No abstract

The toxic dose of rodenticides in children is extremely difficult to be determined because of the uncertain exposure history. We established and validated a method to identify the toxic dose in children of 4-hydroxycoumarin (TDCH). Items were selected by Delphi method and weighted by analytic hierarchy process. Toxic doses were classified into three categories: high dose (>24 points), medium (15-24) and low (<15). Sixty-five children with 4-hydroxycoumarin rodenticide intoxication were included in the study. There were 29(44.6%), 8(12.3%), 28(43.1%) cases in high, medium, and low dose respectively. Patients in high-dose were more likely to have intentionally attempted suicide (5/29, 17.2%) or had no definite history of ingestion (17/29, 58.6%), arrived at the hospital later than 24 h (26/29, 90%), been misdiagnosed initially (25/29, 86.2%), not treated by gastric lavage (27/29, 93.1%), and developed severe hemorrhage. While most patients in low-dose were younger than 6 years (26/28, 92.9%), all have experienced accidental exposure, arrived at the hospital, and received gastric lavage within 24 h, obtained a definite diagnosis, and be asymptomatic. Of 38 patients arrived at hospital within 48 h, patients a score48h ≥ 15 had higher incidence of coagulopathy (6/8, 75.0%) than patients with a score48h < 15 (3/30, 10.0%). Of all patients, 37 in the high and medium dose with a score ≥ 15 has higher incidence (35/37, 94.6%) of prolonged administration with vitamin K1 (≥1 month) than other 28 patients with a score < 15 (0/28, 0%). The TDCH system could not only be used in evaluating toxic doses and predicting coagulopathy in the early stage, but also helps to guide appropriate treatment. Patients with a score48h ≥ 15 were in the high bleeding risk category. And patients with a scores ≥ 15 required treatment with vitamin K1 for more than a month.

Rationale: Epstein-Barr virus (EBV) infection is associated with a variety of diseases and can involve multiple organs and systems, with complex and nonspecific clinical manifestations that are easily misdiagnosed. Chronic EBV infection with persistent erythema multiforme (EM) on the cheek as the main manifestation is very rare and has been reported rarely. Patient Concerns: This article reports a case of an adolescent female with chronic EBV infection who presented with chronic symmetrical erythema lesions on the face for 4 years, exacerbated with photophobia, lacrimation, Henoch-Schonlein purpura (HSP)-like rash, decline in granulocyte and erythrocyte lineages, hematuria, and proteinuria for 1 week. Diagnoses: The disease was initially misdiagnosed as systemic lupus erythematosus (SLE) and later confirmed as chronic EBV infection by skin biopsy. In the case, EBV infection not only caused chronic facial EM, but also induced acute HSP and purpura nephritis (hematuria and proteinuria type). Interventions: The child was treated with 1 week of glucocorticosteroids in adequate doses combined with acyclovir antiviral therapy and 3 sessions of hemoperfusion. After discharge, she took prednisone acetate (15 mg twice a day) orally for 1 month and then discontinued. Outcomes: She was discharged with her rash relieved and normal blood routine test and urine routine test. After 13 months of long-term follow-up, her facial erythema and hyperpigmentation became lighter, and there was no new rash on the whole body, and no abnormality in continuous monitoring of complete blood count and urine test. Lessons: This case suggests the need to be alert for chronic EBV infection in adolescent females with chronic facial EM rash and multiple organs and systems injury, in addition to connective tissue diseases such as SLE.

Background The TRIM8 gene encodes a protein that participates in various biological processes. TRIM8 variants can lead to early termination of protein translation, which can cause a rare disease called neuro-renal syndrome. This syndrome is characterized by epilepsy, psychomotor retardation, and focal segmental glomerulosclerosis. However, we found that some patients may not present the above typical triad, and the reason may be related to their variant sites. Case presentation We report a case of a 6-year-old boy with nephrotic-range proteinuria as the first prominent manifestation of TRIM8 variant. He had stage 3 chronic kidney disease at the time of presentation, specific facial features, and a neurogenic bladder. He had not experienced seizures previously. There were no apparent abnormalities in his growth, intelligence, or motor development. The results of whole exome sequencing showed a TRIM8 variant. Renal biopsy revealed focal segmental glomerulosclerosis and renal tubular cystic dilatation. He did not respond to hormone and angiotensin-converting enzyme inhibitor treatment; however, the symptoms of neurogenic bladder were relieved after treatment with Solifenacin. Conclusion In this case, renal disease was the prominent manifestation; the patient had no other obvious neurological symptoms except a neurogenic bladder. Notably, the variant site is the closest to the C-terminal to date. Based on the analysis of previously reported cases, we found that as the TRIM8 variant became closer to the C-terminal, the renal lesions became more prominent, and there were fewer neurologic lesions. Our findings provide a new understanding of neuro-renal syndrome caused by TRIM8 variant. Patients may only have kidney disease as a prominent manifestation. At the same time, we found that we should also pay attention to the eye lesions of these patients. Therefore, gene analysis is helpful in identifying the etiology and guiding the prognosis of patients with hormone-resistant proteinuria. We suggest that TRIM8 should be included in gene panels designed for the genetic evaluation of hormone-resistant proteinuria.