Associations Between Placental Corticotropin-Releasing Hormone, Maternal Cortisol, and Birth Outcomes, Based on Placental Histopathology.

Preterm birth remains the leading cause of neonatal morbidity and mortality, with complex biochemical pathways requiring continued understanding and assessment. The objective of this study is to assess the associations between maternal cortisol and placental corticotropin-releasing hormone (placental CRH) concentrations with birth outcomes when stratified by placental histopathology. We conducted an analysis of 112 singleton pregnancies who received betamethasone between 23 and 34 weeks' gestation. Maternal blood and saliva were collected prior to betamethasone administration and samples assayed for plasma cortisol (pCort), salivary cortisol (sCort), and placental CRH levels. Placental findings were characterized as inflammatory, maternal vascular underperfusion (MVU), or no pathology, and compared for the outcomes of placental CRH, pCort, and sCort levels, gestational age at birth (GAB), and birthweight percentiles (BWP). Thirty-six subjects were characterized as inflammatory, 38 as MVU, and 38 without placental abnormalities. Histopathology groups differed significantly on placental CRH levels, GAB, and BWP. Post hoc tests suggested that the MVU group had higher placental CRH than the inflammatory or no pathology groups, and despite delivering earlier than the other two groups, the inflammatory group had infants with significantly higher BWP. No differences existed between groups in terms of mean plasma or sCort levels. Higher placental CRH and pCort levels were associated with earlier GAB in the overall sample, but when split by group, these associations remained significant only among the MVU group. Higher placental CRH was also associated with lower BWP in the overall sample but did not remain significant when split by group. Higher sCort was associated with lower BWP only in the MVU group. There is differentiation of placental CRH, cortisol, and birth outcomes when evaluated by placental histopathology. This highlights the importance of evaluating birth outcomes within the context of placental histopathology.

Ascaris Larval Infection and Lung Invasion Directly Induce Severe Allergic Airway Disease in Mice.

Ascaris lumbricoides (roundworm) is the most common helminth infection globally and a cause of lifelong morbidity that may include allergic airway disease, an asthma phenotype. We hypothesize that Ascaris larval migration through the lungs leads to persistent airway hyperresponsiveness (AHR) and type 2 inflammatory lung pathology despite resolution of infection that resembles allergic airway disease. Mice were infected with Ascaris by oral gavage. Lung AHR was measured by plethysmography and histopathology with hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) stains, and cytokine concentrations were measured by using Luminex Magpix. Ascaris-infected mice were compared to controls or mice with allergic airway disease induced by ovalbumin (OVA) sensitization and challenge (OVA/OVA). Ascaris-infected mice developed profound AHR starting at day 8 postinfection (p.i.), peaking at day 12 p.i. and persisting through day 21 p.i., despite resolution of infection, which was significantly increased compared to controls and OVA/OVA mice. Ascaris-infected mice had a robust type 2 cytokine response in both the bronchoalveolar lavage (BAL) fluid and lung tissue, similar to that of the OVA/OVA mice, including interleukin-4 (IL-4) (P < 0.01 and P < 0.01, respectively), IL-5 (P < 0.001 and P < 0.001), and IL-13 (P < 0.001 and P < 0.01), compared to controls. By histopathology, Ascaris-infected mice demonstrated early airway remodeling similar to, but more profound than, that in OVA/OVA mice. We found that Ascaris larval migration causes significant pulmonary damage, including AHR and type 2 inflammatory lung pathology that resembles an extreme form of allergic airway disease. Our findings indicate that ascariasis may be an important cause of allergic airway disease in regions of endemicity.

Firm, hyperpigmented subcutaneous nodule in the inguinal fold of an infant.

Subcutaneous juvenile xanthogranuloma (JXG) of the inguinal fold, an unusual location, was diagnosed in an infant. Subcutaneous JXG should be included in the differential diagnosis of subcutaneous nodules of the lower body, despite the absence of the characteristic yellowish hue usually associated with JXG.

First Reported Case of Postirradiation Pseudosclerodermatous Panniculitis After Stereotactic Body Radiation Therapy for the Treatment of Non-Small Cell Lung Cancer.

Postirradiation pseudosclerodermatous panniculitis is a rare complication of radiation therapy that presents as an indurated plaque and/or subcutaneous nodule in an area of previously irradiated tissue. The histopathologic pattern is of mixed lobular and septal panniculitis with necrotic adipocytes and thickened sclerotic septa as well as dense inflammatory infiltrates consisting mainly of histiocytes. The typical time interval is 1 month to several years after treatment with radiation therapy. This is a case of an 86-year-old man with a medical history significant for diffuse large B-cell lymphoma who was given 3 fractions of stereotactic body radiation therapy for treatment of stage IA non-small cell lung adenocarcinoma of the right upper lobe. Two years later, he presented with several small palpable subcutaneous right axillary nodules, which coalesced into a 6-cm firm multilobulated right axillary mass over several weeks. Histopathology showed sclerosing panniculitis with lipomembranous changes and septal fibrosis. This is the first reported case describing postirradiation pseudosclerodermatous panniculitis in a patient with lung cancer treated with stereotactic body radiation therapy. This diagnosis must be differentiated from other subtypes of panniculitis and complications of radiation therapy.

