Methylprednisolone, dexamethasone or hydrocortisone for acute severe pediatric asthma: does it matter?

OBJECTIVE: Various intravenous (IV) corticosteroids are available for acute severe asthma (ASA) treatment. The choice of IV corticosteroids varies broadly and depends on institution, country, or physician preferences. In this study, we compared the efficacy of IV methylprednisolone, hydrocortisone and dexamethasone in ASA treatment during pediatric intensive care unit (PICU) admission. METHODS: The study was a prospective randomized clinical trial. We enrolled patients of 1-21 years after they were admitted to the PICU requiring continuous beta-2 agonist treatment. Patients were randomized into three groups: Group A: IV Methylprednisolone, Group B: IV Hydrocortisone and Group C: IV Dexamethasone. The primary outcomes measured were durations of beta-2 agonist continuous nebulization treatment. Secondary outcomes, included PICU and hospital length of stay (LOS), pediatric asthma severity score (PASS), need for mechanical ventilation and maximum dose of beta-2 agonist treatment. RESULTS: 61 patients were included in the analysis. 22 patients recruited in Group A, 20 in group B and 19 group C. Median durations of beta-2-agonist treatment were 23 h (QR 16-38) for methylprednisolone, 27 h (QR 16-40) for hydrocortisone, and 32 h (QR 16-48) for dexamethasone (p = 0.90). There was no difference in PICU LOS, hospital LOS, PASS score, B2 agonist maximum dose, or need for ventilation support. CONCLUSIONS: The use of IV methylprednisolone, hydrocortisone, and dexamethasone have equivalent efficacy when used at the appropriate doses. Studies with larger cohorts are needed to compare the effectiveness of IV corticosteroids in the management of ASA in the PICU setting.

The light at the end of the tunnel: an unusual case of acute kidney injury in a pediatric patient: Answers.

Monoclonal gammopathies are a rare diagnosis in pediatric patients. A 19-year-old female patient with past medical history of hypogammaglobulinemia and natural killer cell deficiency and stage III follicular lymphoma, in remission, presented with a right-sided pneumonia, noted to have acute kidney injury and proteinuria. Complement C3 and C4 levels were normal. Anti-double-stranded DNA antibodies, antinuclear antibodies, anti-extractable nuclear antigen antibodies, and antineutrophil cytoplasmic antibodies were negative. A renal biopsy showed numerous fractured tubular casts that were periodic acid-Schiff and silver-stain negative and fuchsinophilic on trichrome stain, with associated giant cells, tubulitis, acute tubular injury, and tubular rupture. The tubular casts had 3+ staining for lambda light chains and 0-1+ staining for kappa light chains. These findings were consistent with light chain cast nephropathy (LCCN). Serum free light chains, serum immunofixation, urine protein electrophoresis, and urine immunofixation studies supported the renal biopsy diagnosis of LCCN. A bone marrow biopsy showed normal trilineage hematopoiesis and also revealed an atypical B cell population detected by flow cytometry. Pathology specimens from lesions in the distal small bowel were characteristic of diffuse large B cell lymphoma (DLBCL). Chemoreduction therapy followed by chemotherapy was initiated for the DLBCL. Three months after initiation of chemotherapy, the patient's creatinine has improved by > 50%. The likely cause of her LCCN was the new diagnosis of a DLBCL. Other risk factors include her history of hypogammaglobulinemia, natural killer (NK) cell deficiency, community-acquired pneumonia, and prior follicular lymphoma. Our patient may be the youngest reported case of LCCN. Treatment of LCCN is based on treating the underlying clonal plasma cell or B cell proliferation, typically with chemotherapy.