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Background Parathyroid hormone (PTH) stimulates aldosterone secretion in human adrenocortex and is regulated by the renin-angiotensin-aldosterone system. We speculated that measurement of PTH may be a valuable aid in the diagnosis of aldosterone-producing adenoma (APA). Methods To test this hypothesis, we recruited 142 patients with adrenal adenoma, of whom 84 had an APA and 58 had a nonfunctioning adrenal adenoma (NFA). Plasma levels of intact PTH, serum potassium, sodium, calcium, phosphate, 25(OH) vitamin D, plasma aldosterone concentration (PAC), plasma renin activity (PRA), and aldosterone to renin ratio (ARR) were measured in every patient. Computed tomography (CT) scanning of the adrenal gland and adrenal hormone levels was used to evaluate the function of the adrenal adenoma. We also evaluated the impact of renin-angiotensin-aldosterone system (RAAS) components on PTH from the recumbent-upright test in 15 patients with APA and 30 patients with NFA. Results Compared with NFA, PTH levels were significantly increased in patients with APA, and serum calcium and phosphate were significantly decreased. When position was changed from supine to upright, the variation in PTH levels was significantly higher in APA patients compared with NFA patients. Receiver operator characteristic (ROC) curves identified the Youden index, which corresponded to the best tradeoff of combined marker (ARR and PTH) with a sensitivity and specificity of 89.3% and 93.1%, respectively. Conclusions The baseline and positional variation of serum PTH levels were significant in APA, thus PTH may be a promising auxiliary index for the clinical diagnosis of APA.

Objective. To investigate the association between the hypertriglyceridemic waist (HTGW) phenotype and prediabetes in Chinese adults aged 40 years and older. Methods. 12757 adults (4101 men and 8656 women) without diabetes or cardiovascular and cerebrovascular diseases, free of using lipid-modified agents, were enrolled in this cross-sectional study. The HTGW phenotype was defined as elevated serum triglyceride concentrations and enlarged waist circumference. A two-hour post 75 g oral glucose tolerance test was performed in all participants. Multiple logistic regression analysis was used to evaluate the relationship of the HTGW phenotype with prediabetes. Results. Individuals with the HTGW phenotype had a higher adjusted odds ratio (OR: 1.70; 95% CI: 1.48–1.95) of prediabetes than those without the phenotype. There existed a strong relationship of the HTGW phenotype with impaired glucose tolerance (IGT) (OR: 1.83; 95% CI: 1.57–2.13), but not with impaired fasting glucose (IFG) (OR: 0.87; 95% CI: 0.65–1.17). Only women with the HTGW phenotype are significantly associated with the combined IFG and IGT (OR: 1.83; 95% CI: 1.28–2.62). Conclusions. The HTGW phenotype was a useful risk indicator and a practical screening tool to benefit in the early diagnosis and intervention for prediabetes, particularly for IGT and the combined IFG and IGT.

Background The aim of the present study was to assess the relationship between night sleep duration and glycemic and triglyceride (TG) levels among people with different glycemic status. Methods In all, 18 121 subjects aged ≥40 years were enrolled in this cross-sectional study, including 4318 with impaired glucose regulation (IGR), 4225 with diabetes, and 9578 with normal glucose regulation (NGR). The IGR + diabetes and NGR groups were divided into three subgroups according to self-reported night sleep duration as follows: (i) 9 h. The associations of sleep duration with HbA1c, fasting plasma glucose (FPG), 2-h post-load plasma glucose (PPG), and TG levels were examined. Results Long night sleep duration (>9 h) was associated with higher HbA1c, FPG, PPG, and TG levels compared with sleep duration of 6–9 h (P 9小时）的患者具有较高的HbA1c、FPG、PPG和TG水平（P值均

Patients with malignant insulinoma always present with symptoms of severe hypoglycemia and have poor life expectancy. In addition, inoperable metastatic malignant insulinomas are very difficult to manage. The aim of this report is to present our successful experiences in diagnosis and treatment of this disease in 6 patients.Six patients (male 2, female 4) with malignant insulinomas were admitted into our hospital. Their clinical histories, including clinical presentations, endocrine evaluations, radiological images, pathological examination and treatments, were reviewed.The diagnosis of malignant insulinoma combined with liver metastases was confirmed in all patients by endocrine evaluation and radiological images. Patients 1-3 underwent surgical management. The primary and metastasized tumors were completely resected. After successful surgery, no hypoglycemia recurred. Patients 4-6 did not undergo surgery because of systemic disease and poor health. Instead, they were administrated with diazoxide 50 mg Three Times a Day (TID), with final doses up to 200-300 mg TID. These 3 patients had good responses to diazoxide administration. After treatment, the frequency and severity of hypoglycemia were improved significantly. All 6 patients had better life quality than previously expected.Combination of surgical and medical approaches can improve life quality and prolong survival of patients with malignant insulinomas.

