Propofol-induced sleep ameliorates cognition impairment in sleep-deprived rats.

PURPOSE: Propofol has been shown to clear sleep debt in rats after sleep deprivation (SD). We examined whether or not propofol-assisted sleep can restore cognitive function in SD rats and explored the possible mechanisms. METHODS: A sleep deprivation model was established by housing 9 to 12 week-old rats to a multiplatform water tank for 96 h. Model rats were then intraperitoneally injected with different concentrations of propofol or 10% fat emulsion (vehicle control). All treatment groups were examined for spatial learning and memory ability in the Morris water maze (MWM). After euthanasia, morphological changes in the hippocampus, hippocampal neurons, and mitochondria were examined by hematoxylin-eosin staining and transmission electron microscopy. Serum and hippocampal levels of IL-1ß, TNF-α, and hippocampal concentrations of ATP and Cyt-c were measured by ELISA (enzyme-linked immunosorbent assay). Immunohistochemistry and Western blotting were performed to assess hippocampal expression of Bcl-2, Bax, and cleaved caspase-3. RESULTS: Results showed that escape latencies in MWM training trials were significantly shorter and target crossings in the memory probe trial significantly greater in propofol-treated SD model rats compared to vehicle-treated SD rats. Propofol also reduced the number of apoptotic bodies in the hippocampal CA1 region. Sleep deprivation reduced IL-1ß and ATP in hippocampus while increasing TNF-α and Cyt-c, and propofol treatment reversed all these changes. There was no significant difference in Bcl-2 expression between propofol- and vehicle-treated SD rats, but pro-apoptotic Bax and cleaved caspase-3 expression levels were significantly reduced by propofol in SD rats. CONCLUSIONS: Propofol-assisted sleep restored cognitive function in SD rats possibly by attenuating mitochondria-mediated neuronal apoptosis in the hippocampus.

Transfer of massive mitochondria from astrocytes reduce propofol neurotoxicity.

Studies have shown that propofol-induced neurotoxicity is mediated by disruption of mitochondrial fission and fusion, leading to an imbalance in energy supply for developing neurons. Healthy mitochondria released from astrocytes migrate to compromised neurons to mitigate propofol-induced neurotoxicity, yet the precise mechanisms involved require further clarification. In our investigation, primary neurons were incubated with propofol, which decreased ATP synthesis and mitochondrial membrane potential, increased ROS generation and neuronal apoptosis. Notably, astrocytes did not respond to the deleterious effects of propofol. The culture medium of neurons or astrocytes incubated with propofol was collected. It was found that mitochondrial ratio was decreased and mitochondrial function was impaired. Non-contact co-culture of neuro-astrocytes facilitated transcellular mitochondrial transfer in both physiological and propofol interventions, but failed to reverse propofol-induced neurotoxicity. The more pronounced damage to neuronal mitochondria induced by propofol compared to that in astrocytes alludes to secondary injury. Damaged neurons incubated with large, functional extracellular mitochondria derived from astrocytes demonstrates transfer of mitochondria to neurons, effectively reversing propofol-induced neurotoxicity. This discovery presents a novel mitochondrial transfer of neuro-astrocytes crosstalk that contributes to neuroprotection and neurological recovery in neurotoxicity.

[Relationship between maternal milk and serum thyroid hormones in patients with thyroid related diseases].

OBJECTIVE: To explore the relationship between maternal milk and serum thyroid hormones in patients with thyroid-related diseases. METHODS: Serum and breast milk samples were collected from 56 breastfeeding mothers. Milk and serum free triiodothyronine (FT3), free thyroxine (FT4), triiodothyronine(T3), thyroxine (T4), and thyrotrophin (TSH) were determined, and T3/T4 was calculated. Using the serum thyroid hormones as the independent variables and milk thyroid hormones as the dependent variables, we performed linear regression analysis. RESULTS: The milk FT3, FT4, T3, T4, TSH, and T3/T4 were (2.30 ± 0.82) pg/ml ,(0.45 ± 0.26) ng/dl, (0.35 ± 0.20) ng/ml, (2.96 ± 1.55) Μg/dl, (0.12 ± 0.08) ΜU/ml, and 0.12 ± 0.04, respectively. Milk FT3 (r = 0.778, P = 0.000), T3 (r = 0.603, P = 0.000), T4 (r = 0.485, P = 0.004), and TSH (r = 0.605, P = 0.000) concentrations were positively correlated with those in serum. CONCLUSION: Thyroid hormones are present in human milk and are positively correlated with those in serum.

