Pilot feasibility study to detect mesenchymal stem cell biomarkers of bronchopulmonary dysplasia in the tracheal aspirate fluid of preterm infants.

OBJECTIVE: This study aimed to detect novel mesenchymal stem cell peptides/biomarkers of bronchopulmonary dysplasia (BPD) in the tracheal aspirate fluid (TAF) of preterm infants. STUDY DESIGN: Participants included infants less than 32 weeks' gestational age or birth weight under 1500 grams who required endotracheal intubation and mechanical ventilation within first 24 hours of life. TAF sample collection was performed at the time of the first clinically indicated routine suctioning. Standardization curves for human levels of osteopontin (Opn), macrophage colony stimulating factor 1 (Csf1), transforming growth factor beta 1 (TGF-ß1), and secretory immunoglobulin A (sIgA) were generated for 15 enrolled participants. RESULTS: We demonstrated that stem cell biomarkers are secreted into the TAF of preterm infants and their concentrations can be easily measured during the first week of life. CONCLUSIONS: Further studies are warranted to determine a causal relationship between these biomarkers and BPD development and severity.

Transfusion-related acute lung injury following PDA ligation in a preterm neonate.

Transfusion-related acute lung injury (TRALI) is a life-threatening complication of blood product transfusion characterized by sudden onset hypoxemic respiratory failure with bilateral lung infiltrates and non-cardiogenic pulmonary edema developing within 6 hours of transfusion. It is believed to be under-recognized, particularly among preterm neonates in whom co-existing developmental lung disease adds diagnostic complexity. Here we report the case of a preterm neonate who developed TRALI during a blood transfusion following PDA ligation.

Massive pneumatosis without necrosis: A case report of Clostridium perfringens sepsis in an extremely low birth weight infant.

Pneumatosis intestinalis and free intraperitoneal air on abdominal radiographs are considered pathognomonic signs of necrotizing enterocolitis (NEC). We report a unique case of late-onset fulminant sepsis due to Clostridium perfringens presenting with shock, extensive pneumatosis intestinalis and free intraperitoneal air in an extremely low birth weight infant without histopathological evidence of bowel necrosis or NEC.

Results of urinary undiversion in children.

Urinary undiversion was performed in 31 patients. Preoperative investigation and criteria for undiversion are discussed. Renal preservation rate is stable in 28 of 31 patients and bladder function satisfactory in 30 of 31 patients. Although prolongation of life and prevention of renal deterioration are of primary concern, psychologic aspects of undiversion must also be considered. Some children who underwent urinary diversion have poor renal reserve and eventually outgrow their kidneys, thus requiring renal transplantation. Their urinary tracts must be prepared for that eventuality.

Smoking is a factor in causing acute chest syndrome in sickle cell anemia.

A link between cigarette smoking and "acute chest syndrome" in sickle cell anemia is suggested. Acute chest syndrome in the patient with sickle cell anemia is characterized by fever, leukocytosis, cough, chest pain, and pulmonary infiltrates in the chest radiograph. This article describes the results of a study of 69 adolescent and young adult sickle cell anemia patients. Twenty-nine of these patients were smokers, three were former smokers, and 37 were nonsmokers. Patients completed respiratory questionnaires that focused on smoking habits and included a history of chest syndrome. Information obtained was confirmed by review of clinical records. The chi-square test demonstrated a strong relationship between cigarette smoking and chest syndrome in sickle cell anemia. All 29 smokers had a history of chest syndrome, but only 24 of 37 nonsmokers had such a history. Although the exact mechanism of the relationship between smoking and the development of acute chest syndrome remains speculative, cigarette smoking joins infection, hypoxia, acidosis, infarction, dehydration, and analgesics as a causative factor in adolescent and adult patients with sickle cell anemia. Behavioral modification of the smoking habit in patients with sickle cell anemia may decrease the frequency of acute chest syndrome and sequelae of sickle cell lung disease.