We describe an elderly male patient who presented with fever of unknown origin and refractory hyponatraemia. Following (18) fluorine-fluorodeoxyglucose positron emission tomography/computed tomography scan and core adrenal biopsy, the diagnosis of diffuse large B-cell non-Hodgkin lymphoma with pituitary and bilateral adrenal involvement was confirmed. After chemotherapy, his symptoms resolved, and all the lesions shrank significantly.

Differentiating between benign and malignant thyroid nodules is important for providing appropriate treatment. In the present study we examined the clinical usefulness of ultrasound in examining calcification patterns in thyroid nodules, and thus predict malignancy. The records of 1,498 Chinese patients who underwent thyroidectomy for nodular thyroid disease were retrospectively examined. All patients underwent thyroid ultrasound within 1 month before surgery. Calcification patterns in thyroid nodules were examined, and tissue samples were analyzed to determine a pathological diagnosis. Calcifications were defined as macrocalcifications, microcalcifications, rim calcifications, or isolated calcifications. A total of 2,122 thyroid nodules were examined, and 259 nodules (12.2%) were found to be malignant. Papillary carcinoma accounted for 85.3% of all malignancies. The majority of benign lesions were nodular goiters. Calcification was detected in 49.6% of malignant nodules and 15.7% of benign nodules. Microcalcifications were significantly more common in malignant nodules as compared to benign nodules (33.7 vs. 6.4%; P

DNA sequencing analysis was used to scan the genes in a Chinese family with clinically diagnosed autosomal genetic hypercholesterolemia. Two mutations were identified in exon 4 of the low-density lipoprotein receptor gene, which is the possible molecular mechanism of etiology of the family. The proband's extremely high level of serum cholesterol and the related manifestations suggested that he was a familial hypercholesterolemia homozygote and that his parents were in a relatively milder condition. DNA sequencing revealed that the proband had an abnormal pattern of exon 4 of the low-density lipoprotein receptor gene due to a heterozygosity (A/G) at nucleotide 386 and a heterozygous single-base deletion (A) at 685. Nucleotide 386 is the second base of codon 129, and A→G mutation (D129G) changed this codon from Asp GAC to Gly GGC . The single-base deletion of A at 685 (685del 1) is a frameshift mutation. It changes the phase of triplets, so that all codons are misread after this site of mutation; consequently, the protein expressed by the gene must be abnormal in structure and function. DNA analysis of the other family members showed that the 2 mutations should be respectively located in different alleles of the proband. Both of the 2 mutations have not been reported previously.

Lipodystrophies is a really rare group of diseases characterized by altered body fat amount and/or repartition and serious insulin resistance.We reported a lean Chinese girl with acquired generalized lipodystrophy, who had a long history of poorly controlled diabetes mellitus (DM) despite with extremely high dose insulin (6 u/kg/d) therapy, combined with severe hypertriglyceridemia and acanthosis nigricans. The differential diagnosis of Lipodystrophies should be considered in lean patients presenting with early onset DM, combined with serious insulin resistance.

To explore the imaging features of congenital adrenal cortex hyperplasia (CAH).A total of 45 patients clinically confirmed as CAH were retrospectively analyzed to investigate the imaging features and strengthening way of the multi-detector-row Computed tomography.The imaging features of all the cases presented as following: 25 with bilateral adrenal hyperplasia, 6 with unilateral adrenal hyperplasia, 6 with adrenal nodular hyperplasia, 2 with adrenal hyperplasia and unilateral solid cystic lesion, 2 with adrenal hyperplasia and double side real cystic lesion, 1 with adrenal hyperplasia and unilateral cystic changes and 3 with normal adrenal. The unilateral or bilateral hyperplasia adrenal could be homogeneously enhanced, while the enhanced performance of other cases was inequitable.The adrenal imaging features of CAH by multi-detector-row CT are variable, with the bilateral adrenal hyperplasia as the main form, which could be restored to normal morphology after hormone replacement therapy.No regression of the tumor size is observed in cases with adrenal mass. CT scanning combined with clinical manifestation and biochemical examination could facilitate the diagnosis of CAH.

