Introduction: Iododerma is a rare, delayed type IV hypersensitivity reaction due to iodine deposition within the skin. With only a few published case reports, iododerma as a syndrome has been associated with exposure to iodine-containing materials such as contrast media, amiodarone, or povidone-iodine solution, with most cases involving lesions along the face and upper extremities (1). Diagnosis of iododerma is difficult, as lesions can raise concern for infection or vasculitis. We highlight a case of iododerma leading to airway compromise which was successfully treated with hemodialysis. Description: A 51 yo F with a PMH of diabetes mellitus, CKD stage IV, and diastolic heart failure presented with symptomatic anemia and underwent workup that included a CT abdomen and pelvis with oral contrast. She returned nine days later with evolving necrotic skin lesions within the perioral and periorbital areas. She developed facial and supraglottic mucosal edema with extensively sloughing bullous lesions and required intubation. A skin biopsy demonstrated neutrophilic infiltrates with a cryptococcoid appearance consistent with neutrophilic dermatosis. Urine and serum iodine were significantly elevated (15143.4 and 10822.5 respectively), consistent with a diagnosis of iododerma. She was started on high dose corticosteroids and initiated on intermittent hemodialysis to assist with clearance of iodine. Following three sessions of hemodialysis, patient had a significant clinical improvement and reduction in iodine levels with successful extubation on hospital day 11. Discussion: Iododerma is largely a diagnosis of exclusion but should be considered in patients with suggestive skin lesions and recent exposure to iodine-containing materials, particularly patients with underlying renal dysfunction. Diagnosis is typically made with a skin biopsy demonstrating neutrophilic infiltrates with structures that mimic Cryptococcus, in conjunction with elevated serum and urine iodine levels (2). While treatment with steroids is typical, we highlight a case where hemodialysis led to rapid clinical improvement in a very severe case of iododerma, suggesting utility in the ICU setting. 1. Tasker et al., 2019. Clin Exp Dermatol, 44: 844-860. 2. Runge et al, 2020. JAAD Case Reports, 6 (4): 319-322.
Abstract Malformations of or injuries to the developing lung are associated with perinatal morbidity and mortality with lifelong consequences for subsequent pulmonary health. One fetal exposure linked with poor health outcomes is chorioamnionitis, which impacts up to 25-40% of preterm births. Severe chorioamnionitis with prematurity is associated with significantly increased risk of pulmonary disease and secondary infections in childhood, suggesting that fetal inflammation may significantly alter developmental ontogeny of the lung. To test this hypothesis, we used intra-amniotic lipopolysaccharide (LPS, endotoxin) to generate experimental chorioamnionitis in prenatal Rhesus macaque ( Macaca mulatta ), a model which shares critical structural and temporal aspects of human lung development. Inflammatory injury directly disrupts the developing gas exchange surface of the primate lung, with extensive damage to alveolar structure, particularly the close association and coordinated differentiation of alveolar type 1 pneumocytes and specialized alveolar capillary endothelium. Single cell RNA sequencing analysis defined a multicellular alveolar signaling niche driving alveologenesis which was extensively disrupted by perinatal inflammation, leading to loss of gas exchange surface and alveolar simplification similar to that found in chronic lung disease of newborns. Blockade of IL1β and TNFα ameliorated endotoxin-induced inflammatory lung injury by blunting stromal response to inflammation and modulating innate immune activation in myeloid cells, restoring structural integrity and key signaling networks in the developing alveolus. These data provide new insight into the pathophysiology of developmental lung injury and suggest that modulating inflammation is a promising therapeutic approach to prevent fetal consequences of chorioamnionitis.
Perinatal inflammatory stress is associated with early life morbidity and lifelong consequences for pulmonary health. Chorioamnionitis, an inflammatory condition affecting the placenta and fluid surrounding the developing fetus, affects 25 to 40% of preterm births. Severe chorioamnionitis with preterm birth is associated with significantly increased risk of pulmonary disease and secondary infections in childhood, suggesting that fetal inflammation may markedly alter the development of the lung. Here, we used intra-amniotic lipopolysaccharide (LPS) challenge to induce experimental chorioamnionitis in a prenatal rhesus macaque ( Macaca mulatta ) model that mirrors structural and temporal aspects of human lung development. Inflammatory injury directly disrupted the developing gas exchange surface of the primate lung, with extensive damage to alveolar structure, particularly the close association and coordinated differentiation of alveolar type 1 pneumocytes and specialized alveolar capillary endothelium. Single-cell RNA sequencing analysis defined a multicellular alveolar signaling niche driving alveologenesis that was extensively disrupted by perinatal inflammation, leading to a loss of gas exchange surface and alveolar simplification, with notable resemblance to chronic lung disease in newborns. Blockade of the inflammatory cytokines interleukin-1β and tumor necrosis factor–α ameliorated LPS-induced inflammatory lung injury by blunting stromal responses to inflammation and modulating innate immune activation in myeloid cells, restoring structural integrity and key signaling networks in the developing alveolus. These data provide new insight into the pathophysiology of developmental lung injury and suggest that modulating inflammation is a promising therapeutic approach to prevent fetal consequences of chorioamnionitis.
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