Ultrasonographic Assessment of Gastric Volume in Fasted Patients Undergoing Gastrointestinal Endoscopy Under Sedation.

Purpose: In this prospective observational study, an ultrasonographic measurement of antral cross-sectional area (ACSA) was conducted to evaluate the gastric content and volume as well as to identify high-risk stomach in non-pregnant adult surgical patients adhering to preanesthetic fasting guidelines. Patients and Methods: Fasted patients undergoing gastrointestinal endoscopy under sedation were included. Ultrasonographic measurements of ACSA were conducted in both semi-recumbent and right lateral decubitus positions before endoscopic procedures. Gastroscopy was employed to guide the measurement of suctioned gastric volume (GV). Ultrasonography was performed to assess gastric contents and identify patients with high-risk stomach. The relationship between ACSA and suctioned GV was also evaluated. Results: ACSA was evaluated in 736 out of 782 patients. A significant positive correlation was discovered between ACSA in the right lateral decubitus position and suctioned GV, which was more reliable than in the semi-recumbent position. To analyze high-risk stomach with a GV > 100 mL, the cutoff value of ACSA in the right lateral decubitus was found to be 7.5 cm2, with the AUC, sensitivity and specificity of 0.80 (95% CI, 0.76-0.82; P<0.001), 82.4% and 67.3%, respectively. A novel mathematical model based on ACSA to estimate GV in non-pregnant fasted adults was presented. Conclusion: Ultrasonographic measurement of ACSA can assist anesthesiologists in estimating the risk of pulmonary aspiration of gastric contents during general anesthesia and sedation.

Magnetic resonance imaging findings of pituitary hyperplasia due to primary hypothyroidism.

OBJECTIVE: To explore the clinical and magnetic resonance imaging (MRI) findings of pituitary hyperplasia due to primary hypothyroidism. METHOD: The clinical presentations, laboratory examinations, and MRI findings of 11 patients with pituitary hyperplasia secondary to primary hypothyroidism diagnosed at our hospitals from the beginning of 2008 to the end of 2011 were retrospectively reviewed. RESULTS: The clinical manifestations in 11 patients included growth arrest(7/8), mental retardation (6/8), cold intolerance and fatigue(6/11), slightly increased body weight (6/11), galactorrhea (3/11), paramenia (8/9), precocious puberty companying vaginal bleeding (2/2),and blurry vision (3/11). Laboratory investigations revealed grossly increased thyroid stimulating hormone, decreased thyroxine, and slightly elevated prolactin levels in all cases. Thyroid antibody was positive in six cases. On MRI, pituitary mass were detected a large intrasellar with/without suprasellar extension in all patients,showing the characteristic of symmetric enlargement. Spherical shape was viewed in 5 cases,with the height of (12.22 ± 3.12)mm. In the other 6 cases, the pituitary mass with the shape of calabash extended superiorly to suprasellar area, with a height of(18.95 ± 2.23)mm. The signal of pituitary mass was isointense to grey matter both on T1 weighted imaging and T2 weighted imaging. Bright short T1 signal in posterior lobe of pituitary was visible. Pituitary stalk was detected only in 4 cases from MRI without dislocation, while the width of pituitary stalk was within the normal limit. CONCLUSIONS: Pituitary hyperplasia should be considered when homogenous enlargement of the pituitary gland is found on MRI. The integration of MRI findings, clinical manifestations, and laboratory findings is helpful for the proper identification of the primary endocrine disease and thus avoid misdiagnosis.

Protective Effects of Remimazolam on Cerebral Ischemia/Reperfusion Injury in Rats by Inhibiting of NLRP3 Inflammasome-Dependent Pyroptosis.