An 18-year-old male patient had presented with diffuse hyperpigmentation after birth and with adrenal insufficiency syndrome since childhood. After puberty, no secondary sexual signs developed. Laboratory examination showed an extremely high concentration of serum triglycerides (9.14 mmol/L) and plasma adrenocorticotropic hormone (>275 pmol/L), however, a low concentration of plasma free cortisone (

This study was conducted to evaluate gender-related differences in clinical characteristics and vascular complications in patients with aldosterone-producing adenomas (APA). Clinical characteristics, biochemical markers and incidence of vascular complications were compared by gender in 187 consecutive patients with APA confirmed by pathological diagnosis. Patients were separated into two groups based on ages either older or younger than 49 years, the average age of menopause among Chinese women (

Leukemia related protein 16 (LRP16) was first cloned from acute myeloid leukemia cells in our laboratory. In the present study, we sought to investigate the role of LRP16 in insulin action and sensitivity, using LRP16-depleted and -overexpressing 3T3-L1 cells. LRP16 silencing resulted in a reduction of the expression and secretion of tumor necrosis factor-alpha (TNF-α) and a concomitant increase in the expression of peroxisome proliferator-activated receptor-gamma (PPAR-γ). Moreover, LRP16 depletion promoted insulin-induced glucose uptake and adipocyte differentiation of 3T3-L1 cells. In contrast, LRP16 overexpression increased TNF-α secretion, suppressed glucose uptake, and attenuated 3T3-L1 cell differentiation. The phosphorylation levels of insulin receptor substrate 1 (IRS-1), phosphatidylinositide 3-kinase (PI3-K), and Akt were increased in LRP16-deficient 3T3-L1 cells, and conversely, diminished in LRP16-overexpressing 3T3-L1 cells, when compared to the corresponding control cells. Additionally, LRP16 overexpression raised the phosphorylation level of mammalian target of rapamycin (mTOR). The pretreatment with rapamycin, a specific inhibitor of mTOR, prevented the TNF-α elevation and PPAR-γ reduction and restored the phosphorylation of IRS-1, PI3-K, and Akt in LRP16-overexpressing cells. Our data collectively indicate that LRP16 acts as a negative regulator of insulin action and adipogenesis in 3T3-L1 adipocytes, which involves the activation of the mTOR signaling pathway.

Subclinical apoplexy of pituitary functional adenoma can cause spontaneous remission of hormone hypersecretion. The typical presence of pituitary growth hormone (GH) adenoma is gigantism and/or acromegaly. We investigated the clinical characteristics of patients with spontaneous partial remission of acromegaly or gigantism due to subclinical apoplexy of GH adenoma.Six patients with spontaneous remission of acromegaly or gigantism were enrolled. The clinical characteristics, endocrinological evaluation and imageological characteristics were retrospectively analyzed.In these cases, the initial clinical presences were diabetes mellitus or hypogonadism. No abrupt headache, vomiting, visual function impairment, or conscious disturbance had ever been complained of. The base levels of GH and insulin growth factor-1 (IGF-1) were normal or higher, but nadir GH levels were all still1 µg/L in 75 g oral glucose tolerance test. Magnetic resonance imaging detected enlarged sella, partial empty sella and compressed pituitary. The transsphenoidal surgery was performed in 2 cases, and the other patients were conservatively managed. All the patients were in clinical remission.When the clinical presences, endocrine evaluation, biochemical examination and imageology indicate spontaneous remission of GH hypersecretion in patients with gigantism or acromegaly, the diagnosis of subclinical apoplexy of pituitary GH adenoma should be presumed. To these patients, conservative therapy may be appropriate.

The accurate and comprehensive assessment of glycemic control in patients with diabetes is important for optimizing glycemic management and for formulating personalized diabetic treatment schemes. This study aimed to analyze the correlation between 1,5-anhydroglucitol (1,5-AG) and glycemic excursions in type 2 diabetic patients.Seventy-one outpatients with type 2 diabetes mellitus were randomly recruited from Chinese People's Liberation Army General Hospital. Using a continuous glucose monitoring system (CGMS), these patients' blood glucose levels were monitored for three consecutive days to obtain mean blood glucose (MBG) data. Intraday glycemic excursions were evaluated using the mean amplitude of glycemic excursions (MAGE), the largest amplitude of glycemic excursions (LAGE), standard deviation of blood glucose (SDBG) and the M-value. Interday glycemic excursion was assessed by absolute mean of daily difference (MODD). Postprandial glycemic fluctuations were evaluated using postprandial glucose excursions (PPGE) and postprandial incremental area under the curve (iAUC). Fasting venous blood samples were collected to measure serum 1,5-AG, whole-blood hemoglobin A1c (HbA1c) and serum glycated albumin (GA). Clinical markers of glycemia and parameters of glycemic excursions from CGMS were analyzed using the Pearson correlation coefficient and multivariate stepwise regression.Pearson correlation analysis revealed that 1,5-AG was significantly correlated with MAGE, SDBG, M-value, LAGE, PPGE and iAUC (r values were -0.509, -0.430, -0.530, -0.462, -0.416 and -0.435, respectively, P0.01), especially in moderately and well-controlled patients, based on defined HbA1c levels. Multivariate stepwise regression analysis revealed a negative correlation between 1,5-AG and the above parameters, but not HbA1c and GA. Finally, HbA1c and GA were positively correlated with MBG and fasting blood glucose (FBG).1,5-AG was much better than HbA1c and GA as a marker of glycemic excursions in type 2 diabetic patients. Based on these results 1,5-AG is the best metric for assessing postprandial glucose levels in moderately and well-controlled patients, while HbA1c and GA were superior to 1,5-AG for monitoring MBG and FBG.

