Pulmonary Calcification in a Congenital Cytomegalovirus Infection

Abstract

A 1-day-old, small for gestational age male infant was born at 39 weeks of gestation via normal, spontaneous vaginal delivery with a birth weight of 2044 g. Physical examination revealed microcephaly but no other external malformations. Congenital cytomegalovirus (CMV) infection was diagnosed by a positive urine CMV polymerase chain reaction performed on day 1. Serologic tests for other congenital infections caused by toxoplasma, rubella, and herpes simplex virus were negative. There was no evidence of hearing loss, retinitis, or hepatitis. Brain calcification was noted on head computed tomography (Figure 1). A chest radiography revealed subtle pulmonary nodules with calcification, which were confirmed by computed tomography (Figures 2 and 3). No respiratory symptoms developed. He received intravenous ganciclovir for 7 days, then oral valganciclovir. After 6 months of treatment with valganciclovir, the pulmonary calcifications were still present. Coexisting congenital infections were ruled out by the negative serology, and congenital tuberculosis was also excluded by maternal history and symptoms. Pulmonary calcification has been reported as an incidental finding in autopsies and prenatal ultrasounds of patients with congenital CMV infection, 1,2 but details in surviving patients with congenital CMV have not been documented. Calcification generally points to an old inflammatory process and in the case of infectious diseases, resolved infections. Brain calcification is commonly observed in cases of congenital CMV infection, 3 and its periventricular distribution is consistent with the pathology observed in CMV neurologic disease. Calcification in the liver and kidneys was also reported previously 1,4 and illustrates the broad tissue tropism associated with CMV infection. Likewise, the peripheral distribution of the pulmonary calcification in this case may be compatible with pneumonitis associated with the CMV infection. ■

Pulmonary Complications of Cytomegalovirus Infection in Neonates and Infants: A Systematic Review of Case Reports and Pooled Analysis

“…A total of 28 articles, encompassing 38 patients, met the inclusion criteria and were included in this systematic review. 3,14,24–49 A detailed flow chart illustrating the study selection process details following the preferred reporting items for systematic reviews and meta-analyses flow diagram is presented in Figure 1. An overview of the characteristics of the included studies is summarized in Table 1.…”

Ginkgolide B protects human pulmonary alveolar epithelial A549 cells from lipopolysaccharide‐induced inflammatory responses by reducing TRIM37‐mediated NF‐κB activation

“…Ubiquitinated IκB is degraded by the 26S proteasome, allowing NF‐κB to enter the nucleus to activate target genes 16. In addition, the p65 subunit of NF‐κB has been shown to be phosphorylated and transferred from the cytoplasm to the nucleus to promote the expression and release of tumor necrosis factor‐α (TNF‐α) and interleukin‐1β (IL‐1β) 19,20, suggesting that LPS could regulate pulmonary inflammation by inducing inflammatory responses in alveolar epithelial cells via the NF‐κB pathway 21,22. As an E3 Ub ligase, the tripartite motif (TRIM) is a protein family that is involved in multiple cellular processes, including apoptosis, inflammation, and cell proliferation 23–27.…”