INTRODUCTION: Remimazolam is a novel benzodiazepine γ-aminobutyric acid A (GABAa) receptor agonist used for sedation and the induction as well as maintenance of general anesthesia. Previous research proved that anesthetic agents acting on GABAa receptor, such as thiopentone, propofol and midazolam, have protective actions for cerebral ischemia/reperfusion (I/R) injury. We here probed into remimazolam for its protective effect and potential mechanism of action against cerebral I/R injury. MATERIAL AND METHODS: A rat model of middle cerebral artery occlusion (MCAO) with focal transient cerebral I/R injury was established and was given tail vein injection of gradient remimazolam (5, 10, 20 mg/kg) after 2 h of ischemia. Following 24 h of reperfusion, neurological function, brain infarct volume, morphology of cerebral cortical neurons, and expressions of corticocerebral NLRP3, ASC, caspase-1, GSDMD, IL-1ß and IL-18 were evaluated. RESULTS: The results showed that remimazolam could effectively improve the neurological dysfunction, reduce the infarct volume and alleviate the damage of cortical neurons after I/R injury. Notably, the expression of NLRP3 inflammasome pathway was down-regulated, suggesting that remimazolam exerted protective actions on I/R injury by suppressing pyroptosis with decreased expression and release of inflammatory factors, and the involvement of the NLRP3 inflammasome pathway might be the core during that process. Overall, our results indicate that NLRP3 inflammation is a promising target. CONCLUSION: Based on this mechanism, remimazolam may be one of the ideal anesthetic drugs for patients with ischemic stroke.

Relationship between Coronary VH-IVUS Plaque Characteristics and CTRP9, SAA, and Hcy in Patients with Coronary Heart Disease.

Coronary heart disease is a common disease threatening human health. In recent years, the incidence of coronary heart disease in China has only increased. It is the most common type of organ disease caused by coronary atherosclerosis, which is observed in the aorta, carotid artery, and femoral artery. The main clinical treatments for coronary heart disease include coronary artery bypass grafting and drug treatment. To investigate the relationship of serum adipocytokine C1q/tumor necrosis factor-related protein 9 (CTRP9), amyloid A (SAA), and plasma homocysteine (Hcy) with coronary artery plaque characteristics in patients with coronary heart disease. Overall, 143 patients with coronary heart disease admitted to our hospital are selected as research participants. The proportion of plaque necrosis core volume is higher in group A than in group B, and the differences are statistically significant (P < 0.05). In group A, necrotic core volume percentage is negatively correlated with CTRP9 levels and positively correlated with SAA and Hcy levels (P < 0.05). Logistic regression analysis revealed that increased systolic blood pressure, increased number of coronary artery lesions, decreased CTRP9 levels, and increased Hcy levels are independent risk factors for thin fibrous cap atherosclerosis in patients with coronary heart disease (P < 0.05). Decreased CTRP9 levels and increased Hcy levels are independent risk factors for coronary heart disease patients with thin fibrous cap atherosclerosis.

[Thyroid-stimulating hormone pituitary adenomas: clinical characteristics, diagnosis and treatment].

OBJECTIVE: To study the clinical characteristics, diagnosis and surgical effects of thyroid-stimulating hormone pituitary adenomas (TSH-omas). METHODS: The clinical data of 19 patients (14 female and 5 male) with TSH-omas were analyzed retrospectively in this study from January 2001 to December 2008. The patients ranged from 20 to 70 years old (average 40.5 years old) and had disease histories from 1 to 228 months (average 55 months). Among these patients, 15 of them complained of thyrotoxicosis symptoms, while the other 4 patients' symptoms were associated with headache and/or visual disturbance caused by the tumor mass effect. Initially, 12 of the 15 patients with thyrotoxicosis symptoms were misdiagnosed with Grave's disease. As a result 2 of them received (131) Iodine, and one received subtotal thyroidectomy. All of these patients underwent transsphenoidal microsurgery. RESULTS: Average follow-up period was 3.6 years (6 months-7 years). Pathological analysis of the surgical specimen showed pituitary adenoma in all patients, immunohistochemistry were positive for TSH in 17 cases, negative for TSH in 2, positive for growth hormone in 2, positive for prolactin in 1, and positive for adrenocorticotrophic hormone in 1. Postoperative MRI revealed that the tumors in 15 patients were removed totally, though 4 patients still had residual tumors. The thyroid hormone level tests suggested that 13 patients could be considered normal 3 months after their tumors were removed, though 2 of patients with normal postoperative MRI and thyroid hormones showed increased levels of TSH. For these 2 patients, tumors did not recur and their thyroid hormone levels returned to normal after pituitary radiotherapy. The cure rate was 11/19 after surgery and 13/19 after surgery plus pituitary radiotherapy. CONCLUSIONS: The screening test for hyperthyroidism patients with high TSH levels is a key point to improve the accuracy rate in early diagnoses of TSH-omas. The transsphenoidal microsurgery is first choice to treat TSH-omas, while pituitary radiotherapy and somatostatin analogs are beneficially adjunctive therapies.

