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BACKGROUND: Hyponatremia is a common clinical electrolyte disorder. However, the association between hyponatremia and acute hypothyroidism is unclear. Acute hypothyroidism is usually seen in patients who undergo preparation for radioactive iodine therapy. AIM: To analyze the incidence and influencing factors of hyponatremia in a condition of iatrogenic acute hypothyroidism in patients with differentiated thyroid cancer (DTC) before 131I treatment. METHODS: The study group consisted of 903 DTC patients who received 131I treatment. The clinical data before and after surgery, as well as on the day of 131I treatment were analyzed. According to the blood sodium level before 131I treatment, patients were divided into the non-hyponatremia group and hyponatremia group. Correlations between serum sodium levels before 131I treatment and baseline data were analyzed. Univariate analysis and binary logistic regression were performed to identify the influencing factors of hyponatremia. RESULTS: A total of 903 patients with DTC, including 283 (31.3%) males and 620 (68.7%) females, with an average age of 43.8 ± 12.7 years, were included in this study. The serum sodium levels before surgery and 131I treatment were 141.3 ± 2.3 and 140.5 ± 2.1 mmol/L, respectively (P = 0.001). However, the serum sodium levels in males and females before 131I treatment were lower than those before surgery. Patients aged more than 60 years and less than 60 years also showed decreased serum sodium levels before 131I treatment. In addition, the estimated glomerular filtration rate (eGFR) in males and females decreased before 131I treatment compared with those before surgery (P = 0.001). Moreover, eGFR in patients over 60 years and under 60 years decreased before 131I treatment, when compared with that before surgery. There were no significant differences in serum potassium, calcium, albumin, hemoglobin, and blood glucose in patients before surgery and 131I treatment (P > 0.05). Among the 903 patients, 23 (2.5%) were diagnosed with hyponatremia before 131I treatment, including 21 cases (91.3%) of mild hyponatremia and 2 cases (8.7%) of moderate hyponatremia. Clinical data showed that patients with mild hyponatremia had no specific clinical manifestations, while moderate hyponatremia cases were mainly characterized by fatigue and dizziness, which were similar to neurological symptoms caused by hypothyroidism and were difficult to distinguish. Correlation analysis showed a correlation between serum sodium before 131I treatment and the preoperative level (r = 0.395, P = 0.001). There was no significant correlation between blood sodium and thyroid-stimulating hormone (TSH) levels and urine iodine before 131I treatment (r = 0.045, P = 0.174; r = 0.013, P = 0.697). Univariate analysis showed that there were significant differences in age, sex, history of diuretic use, distant metastasis, preoperative blood sodium, blood urea nitrogen (BUN), eGFR, TSH and urinary iodine between the two groups (all P < 0.05). Logistic regression analysis showed that factors such as history of diuretic use, distant metastases, preoperative sodium and BUN were all influencing factors of hyponatremia. The Hosmer and Lemeshow test (c2 = 2.841, P = 0.944) suggested a high fit of the model. Omnibus tests of model coefficients indicated the overall significance of the model in this fitted model (P < 0.05). Preoperative serum sodium was a significant factor associated with pre-131I therapy hyponatremia (OR = 0.763; 95%CI: 0.627-0.928; P = 0.007). CONCLUSION: The incidence of hyponatremia induced by 131I treatment preparation was not high. Preparation for radioactive iodine therapy was not a risk factor for the development of hyponatremia in thyroid cancer patients.
RESUMO
OBJECTIVE: to investigate the effects of endostar, a recombined humanized endostatin, on the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenograft in mice. METHODS: lewis lung carcinoma (LLC) xenograft were established in C57 mice by intravenous transplantation of 1 × 10(6) cells. Then tumor-bearing mice were assigned into two groups: control group received caudal vein injections of 0.2 ml of 0.9% sodium chloride for 15 days, and treatment group received 500 µg endostar daily. Six weeks after LLC cell injection mice were sacrificed, and then tumor numbers and size were recorded. The expression of vascular endothelial growth factor-c (VEGF-C) and microlymphatic vessel density (MLVD) were observed by immunohistochemical staining. RESULTS: tumor number and size of control group were significantly higher than those of treatment group. The microlymphatic vessel density (MLVD) was 5.7 ± 1.6 in the treatment group, which was markedly lower than in the control mice (7.8 ± 1.6). Two lymph node metastases were observed in treatment group, and eight in control group. Lymphatic metastases were more frequent in control group than in treatment group. Expression of VEGF-C in control group was significantly higher than that in treatment group. CONCLUSION: endostar significantly inhibits the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenografts, and the inhibitory effect is due to its ability to regulate the expression of VEGF-C of tumors in part.