To evaluate the safety and efficacy of 30 mg pioglitazone hydrochloride combined with sulphonylurea in the treatment of type 2 diabetic patients.A randomized, double blind, placebo-controlled, parallel group, multicenter study was performed. A total of 236 patients, who had fasting plasma glucose (FPG) 7.5 - 13.0 mmol/L and glycosylated hemoglobin A1c (HbA1c) 7.0% - 12.0%, treated with stable dosage of a sulphonylurea for at least 30 days previously, were randomized to receive placebo or pioglitazone 30 mg once daily for 16 weeks. The sulphonylurea and dosage remained unchanged.The patients who had been treated with pioglitazone 30 mg showed significant decrease than that in the placebo group on the average from baseline in FPG [(1.48 ± 2.08) mmol/L vs (-0.17 ± 1.92) mmol/L, P0.05], and in HbA1c [(0.92 ± 0.10)% vs (0.28 ± 0.11)%, P0.05]. Since fasting plasma insulin (FIns) levels decreased (0.24 ± 0.04) mU/L and (0.09 ± 0.04) mU/L in the two groups. The homeostatic model assessment insulin resistant (HOMA-IR) decreased 1.42 ± 2.90 and 0.46 ± 3.53 in two groups. The triglyceride level was decreased 0.36 mmol/L and 0.14 mmol/L, and the HDL-C level increased 0.17 mmol/L and 0.05 mmol/L in two groups. There were significant differences in two groups (all P0.05).The 16-week clinical study demonstrated that pioglitazone hydrochloride with a dosage of 30mg daily, could significantly improve the blood glucose control and enhance the insulin sensitivity, lower triglyceride and raise HDL-C level as an additional therapy to a stable-dose sulphonylurea in Chinese type 2 diabetic patients previously poorly controlled by single sulphonylurea therapy, and furthermore had good safety and compliance.

To explore the effect of LRP (leukemia related protein) 16 on insulin resistance in C2-C12 cells and explore its molecular mechanism.Lipidosome transfection and lentivirus mediated siRNA (small interfering RNA) technology were used to establish LRP 16 overexpression and underexpression cell lines and their corresponding control cell lines. And 2-deoxy-[(3)H]-glucose was used to measure the effect of LRP 16 on insulin-stimulated glucose uptake. The effects of LRP16 on the phosphorylation of IRS (insulin receptor substrate)-1, Akt and the expressions of PI3K (p85), PPAR (peroxisome proliferator actived receptor) γ and GLUT-4 were detected by Western blot. Luciferase was used to study the effect of LRP16 on the transcriptional activity of PPARγ.Insulin-stimulated glucose uptake decreased to 46% of the control when LRP16 was over-expressed [(4700 ± 97) vs. (10200 ± 347), P0.01]. And the insulin-stimulated glucose uptake was 1.73 fold of control when the expression of LRP16 was suppressed in C2-C12 cells [(17600 ± 466) vs (10200 ± 91), P0.05]. The overexpression of LRP16 attenuated the insulin-induced tyrosine phosphorylation of IRS-1, the phosphorylation of Akt and the expressions of PI3K (p85), PPARγ and GLUT-4. But it promoted the insulin-induced phosphorylation of IRS-1 at Ser307 in C2-C12 cells. LRP16 decreased the transcriptional activity of PPARγ in a dose-dependent manner. The transcriptional activity of PPARγ decreased to 43% and 27% of the control when the doses of pcDNA3.1-16 were 0.4 µg and 0.5 µg [(76 ± 11) vs (33 ± 9), P0.01] and 27% [(21 ± 9) vs (76 ± 11), P0.01].LRP16 gene causes insulin resistance in C2-C12 cells by inhibiting the IRS-1 signaling and the transcriptional activity of PPARγ.