Propofol protects hippocampal neurons in sleep-deprived rats by inhibiting mitophagy and autophagy.

BACKGROUND: Sleep deprivation (SD) causes a disturbance in the cognitive function of rats. While propofol has a powerful sedative and hypnotic effect and is an antioxidant, its effect on the cognitive function of rats following SD remains unknown. The purpose of this study was to explore the protective effects of propofol on excessive autophagy and mitophagy in the hippocampus of rats after SD. METHODS: Adult male rats were intraperitoneally injected with 30 mg/kg of propofol after 96 hours of SD. Then we evaluated the effect of propofol on the cognitive function of sleep deprived rats by the Morris water maze. Transmission electron microscopy, Western blotting, PCR, immunohistochemistry, autophagy enhancer and autophagy inhibitor were used to study the effect of propofol on hippocampal neurons of rat with excessive autophagy and mitophagy. RESULTS: The behavioral experimental results of the Morris water maze showed that propofol improved the learning and memory ability of sleep-deprived rats. The expression of Beclin1, PINK1, parkin, p62, and LC3 protein increased significantly after sleep deprivation. While the intervention of propofol could significantly reduce the expression of these proteins, rapamycin treatment eliminated this effect. CONCLUSIONS: Our findings showed that propofol could reduce the impairment of learning and memory in sleep-deprived rats by inhibiting excessive autophagy and mitophagy in hippocampal neurons. This strategy may provide an application basis for the clinical use of propofol in patients with chronic insomnia.

Clinical and pathological features of Riedel's thyroiditis.

OBJECTIVE: To evaluate the clinical and pathological features of Riedel's thyroiditis (RT), and current diagnostic and treatment methods for that disease. METHODS: Five RT cases identified by surgery and pathological examinations at Peking Union Medical College Hospital from 1985 to 2009 were analyzed and compared with the cases reported in the literature in terms of clinical and pathological features. Immunohistochemical staining of kappa and lambda light chains was carried out for RT tissues from all the five patients. RESULTS: All the five cases were females, aged 45-55 years. Elevation of serum thyroid autoantibodies was found in only one patient, who had longer disease duration than the others. Pathological examination revealed invasive fibrosclerosis of the thyroid follicles, thyroid capsule, and the surrounding tissues. In RT tissues, the number of cells containing lambda chains was a little higher than those containing kappa chains. CONCLUSIONS: RT is a rare disease which might be more common in middle-aged females than in other populations. Pathological features include the destruction of thyroid follicle, extension into surrounding tissues by inflammatory cells and fibrous tissues. Immunohistochemical staining of kappa and lambda chains could help diagnose RT.

Dose-dependent neurotoxicity caused by the addition of perineural dexmedetomidine to ropivacaine for continuous femoral nerve block in rabbits.

OBJECTIVE: This study was designed to evaluate the neurotoxicity of dexmedetomidine combined with ropivacaine for continuous femoral nerve block in rabbits. METHODS: Thirty New Zealand rabbits were randomly divided into 5 groups of 6 rabbits each and received a continuous femoral nerve block with saline; 0.25% ropivacaine; or 1, 2, or 3 µg/mL of dexmedetomidine added to 0.25% ropivacaine (Groups A-E, respectively). Sensory and motor function was assessed after the nerve block. The rabbits were anesthetized and killed after 48 hours of a continuous femoral nerve block, and the femoral nerves were removed for light and electron microscopy analyses. RESULTS: The behavior scores were highest in Group A at 2 and 6 hours after injection. The scores were higher in Groups B and C than in Groups D and E at these same time points. All groups showed normal pathological tissues in the femoral nerves under optical microscopy. Under electron microscopy, histological abnormalities were observed only in Group E; none of the other groups exhibited pathological abnormalities. Quantitative analysis of the myelin sheath area revealed no significant difference in the axonal area, total area of the myelin sheath, or ratio of the total axonal area to the total area of the myelin sheath in all groups. CONCLUSION: The lowest doses of dexmedetomidine (1 and 2 µg/mL) combined with 0.25% ropivacaine for continuous femoral nerve block resulted in no neurotoxic lesions, but the higher dose (3 µg/mL) resulted in neurotoxic lesions in this rabbit experimental model.

[Octreotide in the diagnosis and treatment of pituitary thyrotropin-secreting adenoma].

