Objectives:Thiopurines, commonly used to treat inflammatory bowel disease, cause lymphopenia and red blood cell macrocytosis, requiring therapeutic monitoring. Mean corpuscular volume/white blood cell (MCV/WBC) ratio has been proposed as a surrogate for therapeutic monitoring. Our aim was to investigate MCV/WBC ratio for assessing clinical response to thiopurines among pediatric patients with inflammatory bowel disease.Methods:We performed a retrospective cross-sectional study at a tertiary care center using laboratory results and standardized physician global assessments (PGA) among pediatric patients taking thiopurines. Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), fecal calprotectin, and 6-thioguanine nucleotides were assessed when available. The primary outcome was association between MCV/WBC ratio and clinical remission assessed by ESR, CRP, calprotectin, or PGA. We also used a composite outcome requiring all available data to be normal. Analyses were limited to 1 occurrence per patient, >60 days after starting thiopurine, and comparators were required to be within 14 days of one another.Results:A total of 471 patients met inclusion criteria. MCV/WBC ratio poorly predicted quiescent disease as defined by PGA (area under receiver operating characteristic curve [AuROC] 0.55, 95% confidence interval [CI] 0.43–0.66). MCV/WBC ratio better predicted quiescent disease defined as normal CRP (AuROC 0.64, 95% CI 0.58–0.70) or normal ESR (AuROC 0.59, 95% CI 0.52–0.66). When the composite outcome measure was used, MCV/WBC ratio had an AuROC of 0.65 (95% CI 0.59–0.70), indicating it is reasonably accurate in discriminating between clinical remission and active disease.Conclusions:MCV/WBC ratio is a noninferior, easy, and low-cost alternative to thiopurine metabolite monitoring.

Objectives: Corticosteroids have long been used to treat inflammatory bowel disease. However, cumulative corticosteroid exposure is associated with adverse effects, particularly in growing children. Professional guidelines recommend steroid-sparing strategies. It remains unknown whether corticosteroid use has decreased in children with inflammatory bowel disease. Methods: We performed retrospective cohort study using data from 2007 to 2018 from the international multi-center ImproveCareNow Network, a pediatric inflammatory bowel disease quality improvement collaborative. Pediatric patients diagnosed with inflammatory bowel disease were included. Patients with missing diagnosis or corticosteroid use data were excluded. We performed serial cross-sectional analyses of period prevalence and used multivariate regression models. Results: 27,321 patients were included (65% Crohn disease, 28% ulcerative colitis, 7% indeterminate colitis). Corticosteroids were used in 10,206 (37%). Corticosteroid use decreased from 28% (2007) to 12% (2018). Black patients received corticosteroids more commonly than white patients. This disparity improved as corticosteroid use decreased in both groups. Most corticosteroid use occurred <120 days after diagnosis. Corticosteroid or 5-aminosalicylate use <120 days after diagnosis predicted later corticosteroid use. Anti-tumor necrosis factor-alpha medication use <120 days after diagnosis was associated with a reduction in corticosteroid use. As corticosteroid use decreased, steroidsparing therapy use increased and height and weight z scores improved, particularly among children with Crohn disease. Despite improvement across the network, variation in corticosteroid usage remains. Conclusions: Corticosteroid use among pediatric patients with inflammatory bowel disease in the ImproveCareNow Network has decreased over time. Racial disparities in corticosteroid use were found, but gradually improved.

A 2-week-old male presented with poor feeding and weight loss. His birth history included an uncomplicated pregnancy followed by a normal term vaginal delivery with a birth weight of 3.23 kg, and an uncomplicated newborn stay.During his second week of life, he developed nonbloody, nonbilious emesis with nearly every feed. On the day of admission, he presented to his pediatrician for decreased oral intake, decreased urine output, and increased sleepiness requiring arousal for feedings. Given the concern for dehydration the patient was sent to the emergency room. Vital signs revealed a temperature of 99.1°F, respiratory rate of 36 breaths/min, heart rate of 187 beats/min, and oxygen saturation of 97% on room air. He weighed 3.03 kg, down 6% from his birth weight. His examination was pertinent for a flat anterior fontanelle, dry mucous membranes, 2+ brachial and femoral pulses, normal skin turgor with normal male genitalia, and absence of abnormal skin discoloration or birthmarks. Laboratory tests revealed sodium of 123 mmol/L, potassium 5.9 mmol/L, chloride 90 mmol/L, bicarbonate 20 mmol/L, blood urea nitrogen 18 mg/dL, creatinine 0.5 mg/dL, glucose 112 mg/dL, and calcium 10.6 mg/dL. His complete blood count and urinalysis were unremarkable. Abdominal and chest radiographs were normal. He received two 20 mL/kg normal saline boluses and was started on maintenance intravenous fluids of normal saline. He was transferred to our institution for evaluation of possible pyloric stenosis.At our institution, the patient's pyloric ultrasound was normal. On arrival a venous blood gas showed a pH 7.29, partial pressure of carbon dioxide of 48 mm Hg, partial pressure of oxygen of 33 mm Hg, and bicarbonate 23 mmol/L. He remained hyponatremic with serum sodium of 126 mmol/L. His serum creatinine was <0.1 mg/dL verifying normal glomerular filtration rate. He received 40 mL/kg of normal saline bringing his total sodium repletion since start of fluid resuscitation to 18 mEq/kg, with a corrected sodium of only 131 mmol/L and stable potassium level of 5.9 mmol/L. The patient was admitted for persistent hyponatremia and poor feeding.Because of persistent hyponatremia, mild hyperkalemia, and concerns for an abnormality in the adrenal axis, pediatric nephrology and endocrinology were consulted. The patient had a normal renal ultrasound with no evidence of obstruction, normal parenchymal thickness, echogenicity, and corticomedullary differentiation. A cranial ultrasound was unremarkable. Further evaluation revealed an adrenocorticotropic hormone (ACTH) level of 12 pg/mL and a cortisol level of 1.6 µg/dL (age appropriate level of 2 µg/dL). Follow-up cortisol levels were 1.7 and 1.0 µg/dL. Given persistently low cortisol levels, a low-dose ACTH stimulation test was performed, which showed appropriate rise in cortisol. His 17-hydroxyprogesterone level was 0.5 ng/mL and 11-deoxycorticosone level was 22 ng/dL, both appropriate for age. Interrogation of the aldosterone axis yielded markedly elevated aldosterone and renin levels of 816 ng/mL/h an...