Parotid gland swelling in HIV diffuse infiltrative CD8 lymphocytosis syndrome.

HIV can affect salivary gland tissue. Parotid swellings have been observed in a subset of patients who are HIV-positive; the swellings are the result of a condition that has been termed diffuse infiltrative CD8 lymphocytosis syndrome. Initially the glandular enlargement results from a massive CD8 cell lymphoproliferation, but with time lymphoepithelial cysts become manifest. Two case reports are presented to illustrate this progression of diffuse infiltrative CD8 lymphocytosis.

Sialosis of unknown origin.

Sialosis (sialadenosis) is defined as an asymptomatic, non-inflammatory, non-neoplastic parenchymal salivary gland disease accompanied by a persistent painless bilateral swelling of the salivary glands, most commonly involving the parotid glands. There is no sex predilection, and the peak age incidence is between 30 and 70 years of age. Sialosis occurs in three different groups of patients: alcoholics, diabetics and the malnourished. An autonomic neuropathy, seen as a demyelinating polyneuropathy, seems to be the common underlying basis for this seemingly disparate group of patients with sialosis.

Effect of prenatal glucocorticoid treatment on size at birth among infants born at term gestation.

OBJECTIVE: To determine whether prenatal treatment with a single course of glucocorticoids (GCs) affects size at birth among full-term infants independent of fetal size before GC administration or exposure to preterm labor (PTL). STUDY DESIGN: In all, 105 full-term infants were recruited into three study groups (30 GC treated; 60 controls matched for gestational age (GA) at birth and sex; and 15 PTL controls without GC exposure). Size of the infants was estimated before treatment using two-dimensional (2D) ultrasound and by direct measurement at birth. RESULTS: Length, weight and head circumference at birth were smaller among GC-treated infants compared with matched controls (P's<0.01), although fetal size did not differ before treatment (P's>0.2). Exposure to PTL did not account for this effect. CONCLUSIONS: Prenatal treatment with a single course of GCs was associated with a reduction in size at birth among infants born at term gestation. This effect cannot be explained by differences in fetal size before treatment or exposure to PTL.

Shock, metabolic acidosis, and coma following ibuprofen overdose in a child.

OBJECTIVE: To report a child who developed shock, loss of consciousness, and metabolic acidosis following an ibuprofen overdose. CASE SUMMARY: A 6-year-old boy with no prior medical problems ingested approximately thirty 200-mg tablets of ibuprofen. The patient developed shock, coma, and metabolic acidosis. He was treated successfully with intubation and mechanical ventilation, fluid resuscitation, and decontamination with activated charcoal. The patient was discharged without any clinical sequelae. DISCUSSION: Serious adverse complications following ibuprofen overdose have been reported rarely in children. We reviewed literature pertaining to the etiology, pharmacology, pathophysiology, and management of complications following ibuprofen overdoses, as well as other case reports. CONCLUSIONS: Coma, metabolic acidosis, and shock were noted in a child who ingested a large quantity of ibuprofen. These complications have been described rarely in children. We attribute his favorable clinical outcome to early and aggressive intervention consisting of tracheal intubation, fluid resuscitation, and decontamination with activated charcoal. Although ibuprofen overdoses are usually benign, healthcare professionals should be aware of the various potentially serious complications that may occur.