OBJECTIVE: To evaluate the efficacy of octreotide in the diagnosis and treatment of pituitary thyrotropin (TSH)-secreting adenoma. METHODS: A 34-year man presented with central hyperthyroidism and pituitary TSH-secreting macroadenoma was reported. (99 m)Tc-octreotide scan and magnetic resonance imaging were completed to make the location diagnosis of the adenoma. Octreotide in 0.1 mg dose was subcutaneously injected every 8 hours for 10 days. Serum TSH level and tumor size were observed and trans-sphenoidal adenoma resection was completed. RESULTS: Pituitary TSH-secreting adenoma displayed positive sign in (99 m)Tc-octreotide scan. Antithyroid drug was of no help in depressing thyroid function to normal. However, octreotide treatment could revert thyroid function to normal rapidly. A significant shrinkage of tumor mass from 3.0 cm x 2.0 cm x 2.5 cm to 2.0 cm x 2.0 cm x 1.5 cm was observed and a shrinkage of thyroid gland from III to II also observed. CONCLUSIONS: (99 m)Tc-octreotide scan is one of the useful tools for location diagnosis of TSH-secreting adenoma. Octreotide can effectively control central hyperthyroid and make tumor shrink, and it can be a satisfactory method of preoperative preparation for TSH-secreting adenoma.

[A family with familial dysalbuminaemic hyperthyroxinaemia].

OBJECTIVE: To report a family of familial dysalbuminaemic hyperthyroxinaemia(FDH). METHODS: Four members, including the female proband, mother, daughter and brother, went through the measurement of thyroid hormone and thyroid-stimulating hormone (TSH). Electrophoretic analysis of the patient's serum proteins was carried out after the patient's serum being incubated with fluorescein isothiocyanate (FITC) labeled thyroxine(T4), The point mutation of Alb gene was determined in all members. RESULTS: The measurements of thyroid hormane and TSH showed that in three members (the proband, her mother and her daughter), the total thyroxine(TT4) serum level was high, the total triiodothyronine(TT3), FT4, FT3 and TSH serum levels were normal. And the enhanced albumin binding of fluorescenced T4 by electrophoresis showed a mutation transition 653 G-->A on DNA coding region of albumin. But in the proband's brother, the thyroid function and the results of electrophoresis of thyroxine-binding protein and determination of albumin gene were normal. CONCLUSION: A family with FDH in China is firstly reported here, a mutation at albumin gene DNA coding region 653G-->A causing enhanced albumin binding of T4 results in high T4 level.

[Effects of maternal hyperthyroidism and antithyroid drug therapy on congenital malformation of newborn infants].

OBJECTIVE: To evaluate the relationship between the incidence of congenital malformations of newborns and maternal hyperthyroidism with antithyroid drug (ATD) therapy during pregnancy. METHODS: The clinical data of 100 cases of pregnant women with hyperthyroidism and their 101 offsprings born in Peking Union Medical College Hospital during 1983-2003 were analyzed retrospectively. According to the maternal thyroid function, and antithyroid drugs taken during the first trimester of pregnancy, subjects were divided into different groups. The incidence of congenital malformations of newborns and risk factors, especially the effects of maternal hyperthyroidism with antithyroid drug therapy were analysed. RESULTS: The prevalence of congenital malformation in infants born to mothers who had hyperthyroidism during pregnancy (6.9%, 7/101) was significantly higher than that of all the infants born in the same hospital during the same period (0.9%, 212/22 765, P < 0.01). The difference of the incidence of malformed infants born to mothers with hyperthyroidism (9.6%, 5/52) or euthyroidism (4.1%, 2/49) during the first trimester was not significant (P > 0.05). The incidence of malformed infants whose mothers received methimazole (MMI; 41.7%, 5/12) was significantly higher than that of mothers treated with propylthiouracil (PTU) (3.6%, 1/28) and without ATDs (1.6%, 1/61), respectively (P < 0.01). The Loglinear model analyses showed that mothers receiving MMI during the first trimester of pregnancy was independent risk factor for the increased incidence of malformation of their infants (L.R. square = 15.668, P = 0.0003). CONCLUSIONS: The risk of congenital malformation in infants whose mothers take MMI during the first trimester may be increased. Therefore, we suggest that MMI should not be used as a choice of drug in treatment of pregnant women with hyperthyroidism.