Recurrent autoimmune hypophysitis is a rare autoimmune endocrine disease involving lymphocytic infiltration and chronic pituitary inflammation. It is even more rare than primary hypophysitis. The objective of the study was to evaluate the efficacy of glucocorticoid treatment combined with azathioprine for treating three cases of recurrent autoimmune lymphocytic hypophysitis encountered within a two-year period. The clinical features and follow-up data of these cases were analyzed, including results of treatment with glucocorticoids combined with azathioprine. All three patients were female and presented with the following clinical characteristics: case 1 was a 22-year-old with headache and diplopia; case 2 was a 70-year-old with dry mouth, polydipsia, and polyuria; case 3, a 32-year-old, with polydipsia, polyuria and menstrual disorders with headache and dizziness. Regarding recurrence, case 1 recurred 4 months after surgery and again 14 months after discontinuing prednisone; case 2 relapsed 16 months after receiving high-dose methylprednisolone pulse therapy; and case 3 recurred during the period of prednisone dose reduction. The patients were treated with glucocorticoids plus azathioprine, and positive responses were seen in all three cases. Symptoms were relieved, and MRI revealed significant reduction of lesions during follow-up. Pituitary function resumed in cases 1 and 3; permanent hypopituitarism was present in case 2. At last follow-up, MRI showed no further recurrence of disease in any patient. Treatment and responses of these patients with autoimmune hypophysitis suggest that glucocorticoid therapy combined with azothioprine is effective treatment for recurrent autoimmune hypophysitis. Endocrine and radiologic studies are an essential part of follow-up.

To retrospectively evaluate the diagnostic accuracy of ultrasonographic (US) features for the pre-operative differentiation of benign and malignant thyroid nodules by using pathological diagnosis as the reference standard.A total of 1501 patients with 2123 thyroid nodules (1864 malignant, 259 benign) diagnosed intra-operatively and undergoing pre-operative ultrasonography at our hospital were recruited. The following characteristics of US images were evaluated: nodule size, shape, margin, echotexture, echogenicity, presence and type of calcification, blood flow inside or around nodules and the presence of ipsilateral cervical lymphadenectasis.(1) The risk of malignancy was higher in a solitary nodule than in a non-solitary nodule [16.7% (109/653) vs 10.2% (150/1470), P=0.000]. The mean diameter of benign nodules was larger than that of malignant nodules [(2.4±1.4) vs (2.1±1.9) cm, P=0.009]. (2) Microcalcification, irregular shape, ill-defined border, solid and hypoechogenicity were more common in malignant nodules. Irregular shape had the highest sensitivity and positive predictive value while microcalcification had the highest diagnostic accuracy. (3) Nodules with a rich blood flow inside tended to have a higher risk of malignancy. The distribution pattern of blood flow around the nodules was not associated with the differentiation of benign and malignant thyroid nodules. Nodules with the presence of ipsilateral cervical lymphadenectasis had a higher risk of malignancy than those without lymphadenectasis [28.3% (80/283) vs 9.6% (92/963), P0.01]. (4) If microcalcification, irregular shape, ill-defined border, solid, hypoechogenicity and the presence of ipsilateral cervical lymphadenectasis were treated as the characteristics of malignancy, a higher frequency of these characteristics was correlated with a higher risk of malignancy.Despite a lack of specific US imaging characteristics in malignant thyroid nodules, microcalcification and irregular shape appear closely correlated with malignancy. A combined use of conventional US characteristics may improve the accuracy of differential diagnosis.

To study the cerebrospinal fluid (CSF) and serum level of human chorionic gonadotropin (HCG) in patients with intracranial germinoma and to evaluate its diagnostic and therapeutic value.Thirty-one patients with intracranial germinoma receiving estimation of HCG in CSF and serum in our hospital were retrospectively analyzed in terms of HCG level, its influencing factors and the relationship of HCG with clinical features.HCG levels in CSF of the 31 cases ranged from 0.17 IU/L to 5316.98 IU/L with a median value of 3.44 IU/L. The sensitivity of diagnosis increased from 80.6% to 90.3%, when the cut point of HCG in CSF changed from 0.60 IU/L to 0.50 IU/L. The sensitivity increased from 83.9% to 93.5% when the cut point of the ratio of CSF/serum HCG decreased from 1.8 to 1.7. HCG level of germinoma located in pineal region was higher than that in basal ganglia region, while it is lowest in sellar region. The ratio of CSF/serum HCG in different parts showed no difference. Multiple risk factors analysis revealed that serum HCG (r = 0.886, P = 0.0001) and tumor size (r = 0.748, P = 0.0211) were positively correlated with the HCG level in CSF, while course of the disease, age and gender were not correlated. After radiation therapy, HCG in CSF and serum decreased dramatically as compared with those before radiation.The HCG level and its dynamic change were sensitive marker of intracranial germinomas. Based on our analysis, HCG in CSF over 0.50 IU/L and the its ratio in CSF/serum over 1.7 were highly indicative of the possibility of intracranial germinomas.

A rare case with ectopic adrenocorticotrophic hormone syndrome (EAS) caused by medullar thyroid carcinoma (MTC) in mediastinum was reported. This 49 year-old male patient initially presented with serious and intractable hypokalemia. Endocrine evaluations showed increased levels of adrenocorticotrophic hormone (ACTH) and urinary free cortisol, which could not be suppressed more than 50% by high-dose dexamethasone suppression test. Computed tomography (CT) scan detected a 5×5×5 cm mass at the bottom of thyroid in anterior mediastinum. The patient underwent total thyroidectomy with central compartment and ipsilateral modified radical neck dissection. Pathological examination showed an infiltrating thyroid medullary carcinoma with abundant amyloid deposition, meanwhile immunohistochemical positive for ACTH. After surgery, serum levels of kalium, as well as cortisol and ACTH returned to normal range. During follow-up, the patient's clinical manifestation of Cushing syndrome relieved.

