Retrospective analysis of clinical characteristics of and treatment strategies for patients with long-acting anticoagulant rodenticide poisoning.

OBJECTIVE: Long-acting anticoagulant rodenticide (LAAR) poisoning remains a serious public health problem. The aim of this study was to explore the clinical characteristics of different LAARs and a method of making a decision on the VK1 treatment course and the time to stop VK1 treatment safely. METHOD: This retrospective study compared the clinical characteristics of two LAARs poisoning patients and used multivariate regression method to explore the relationship between blood LAAR concentration and vitamin K1 dose/treatment time. RESULT: A total of 115 patients with LAAR poisoning were included in this study after screening. Of these, 50 patients attempted to commit suicide. The median LAAR concentration of the patients at admission was 409 (157-1174) ng/mL, and the VK1 treatment duration was 14 (8-34) days. The total VK1 treatment time in patients with LAAR poisoning was positively correlated with admission LAAR concentration. During the maintenance treatment period, the VK1 dosage was positively correlated with blood LAAR concentration. CONCLUSION: Low dose of VK1 during the maintenance period is indicative of the blood LAAR concentration being relatively low. This provides a basis for judging the LAAR content in the body during the maintenance treatment period.

Epidemiology, clinical presentation, treatment, and follow-up of chronic mercury poisoning in China: a retrospective analysis.

BACKGROUND: There are no reports on the incidence of chronic mercury poisoning in a large population in China. This study investigated the epidemiology, clinical manifestations, treatment, and follow-up of Chinese patients with chronic mercury poisoning. METHODS: Data for 288 mercury poisoning patients were collected at our hospital from July 2014 to September 2019, including sex, age, admission time, blood mercury content, urine mercury content, creatinine, urinary mercury/creatinine ratio, 24-h urinary protein levels, electromyography (EMG) findings, renal biopsy, and follow-up. Patient characteristics were evaluated by statistical and correlation analyses. RESULTS: First, mercury poisoning in China mainly occurred through occupational exposure and the inappropriate use of mercury-containing cosmetics and Chinese folk remedies (CFRs). Second, the most common symptoms were nervous system (50.3 %), kidney (16.4 %) and breathing (8.0 %). Mercury poisoning-induced Nephrotic syndrome (NS) and peripheral neuropathy are common long-term complications. The complications of occupational and cosmetics-induced mercury poisoning are consistent with international belief. However, the NS caused by CFRs is mainly membranous nephropathy and the probability of peripheral neuropathy caused by CFRs is higher than other pathogens. Third, follow-up data shows that 13 patients with EMG-confirmed neurological injury, 10 showed full recovery after 38.50 ± 8.03 months. Furthermore, among 18 patients with NS, 15 had normal urine protein and serum albumin levels after 22.67 ± 10.26 months. CONCLUSIONS: Regulation of skin-lightening cosmetic products, safety surveillance of CFRs, and prevention and control of occupational exposure must be improved to decrease the incidence of mercury poisoning in China.

[Mutation analysis of the pathogenic gene in a Chinese family with hereditary hemochromatosis].

Hereditary hemochromatosis (HHC) is a rare autosomal recessive disorder. We recruited a consanguineous Chinese family including the proband with HHC and other four members without HHC. Using whole-exome sequencing, we identified two homozygous mutations (c.G18C [p.Q6H] and c.GC962_963AA [p.C321X]) in the hemojuvelin gene (HJV) in the proband with HHC. No mutation was found in other four previously identified HHC related genes, HAMP, TFR2, FPN and HFE. The functional impact of p.Q6H mutation is weak whereas p.C321X, a premature termination mutation, results in a truncated HJV protein, which lacks the glycosylphosphatidylinositol (GPI) anchor domain. In addition to the mutations in HJV, other 12 homozygous mutations were identified in this patient. However, none of these mutations showed strong damaging impact and the mutated genes are not related to iron metabolism. Our in-house data further demonstrated that p.C321X is absent in the general Chinese population, suggesting that the homozygous mutation p.C321X in HJV is causative in the patient with HHC. Accordingly, all of the four members without HHC from the same family carried wild-type alleles or heterozygous mutations, but not the homozygous mutation in this site. Thus, we found for the first time that the homozygous mutation p.C321X in HJV can result in HHC, which will help genetic diagnosis and prenatal counseling for HHC.