[Effects of maternal hyperthyroidism and antithyroid drug therapy on thyroid function of newborn infants].

OBJECTIVE: To evaluate the relationship between the incidence of abnormal thyroid function of newborns and maternal hyperthyroidism with antithyroid drug therapy. METHOD: The clinical data of 35 neonates born to mothers with hyperthyroidism from 1983 to 2003 in Peking Union Medical College Hospital were retrospectively analyzed. According to the maternal thyroid function and the antithyroid drugs taken during pregnancy, subjects were divided into different groups. RESULTS: The proportion of abnormal thyroid function in newborn was 48.6% (17/35). The prevalences of primary hypothyroidism, subclinical hypothyroidism, hypothyroxinemia, and central hypothyroidism were 29.4%, 29.4%, 35.3%, and 5.9%, respectively. The incidence of abnormal thyroid function of neonates whose mothers did not take the antithyroid drugs (ATDs) until the third trimester of pregnancy was significantly higher than those without and with ATDs during the first or second trimester (P < 0.01). The incidence of abnormal thyroid function significantly increased in premature neonates, neonates whose mothers with modest or heavy pregnant hypertension, or neonates whose core serum thyroid-stimulating hormone or serum anti-thyroid peroxidase antibodies levels were abnormal. CONCLUSION: The risk of abnormal thyroid function of infants whose hyperthyroid mothers did not take ATDs until the third trimester of pregnancy may be increased. Prompt diagnosis and appropriate treatment of hyperthyroidism in pregnant women are essential for the prevention of neonatal thyroid functional abnormality.

[The clinical characteristics of symptomatic propylthiouracil-induced hepatic injury in patients with hyperthyroidism].

OBJECTIVE: To study the clinical characteristics and factors of symptomatic propylthiouracil (PTU)-induced hepatic injury in patients with hyperthyroidism. METHODS: A retrospective study of the patients diagnosed with symptomatic PTU-induced hepatic injury, admitted to Peking Union Medical College (PUMC) Hospital from January 1993 to December 2002, were carried out with regard to clinical characteristics, laboratory findings and management. In addition, a comparative study was carried out in hyperthyroidism with symptomatic, asymptomatic and without PTU-induced hepatic injury at the same time. Symptomatic PTU induced hepatic injury was defined as the development of hepatitis symptoms or jaundice with at least 3-times elevation of liver function test without other causes. RESULTS: Nine hundred fourteen patients were admitted to PUMC Hospital from January 1993 to December 2002. Clinically overt symptomatic hepatic injury developed in twelve patients [1.3%, age (30 +/- 9) yr, male:female ratio, 1:11] between 7 and 77days after PTU administration. Abdominal distention and fatigue developed in all patients. Serum level of ALT and total bilirubin (TBil) increased to (531.7 +/- 352.0) 113 - 1425 U/L and 67.6 (17.1 - 567.7) micro mol/L, respectively. Prothrombin time prolonged in three cases and plasma ammonia elevated in one case. The types of hepatic injury were hepatocellular in eight, cholestatic in one and mixed in two. None resulted from viral hepatitis and autoimmune hepatitis. There was significant difference in history of side effects of antithyroid agents, PTU dose and abnormal ratio of serum ALT among patients with symptomatic, asymptomatic and without hepatic injury (P < 0.05). However, there were no statistic differences in age, sex, serum levels of T(4), T(3), and increased thyroglobulin antibody, thyroid peroxidase antibody and thyrotrophin receptor antibody at initial diagnosis. The liver function test normalized in all patients from 14 to 140 days after the PTU withdrawal. CONCLUSIONS: Symptomatic hepatic injury usually develops with PTU administration in the first few months, though it is unusual. It may be difficult to predict its development and the patient should be monitored for the liver function in the early stage of PTU administration.

[Effect of universal salt iodization on the dosage of antithyroid drug].

