Objective:To analyze the clinical data of primary hyperthyroidism patients complicated with thyroid microcarcinoma, and to guide clinical diagnosis and treatment.Methods:From January 2013 to March 2019, the clinical data of 42 cases of hyperthyroidism with thyroid microcarcinoma(study group) and 410 cases of thyroid microcarcinoma without hyperthyroidism(control group) who underwent surgical treatment in the People's Hospital Affiliated to Hubei University of Medicine were retrospectively analyzed.The epidemiological characteristics, clinical diagnosis and treatment, clinical stage, B-ultrasound characteristics, thyroid function and antibody, pathological data and prognosis of the two groups were compared.Results:In study group and control group, the proportion of microcalcification detected by B-ultrasonography was 61.9%(26/42) and 33.4%(137/410), respectively, the difference was statistically significant between the two groups(χ 2=13.411, P<0.05). In study group and control group, 47.62%(20/42) and 69.02%(283/410) of multifocal nodules were detected by B-ultrasound, the difference was statistically significant between the two groups(χ 2=7.899, P<0.05). The diagnostic rates of intraoperative frozen-section examination of the study group and the control group were 61.9%(26/42) and 66.1%(271/410), respectively, the difference was statistically significant between the two groups(χ 2=4.460, P<0.05). The lymph node metastasis rates of the study group and the control group were 9.5%(4/42) and 26.8%(110/410), respectively, the difference was statistically significant between the two groups(χ 2=6.049, P<0.05). The middle follow-up period was 37 months(1 month to 74 months). There was no recurrence of thyroid cancer in the study group, 2 cases with recurrence of hyperthyroidism after operation, and 3 cases with recurrence in the control group, with secondary surgical resection.There were no deaths in the two groups during follow-up. Conclusion:Thyroid cancer should be paid attention to when hyperthyroidism combined with nodules, but the prognosis of hyperthyroidism with microcarcinoma is better.The operation method tends to be bilateral lobectomy, which can prevent the recurrence of hyperthyroidism.In order to reduce the chance of parathyroid gland and recurrent laryngeal nerve injury, there may be no need of preventive lymph node dissection in area VI.

Aristolochic acid (AA), extracted from Aristolochiaceae plants, plays an essential role in traditional herbal medicines and is used for different diseases. However, AA has been found to be nephrotoxic and is known to cause aristolochic acid nephropathy (AAN).AA-induced acute kidney injury (AKI) is a syndrome in AAN with a high morbidity that manifests mitochondrial damage as a key part of its pathological progression. Melatonin primarily serves as a mitochondria-targeted antioxidant. However, its mitochondrial protective role in AA-induced AKI is barely reported. In this study, mice were administrated 2.5 mg/kg AA to induce AKI. Melatonin reduced the increase in Upro and Scr and attenuated the necrosis and atrophy of renal proximal tubules in mice exposed to AA. Melatonin suppressed ROS generation, MDA levels and iNOS expression and increased SOD activities in vivo and in vitro. Intriguingly, the in vivo study revealed that melatonin decreased mitochondrial fragmentation in renal proximal tubular cells and increased ATP levels in kidney tissues in response to AA. In vitro, melatonin restored the mitochondrial membrane potential (MMP) in NRK-52E and HK-2 cells and led to an elevation in ATP levels. Confocal immunofluorescence data showed that puncta containing Mito-tracker and GFP-LC3A/B were reduced, thereby impeding the mitophagy of tubular epithelial cells. Furthermore, melatonin decreased LC3A/B-II expression and increased p62 expression. The apoptosis of tubular epithelial cells induced by AA was decreased. Therefore, our findings revealed that melatonin could prevent AA-induced AKI by attenuating mitochondrial damage, which may provide a potential therapeutic method for renal AA toxicity.