To investigate the characteristics of glycemic excursion of different subtypes of glucose tolerance.Assessed by oral glucose tolerance test (OGTT) repeated twice, 81 individuals were divided into 4 groups: normal glucose tolerance (NGT, n = 18), isolated impaired fasting glycemia (IFG, n = 12), isolated impaired glucose tolerance (IGT, n = 19), combined IFG/IGT (n = 11), and newly diagnosed type 2 diabetes mellitus (T2DM, n = 21). And then continuous glucose monitoring system (CGMS) was used for 72 hours to monitor the blood glucose (BG) level before drug intervention.(1) The levels of largest amplitude of glycemic excursions (LAGE), mean blood glucose (MBG), and standard deviation of mean level of blood glucose fluctuation (SDBG) increased gradually with the deterioration of glucose tolerance. The mean amplitude of glucose excursion (MAGE) readout of the IGT group was (3.2 +/- 1.2) mmol/L, significantly higher than that of the NGT group [(1.6 +/- 0.5) mmol/L, P0.05], and significantly lower than that of the T2DM group [(5.2 +/- 1.9) mmol/L, P0.05]. The level of frequency of glucose excursion (FGE) decreased along with the decrease of glucose tolerance: NGT group [(6.1 +/- 3.4)]IGT/IFG group [(5.5 +/- 2.5)]T2DM group [(4.8 +/- 1.8)]. Among the three components of IGR, the IGT group showed highest MAGE (3.2 +/- 1.2) mmol/L and lowest FGE level (4.9 +/- 1.8). (2) The level of absolute mean of daily difference (MODD) increased in the following order: NGT group [(0.8 +/- 0.3) mmol/L], IGT group [(1.1 +/- 0.4) mmol/L], IFG/IGT group [(1.2 +/- 0.4) mmol/L], and T2DM group [(2.0 +/- 1.0) mmol/L] (all P0.05). (3) The fasting glucose level deteriorated the most rapidly in the IFG group, while it reached the highest postprandial peak in the IFG/IGT group. The blood glucose curve increased along the order of NGT, I-IGT, IFG/IGT, IFG, and T2DM. (4) When the level of glycosylated hemoglobin (HbA1c) level was less than 7%, the fasting phase of curve virtually coincided with each other among individual groups with different HbA1c levels; however, the postprandial peak separated slightly. When the HbA1C level was between 7.0% and 7.9%, the postprandial peaks of individual groups with different HbA1c levels dispersed markedly. When the HbA1c level was higher than 8%, the fasting blood glucose curve moved upwards significantly with increasing postprandial excursion.(1) With the deterioration of glucose regulation, the intraday and day-to-day blood glucose excursions become increasingly fluctuant. (2) The amplitude of glycemic excursion is lower in the NGT group than in the T2DM group, however, the frequency of glycemic excursion is higher in the NGT subject than in the T2DM subjects. The glucose excursion profile of the IGR subjects is between the NGR and T2DM subjects. (3) The characteristics of glucose excursion of the IGT group are similar to those of the T2DM group, and the characteristics of the IFG group are similar to those of the NGT group. (4) The loss of postprandial glycemic control precedes evident deterioration in fasting phase of IGR.

To investigate the clinical characteristics of multiple endocrine neoplasia type 1 (MEN1) patients presenting with hypoglycemic coma as chief manifestation and the related clinical experience in diagnosis and therapy.We analyzed the clinical data of 4 patients who were hospitalized because of recurrent hypoglycemic coma and diagnosed as having MEN1 by endocrinological, radiological and pathological examinations.In the 4 cases of Whipple trilogy, radiological examination showed occupying lesion in the pancreas and pathological examination confirmed the diagnosis of insulinoma. In 2 cases the insulinomas were multiple. In this series, one case was complicated with pituitary adenoma, parathyroidoma (recurrent after operation) and adrenocortical adenoma, one case with pituitary adenoma, parathyroidoma (2 tumors) and adrenal nodular hyperplasia, one case with pituitary adenoma and parathyroidoma, and the remaining one with pituitary adenoma and suspectible parathyroidoma.For patients with insulinoma, MEN1 should be considered. In patients with MEN1, the presence of multiple or ectopic parathyroid adenomas (or hyperplasia) and insulinomas should be inspected during operation. After operation, examinations should be regularly performed to identify whether the diseases relapse or new endocrine neoplasias occur.

