Association between iron deficit repletion with ferric carboxymaltose relative to iron sucrose in children with inflammatory bowel disease: A retrospective cohort study.

BACKGROUND: Iron deficiency and iron deficiency anemia are common in pediatric inflammatory bowel disease and often require supplementation with iron. There is a paucity of literature regarding optimal iron formulation. The aim of this study is to compare outcomes in pediatric patients with inflammatory bowel disease receiving either iron sucrose or ferric carboxymaltose during inpatient hospitalizations. METHODS: This was a single-center retrospective study of pediatric patients with inflammatory bowel disease admitted for newly diagnosed disease or flare who received either iron sucrose or ferric carboxymaltose. Linear regression was used to assess differences in iron repletion. Longitudinal linear mixed-effects models and generalized estimating equations compared hematologic and iron outcomes 6 months post-iron repletion. RESULTS: Thirty patients received ferric carboxymaltose. Sixty-nine patients received iron sucrose. Baseline hemoglobin and iron deficits were similar in both groups. A larger percentage of iron deficit was repleted in the ferric carboxymaltose group (81.4%) compared with iron sucrose (25.9%) (P < 0.001) with fewer infusions. Cumulative doses of ferric carboxymaltose administered (18.7 mg/kg) were higher than iron sucrose (6.1 mg/kg) (P < 0.001). Hemoglobin increased more quickly with ferric carboxymaltose compared with iron sucrose (P = 0.04 and P = 0.02, respectively). Total iron binding capacity and red cell distribution width levels decreased more over time with ferric carboxymaltose vs iron sucrose (P < 0.01 and P = 0.01, respectively). No adverse effects were seen. CONCLUSIONS: Hematologic and iron parameters responded more quickly with fewer infusions in patients who received ferric carboxymaltose vs iron sucrose. Patients who received ferric carboxymaltose achieved a higher percentage of iron deficit repleted.

Analysis of transition from intravenous iron sucrose to ferric carboxymaltose infusions in pediatric patients with intestinal failure.

BACKGROUND: Iron supplementation is required for pediatric patients with intestinal failure (IF). There is a paucity of literature on optimal iron formulation and outcomes in this patient population that requires ongoing supplementation. The aim of this study was to assess outcomes in pediatric patients with IF receiving iron sucrose (IS) vs ferric carboxymaltose (FCM) iron infusions. METHODS: This was a single-center observational cohort study of pediatric patients with IF requiring ongoing intravenous iron supplementation. Patients were transitioned from IS to FCM as iron therapy. Longitudinal linear mixed-effects models and generalized estimating equations were used to compare outcomes, including hematologic, iron, and growth parameters for 12-month treatment duration on each iron formulation. Adverse effects were descriptively summarized. RESULTS: Twenty-three patients were included. Sixteen received IS and later switched to FCM, five received IS only, and two received FCM only. Most patients' etiology of IF was short bowel syndrome (FCM: 81%, IS: 83%). No differences were seen over time for iron, hematologic, and growth metrics between IS and FCM. The median number of infusions over 12 months for those taking IS was 15 (interquartile range [IQR] = 13-26) and 2 for FCM (IQR = 1-2). Asymptomatic hypophosphatemia was noted in both groups. Similar central line-associated bloodstream infection rates were noted. CONCLUSION: IS and FCM infusions both maintained hematologic and iron parameters with no significant difference noted between the two types of iron, though the number of FCM infusions was significantly less. No significant adverse effects were noted.

Adjunctive Dietary Therapy Is Associated With Improved Gastrointestinal Symptoms in Steroid-Refractory Gastrointestinal Graft-Versus-Host Disease: A Case Series.

Acute gastrointestinal graft-versus-host disease (GI GVHD) is a complication after hematopoietic stem cell transplant with high morbidity and mortality. In particular, steroid-refractory GI GVHD can be difficult to treat. Recent investigations have revealed that patients after transplant can experience intestinal dysbiosis contributing to the progression of GVHD. Modulation of the gut microbiome through dietary intake could potentially improve the intestinal dysbiosis in GI GVHD. In this case series, we present 3 patients where dietary therapy was used in conjunction with immunosuppression to achieve clinical remission of GI GVHD.