A novel association of biventricular cardiac noncompaction and diabetic embryopathy: case report and review of the literature.

Diabetic embryopathy refers to a constellation of congenital malformations arising in the setting of poorly controlled maternal diabetes mellitus. Cardiac abnormalities are the most frequently observed findings, with a 5-fold risk over normal pregnancies. Although a diverse spectrum of cardiac defects has been documented, cardiac noncompaction morphology has not been associated with this syndrome. In this report, we describe a novel case of biventricular cardiac noncompaction in a neonate of a diabetic mother. The patient was a late preterm female with right anotia, caudal dysgenesis, multiple cardiac septal and aortic arch defects, and biventricular cardiac noncompaction. Examination of both ventricles demonstrated spongy myocardium with increased myocardial trabeculation greater than 50% left ventricular thickness and greater than 75% right ventricular thickness, with hypoplasia of the bilateral papillary muscles, consistent with noncompaction morphology. Review of the literature highlights the importance of gene expression and epigenomic regulation in cardiac embryogenesis.

A case of congenital pyloric atresia with dystrophic epidermolysis bullosa.

Pyloric atresia with epidermolysis bullosa (EB) dystrophica is a rare entity that may not be immediately recognized. We describe the fourth confirmed case of pyloric atresia associated with the dystrophic subtype of EB diagnosed by standard pathologic measures, and discuss the clinical disease features and recent advances in the pathophysiology.

A rudimentary tragus in the nasopharynx: case report, literature review, and discussion of embryologic development.

We describe the rare case of a nine year-old girl with a several month history of mouth breathing and nasal obstruction due to a rudimentary tragus in the nasopharynx. We focus on the accessory tragus and its origins by describing the embryologic development of the external ear. Based on our review of the medical literature, this is the first report of a nasopharyngeal mass with a pathologic diagnosis of a rudimentary tragus.

Colorectal stents orient specimens and induce artifacts that mimic Crohn disease.

Colorectal malignancies may be stented to alleviate obstruction. The stent is a polarized and braided network of metallic wires. Pathology associated with colorectal stents is yet to be described. The authors reviewed 7 cases involving stented colorectal segments from patients lacking clinical suspicion of Crohn disease. In 4 cases, orientation of the specimens and stents matched the corresponding anatomic landmarks. In 3 cases, the specimens lacked helpful anatomic landmarks, and orientation was possible only after correlating with the intrinsic polarity of the stents. Stented areas showed artifacts resembling Crohn disease, including rounded cobblestones, pseudopolyps, and simple fissures, as well as unique artifacts including rhomboid cobblestones, complex fissures, oblique fissures with remarkably straight edges, and conical fragments of tissue that appeared to float. Crohn disease was misdiagnosed in 1 case in which the stent was removed intraoperatively and was never received. Colorectal stents help orient ambiguous specimens and induce patterned injury that can be confused with Crohn disease.

An in vivo evaluation of a novel spiral cut flexible ureteral stent.

OBJECTIVE: The flow characteristics, ureteral conformance, and histopathologic changes of a novel spiral cut flexible ureteral stent (Percuflex Helical, Boston Scientific, Boston, MA) were evaluated in vivo in an acute and chronic porcine model. MATERIALS AND METHODS: Flow characteristics and ureteral conformance of the novel stent were determined in 6 acute and 6 chronic swine models and compared with a control ureteral stent (Percuflex Plus, Boston Scientific). The flow characteristics were determined in vivo after ligating the renal vessels and via a nephrostomy tube delivering a standard rate of 0.9% saline at 35 cm H(2)O. Flows in the unobstructed ureter, normal stent, intraluminally obstructed stent, extraluminal obstructed stent, and both intraluminally and extraluminally obstructed conditions were determined. In the chronic animals, flow was determined at day 10, with the stent in place and immediately after stent removal. Conformance and hydronephrosis was assessed on pyelograms. Histopathologic changes were also evaluated in the chronic animals. RESULTS: The acute and chronic flow characteristics in the novel stent were equivalent to the control stent. Size and weight of the kidney, degree of hydronephrosis, stent migration, and presence of urinary tract infection were also similar between the test and control stents. There were no differences seen in histopathologic grading or degree of encrustation in either stent. The novel stent appeared to conform better to the shape of the ureter in both acute and chronic animals. CONCLUSION: The novel helical stent appears to drain as well as a standard stent and causes no increased degree of histopathologic changes in the ureter.