Autoimmune hypothalamitis is a rare autoimmune neuroendocirne disease. A case of a 70-year-old female with autoimmune hypothalamitis was reported. The chief clinical characteristics were diabetes insipidus and adenopituitary function deficiency. Cranial magnetic resonance imaging (MRI) scan indicated a mass in the hypothalamus. The diagnosis of autoimmune hypothalamitis was presumed. After treatment with prednisone, there was a marked reduction in the mass and the hypothalamus-adenopituitary function partially improved. However, after glucocorticoid therapy was withdrawn, the hypothalamic lesion relapsed progressively. High dose methylprednisolone pulse therapy (HDMPT) in combination with azathioprine was initiated thereafter. During follow-up, MRI scan indicated the lesion shrank strikingly, and the patient's clinical condition improved as well. In view of the good response of the hypothalamic lesion to glucocorticoid and immunodepressant, the putative diagnosis of autoimmune hypothalamitis was confirmed. This case report suggested that HDMPT in combination with azathioprine therapy might be an effective trial for autoimmune hypothalamitis treatment.

To investigate the molecular diagnosis method and possible molecular mechanism of the etiology of a hereditary genetic hypercholesterolemia family by scanning and analyzing the related genes of hereditary hypercholesterolemia in a clinically diagnosed proband and his family members.Molecular diagnosis was performed with PCR and then DNA sequencing of the promoter and 18 exons of low-density lipoprotein receptor (LDLR) gene and 3500 - 3531 fragment of apolipoprotein B-100 gene was carried out. The sequencing results were compared with the normal nucleotide sequence queried from the GeneBank database to discover the mutations.Familial defective apolipoprotein B-100 was excluded, as no mutation was detected in the apolipoprotein B 3500 - 3531 fragment. Two new point mutations were detected in the exon 4 of the proband's LDLR gene, they were heterozygous 685delA (Del A at 685) and 386AG. The sequencing in his parents and other family members showed that the two mutations were paternal origin (685delA) and maternal origin (386AG) respectively and should be located in different alleles of the proband.Molecular diagnosis in the family shows that the proband is a compound heterozygote and the newly detected LDLR gene mutations of 685delA and 386AG are the possible molecular etiological basis of the disease in this family.

Lymphocytic hypophysitis is a rare inflammatory lesion of pituitary gland. To enhance the knowledge of lymphocytic hypophysitis, herein we reported 3 cases of lymphocytic hypophysitis and reviewed the literature.The clinical data of 3 patients diagnosed as having lymphocytic hypophysitis were analysed.All the three patients were young females, one of them (case 1) was affected in the postpartum period, however, the others were neither pregnant nor in postpartum period. Clinically, the most frequently seen symptoms and signs were attributable to pituitary hypofunction, headache and diabetes insipidus. Pituitary MRI revealed enhanced mass with pituitary stalk enlargement expanding the pituitary fossa, extending into suprasellar area and compressing optic chiasm. Typically the lesion appeared hypointense or isointense on T1-weighted imaging, but hyperintense on T2-weighted imaging. Histopathological examination showed extensive destruction of anterior acini of the pituitary with a dense infiltration of lymphocytes, plasma cells, histocytes and other inflammatory cells. Two patients (case 2 and 3) were successfully treated for mass reduction of pituitary gland and restoration of pituitary function with high dose methylprednisolone pulse therapy (HDMPT).Lymphocytic hypophysitis is a rare autoimmune endocrinopathy which can affect young woman in the postpartum period, or in the peripartum period, characterized by focal or extensive lymphocytic infiltration of anterior pituitary acini. It may cause pituitary expansion and a varying degree of hypopituitarism mimicking the features observed in pituitary adenoma. HDMPT was proved to be effective for mass reduction of pituitary gland and restoration of pituitary function.

To investigate the expression of G proteins alpha subunit mRNA in different thyroid diseases.Twenty-three thyroid specimens were obtained during surgery, 5 from patients with Graves' disease (GD), 7 from patients with multinodular goiter (MNG), 6 from patients with eufunctioning thyroid adenoma (EFTA) and 5 from patients with thyroid papillary cancer (TPC). The expression of stimulating and inhibiting G proteins alpha subunit mRNA were determined by reverse transcription-polymerase chain reaction (RT-PCR).(1) The expression of G(s)alpha mRNA in TPCs (1.67 +/- 0.25) was significantly higher than that in normal thyroids (1.10 +/- 0.14) and MNGs (0.96 +/- 0.31), P0.05 and P0.01. The expression in GDs (1.47 +/- 0.11) and EFTAs (1.36 +/- 0.28) was significantly higher than that in MNGs (P0.05), but comparable to that in normal thyroids. (2) The expression of G(i)alpha-2 mRNA in GDs (0.68 +/- 0.26) was lower than that in MNGs (1.15 +/- 0.35), P0.05, but there was no difference in the expression of G(i)alpha-1 and G(i)alpha-3 mRNA among different thyroid diseases.The results indicated that G(s)alpha could play an important role in the pathogenesis of thyroid papillary cancer and G proteins had different expression in different thyroid diseases.