Late graft loss after intestinal transplantation.

PURPOSE OF REVIEW: Despite improvement in short-term outcomes after intestinal transplantation in the last 20 years, long-term rates of graft attrition and patient survival remain unchanged, with worse outcomes compared with other solid organ transplants. This review investigates the multiple causes of late graft loss, including chronic rejection, infection, graft-versus-host disease, posttransplant lymphoproliferative disorder and postsurgical complications. RECENT FINDINGS: New insights into immunology of the intestine and evolution of immunosuppression, as well as review of current persistent causes of late graft loss, shed light on findings that may help improve long-term intestinal allograft survival. SUMMARY: Although intestinal transplantation remains a life-saving intervention with significant advancements since its inception, further understanding of mechanisms of injury is needed to improve long-term outcomes and prevent late intestinal graft loss.

Ulcerative Colitis: Making the Diagnosis.

Ulcerative colitis is an inflammatory condition of the colon. The diagnosis of ulcerative colitis is based on clinical presentation, endoscopic evaluation, and histologic parameters in the absence of demonstrable alternate etiology. The differential diagnosis remains broad, and infection in particular must be considered and excluded. Although laboratory and radiographic findings can aid in the diagnosis of ulcerative colitis, endoscopy remains the gold standard for diagnosis. A correct diagnosis and disease staging are imperative because these factors affect treatment options and prognosis.

Dietary Management of Pediatric Inflammatory Bowel Disease.

Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, is a life-long relapsing and remitting condition characterized by inflammation of the intestine. While the exact pathogenesis of IBD is unclear, the current belief is that both genetic and environmental factors play a role in development of disease. Management options include nutritional, pharmacological, and surgical therapies. In particular, nutritional therapies for IBD have garnered significant interest due to their limited side effect profile, bowel-sparing nature, and naturalistic approach. This review will examine the role of diet in the pathogenesis and malnutrition in IBD, and will discuss dietary approaches to management of IBD, including exclusive enteral nutrition, specific carbohydrate diet, anti-inflammatory diet, and food supplements (specifically curcumin and long-chain n-3 polyunsaturated fatty acids). Past and recent literature on these subjects were reviewed in Medhub and Scopus databases for this review article with a focus on pediatric and high-quality publications. At this time, these approaches seem to be safe and show promise of an efficacious sole or supplemental role in the treatment of IBD, but randomized, prospective studies are lacking. Additional studies investigating these diets and food supplements are needed to provide more information on their efficacy, mechanism, applicability, and safety.

Peculiarities in Ankle Cartilage.

Posttraumatic osteoarthritis (PTOA) is the most common form of osteoarthritis (OA) of the ankle joint. PTOA occurs as a result of several factors, including the poor regenerative capacity of hyaline articular cartilage as well as increased contact stresses following trauma. The purpose of this article is to review the epidemiology, pathogenesis, and potential targets for treatment of PTOA in the ankle joint. Previous reviews primarily addressed clinical approaches to ankle PTOA, while the focus of the current article will be specifically on the newly acquired knowledge of the cellular mechanisms that drive PTOA in the ankle joint and means for potential targeted therapeutics that might halt the progression of cartilage degeneration and/or improve the outcome of surgical interventions. Three experimental treatment strategies are discussed in this review: (1) increasing the anabolic potential of chondrocytes through treatment with growth factors such as bone morphogenetic protein-7; (2) limiting chondrocyte cell death either through the protection of cell membrane with poloxamer 188 or inhibiting activity of intracellular proteases, caspases, which are responsible for cell death by apoptosis; and (3) inhibiting catabolic/inflammatory responses of chondrocytes by treating them with anti-inflammatory agents such as tumor necrosis factor-α antagonists. Future studies should focus on identifying the appropriate timing for treatment and an appropriate combination of anti-inflammatory, chondro- and matrix-protective biologics to limit the progression of trauma-induced cartilage degeneration and prevent the development of PTOA in the ankle joint.