OBJECTIVE: To investigate the effect of universal salt iodization (USI) on antithyroid drug. METHODS: One hundred and one patients with untreated hyperthyroidism were randomly divided into two sex and age-matched groups: group A (n = 45, consuming pure salt without iodine) and group B (n = 56, consuming iodated salt). The same dosage of 300 mg propylthiouracil (PTU) was given to both groups at beginning, the serum TT4. TT3, FT4, FT3, and TSH were measured before and 1, 2, 3, 6 months after PTU treatment, when the serum TT4, TT3, FT4. FT3, and TSH were back to the normal ranges, the dosage of PTU was decreased to maintain the normal levels of serum thyroid hormones. RESULTS: The urine iodine and serum thyroid hormone levels were not significantly different between group A and group B before the treatment (P > 0.05). The urine iodine of group A was significant lower 2 - 3 months after the treatment (148.4 micro g/L) than before the treatment (213.4 micro g/L, P < 0.01). There were not significant differences in serum TT4, TT3, FT4, and FT3 between group A and B before the treatment (all P > 0.05). One month after the treatment the serum TT4 and TT3 in group A were (153 +/- 50) nmol/L and (3.6 +/- 1.2) nmol/L respectively, both significantly lower than those of the group B [(177 +/- 64) nmol/L and (2.7 +/- 1.5) nmol/L respectively, P = 0.041 and 0.033], however, there was no significant difference in other serum thyroid hormones between the group A and group B. The dosage of PTU was not significantly different between group A and B 1 month after the treatment, but became significantly higher in group B than in group A 2, 3, and 6 months after the treatment (214,189, and 178 mg/d respectively vs. 190, 147, and 116 mg/d respectively, and 24, 42, and 62 mg/day more respectively, all P < 0.05). CONCLUSION: Hyperthyroidism can be effectively controlled by PTU while the patients consume iodated salt, but the dosage of PUT needed should be higher than while the patients consume pure salt.

[Clinical validity of anti-thyroperoxidase antibody and anti-thyroglobulin antibody].

OBJECTIVE: To evaluate the clinical validity of anti-thyroperoxidase antibody (anti-TPOAb) and anti-thyroglobulin antibody (anti-TgAb). METHOD: Serum levels of anti-TPOAb and anti-TgAb were assayed using chemiluminescence immunoassay in 434 subjects, including 51 patients with Hashimoto's thyroiditis, 58 with Graves' disease, 68 with nodular goiter, 56 with thyroid adenoma and carcinoma, 56 with subacute thyroiditis, 65 with euthyroid non-thyroid endocrine disease, 35 with euthyroid non-thyroid autoimmune diseases, and 45 euthyroid controls. RESULTS: The highest level and most positive results of serum anti-TgAb and anti-TPOAb were observed in patients with Hashimoto's thyroiditis (median 373 and 6 974 U/ml, positive rate 84.3% and 86.3%), followed by patients with Graves' disease (median 84 and 1 369 U/ml, positive rate 44.8% and 72.4%). Serum anti-TgAb and anti-TPOAb were also more common in patients with subacute thyroiditis and other autoimmune diseases than in the controls. CONCLUSION: The assay of serum anti-TPOAb and anti-TgAb by chemiluminescence immunoassy are useful in the differential diagnosis of autoimmune thyroid disease.

[Propylthiouracil-induced overt hepatic injury in patients with hyperthyroidism].

OBJECTIVE: To study the incidence, clinical features and related factors of propylthiouracil (PTU)-induced hepatic injury in patients with hyperthyroidism. METHODS: A prospective study were carried out in 70 patients of hyperthyroidism with normal liver function. Every patient was treated with PTU 300 mg/d until the thyroid functions recovered to normal, following by decease and maintenance PTU dose in period of six months. Liver function, including serum levels of alanine aminotransferase (ALT), alkaline phosphatase (ALP), aspartate aminotransferase (AST), total bilirubin (TBIL) and direct bilirubin (DBIL), thyroid function (serum thyroxine, triiodothyronine, free thyroxine, and free triiodothyronine and thyrotropin) and blood routine items were measured before therapy and once a month for six months after PTU therapy was begun. RESULTS: Sixty-four cases of 70 patients completed the therapy for 6 months. Hepatic injury developed in 33 patients (51.6%). Asymptomatic, transient hepatic injury was shown in 22 patients (34.4%). Slight symptomatic hepatic injury occured in 6 cases (9.4%) and overt hepatic injury in 5 patients (7.8%) after PTU administration. However, all the patients who developed overt hepatic injury did not stop PTU. Hepatic function returned normal one month after stopping PTU. No one finally suffered from viral hepatitis and autoimmune hepatitis in patients of symptomatic and overt hepatic injury. CONCLUSIONS: PTU-induced symptomatic hepatic injury is not rare and usually develops within the first few months of PTU administration. Its clinical course is relatively benign. However, it may be difficult to predict its development, so all patients should be monitored for liver function test during the administration in early stage.