Granulocyte-macrophage colony-stimulating factor increases surfactant phospholipid in premature rabbits.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a hematopoietic cytokine that is low in airway specimens from immature lungs at birth. In adult mice, an absence of GM-CSF causes excessive accumulation of alveolar surfactant due to a lack of catabolism. Our aim was to investigate whether recombinant human GM-CSF (rhGM-CSF) affects the pool sizes or the turnover of disaturated phosphatidylcholine (DPC) in preterm (gestation 29 d) rabbits at birth and in term rabbits, age 3 d. 3H-labeled dipalmitoyl phosphatidylcholine, 14C-acetate, and either rhGM-CSF (125 or 25 microg/kg body weight) or placebo were given intratracheally. Thereafter, the intra- and extracellular surfactant fractions were isolated and quantified for DPC and radioactivity. In preterm animals, GM-CSF increased dose-dependently within 24 h both the pool sizes of surfactant DPC and the 3H,14C-labeling of surfactant DPC (p < 0.05). The expression of surfactant protein B mRNA was unaffected, whereas surfactant protein B in bronchoalveolar lavage increased. The number of cells in the whole lung, the type II alveolar epithelial cells, and the lavageable alveolar macrophages were unaffected. At term, rhGM-CSF increased the turnover but did not affect the pool sizes of surfactant DPC. Intraperitoneal rhGM-CSF increased blood eosinophils but had no effect on surfactant DPC. Depending on the degree of lung maturity, GM-CSF in the alveolar space may either up-regulate the pool size or increase the turnover of surfactant phospholipid after birth.

Acquired immunodeficiency syndrome-associated renal disease in children.

Five children with acquired immunodeficiency syndrome (AIDS) and clinically significant renal disease had detailed pathologic examination of renal tissue (biopsy specimens, autopsy specimens, or both). All patients had proteinuria, hypoalbuminemia, and edema; one patient had persistent azotemia. In two cases, renal disease was the first manifestation of human immunodeficiency virus (HIV) infection. All patients had progressive renal disease, and four of the five died. Pathologic studies revealed focal glomerulosclerosis and mesangial proliferative glomerulonephritis with deposits of immunoglobulins and complement demonstrated by immunofluorescence and electron microscopy. Characteristic tubuloreticular structures were also demonstrated in the glomerular endothelial or epithelial cells in two cases. Renal disease is part of the multisystem involvement in children with AIDS. The pathogenesis of renal disease is not known, but circulating immune complexes are known to occur in children with HIV infection and may be involved.

Pneumococcal polysaccharide immunization of children with sickle cell disease. I. Clinical reactions to immunization and relationship to preimmunization antibody.

Vaccine reaction data were obtained from 154 patients with sickle cell disease immunized with tetradecavalent pneumococcal polysaccharide vaccine. There was a high rate (70%) of mild reactions, primarily at the site of injection. Fever over 100 degrees F was uncommon and precipitation of symptoms similar to sickling crisis was rare. Development of local reactions was associated with the level of preimmunization pneumococcal antibody titer.

Pneumococcal polysaccharide immunization of children with sickle cell disease. II. Serologic response and pneumococcal disease following immunization.

One-hundred seventy-four children with sickle cell disease (SCD) were immunized with a single dose of tetradecavalent pneumococcal vaccine. Preimmunization and postimmunization antibody against 13 of the 14 pneumococcal capsular antigens was measured by indirect hemagglutination (IHA). The ability of each antigen to stimulate antibody following immunization was characterized by one of three types of responses: (1) poor antibody response regardless of the age at immunization (capsular types 6A, 14, and 19F); (2) improving antibody response with advancing age at immunization (capsular types 1, 4, 9N, 12F, 18C, and 23F); and (3) good antibody response regardless of age at immunization (capsular types 2, 3, 7F, and 8). An increase in antibody following immunization was significantly correlated (P less than 0.0005) with an increasing level of preimmunization antibody titer for all 13 antigens. Through the first 24 months of study, two episodes of pneumococcal sepsis caused by group 23 pneumococci were documented in two children immunized prior to 24 months of age (incidence rate, 4.40/100 patient-years in children less than 5 years of age), and one additional episode caused by a group 23 pneumococcus occurred in a 5 7/12-year-old child (incidence rate, 0.66/100 patient-years in children greater than 5 years of age). These observations suggest that anamnestic immune response significantly contributed to the enhanced antibody response observed in older children and adults. Only modest vaccine efficacy may be expected among children with SCD who receive a single dose of pneumococcal vaccine.