD compared to 40 age- and sex-matched healthy children. All participants underwent thorough clinical examination, laboratory investigations, 24-h Holter monitoring, and 2D/4D echocardiographic study (conventional and advanced modalities).
Pediatr Transplant
March 2025
Department of Psychosocial Oncology and Palliative Care, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Background: Some adult transplant surgeons consider transplant to be contraindicated in patients receiving palliative care (PC). Little is known about pediatric transplant surgeons' attitudes toward PC. We sought to ascertain pediatric kidney transplant surgeons' perspectives regarding the routine integration of PC for children with chronic kidney disease.
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December 2024
State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and Xijing Hospital of Digestive Diseases, Air Force Medical University, Xi'an, Shaanxi 710032, China.
Metabolic dysfunction-associated steatohepatitis (MASH) is one of the most common chronic liver diseases and is mainly caused by metabolic disorders and systemic inflammatory responses. Recent studies have indicated that the activation of the mammalian (or mechanistic) target of rapamycin (mTOR) signaling participates in MASH progression by facilitating lipogenesis and regulating the immune microenvironment. Although several molecular medicines have been demonstrated to inhibit the phosphorylation or activation of mTOR, their poor specificity and side effects limit their clinical application in MASH treatment.
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