In men, obesity has generally been associated with reduced plasma testosterone levels and with elevation of the plasma free fatty acids (FFAs). In this study, we investigated the effects of saturated FFAs including palmitic acid (PA) and stearic acid (SA), and polyunsaturated FFA arachidonic acid (AA) on the survival of rat testicular Leydig cell cultured in vitro. PA and SA markedly suppressed Leydig cell survival in a time- and dose-dependent manner. In contrast, AA stimulated the cell proliferation at 5-10 times of physiological concentration. The suppressive effect of PA and SA on cell survival was caused by apoptosis evidenced by DNA ladder formation and Annexin V-EGFP/propidium iodide staining of the cells. The apoptotic effect of PA was possibly mediated by ceramide generation because it could be completely blocked by ceramide synthase inhibitor fumonisin B1 and exogenous ceramide itself could directly induce apoptosis in vitro. Surprisingly, the apoptosis induced by PA could be partly prevented by AA. These results indicate that PA and SA induce apoptosis in testicular Leydig cells by ceramide production and these apoptotic effects may be a possible mechanism for reproductive abnormalities in obese men, and AA can partly prevent the apoptotic effect induced by saturated FFA.

We report a rare case of recurrent lymphocytic hypophysitis (LyH) after transsphenoidal surgery and high dose methylprednisolone pulse therapy (HDMPT). The patient was treated with azathioprine, and achieved spontaneous pregnancy. A 22-year-old nulliparous female was seen in June 2004 due to headaches, diplopia and left eye ptosis, and bilateral milky nipple discharge. Six months prior she had undergone transsphenoidal pituitary tumor resection at another hospital, and the histopathological diagnosis was ‘‘pituitary tumor with inflammatory response.’’ The patient had no significant medical history, menarche at age 16, and regular cycles until March 2004. Physical examination was normal except for left eye ptosis and adduction limitation, and bilateral milky nipple discharge. Routine laboratory tests and T3, T4, TSH, LH, FSH, E2, prolactin, ACTH, cortisol, and 24 h urinary free cortisol were within normal limits. Thyroid autoantibodies (TGAb and TPOAb) and TSH receptor antibody were negative. Magnetic resonance imaging (MRI) showed abnormal, enhancing, irregular soft tissue signals with unclear boundaries in the sellar region and suprasellar cistern. Histopathological examination revealed lymphocyte, histiocyte, and neutrophil infiltration in the pituitary tissue, consistent with LyH. High dose methylprednisolone pulse therapy (HDMPT) was begun, and her symptoms rapidly improved. MRI showed the pituitary significantly reduced in size and the lesions had disappeared. The patient was asymptomatic until December 2005 when she experienced headaches, diplopia, and nausea and vomiting. MRI showed normal hypothalamic and pituitary morphology, and abnormal enhancement on the right side of the dorsum sellae and near the tentorium cerebelli. She was treated with azathioprine 100 mg/day for 16 weeks, and prednisone 30 mg/ day (decreased 5 mg/week until withdrawal). After treatment, she experienced regular menstrual cycles and conceived spontaneously in April 2009. Her pregnancy and delivery were uneventful with no LyH relapse during pregnancy or to date. The natural course of LyH can include sellar massoccupying effects, pituitary disorders, diabetes insipidus, and hyperprolactinemia [1]. MRI findings are not specific enough to distinguish LyH from pituitary adenomas; thus careful correlation with clinical and laboratory findings is critical [1]. Transsphenoidal resection of pituitary lesions, drugs (corticosteroids, azathioprine, and methotrexate), and radiotherapy have all been used to treat LyH; however, none are effective in all cases [1, 2]. Lecube et al. [3] first reported the successful treatment of LyH using azathioprine in a patient who failed corticosteroid treatment, and subsequently other authors have reported success with azathioprine [4]. Lymphocytic hypophysitis (LyH) is significantly correlated with pregnancy; of 210 reported cases in females, 120 (57%) occurred during pregnancy or the postpartum period, primarily in the final month of pregnancy or first 2 months postpartum [5]. If onset is during pregnancy, complications or adverse effects on the fetus are unlikely, and the condition may gradually resolve after delivery. A history of pregnancy-related LyH is not associated with relapse Z. Lu and G. Yang contributed equally.

Objectives To explore the relationship between depressive symptoms and waist-to-hip ratio, dyslipidemia, glycemic levels or blood pressure among diabetic and non-diabetic Chinese women. Methods 11,908 women aged ≥40 years were enrolled in this cross-sectional study, including 2,511 with type 2 diabetes and 9,397 without. Depressive symptoms (defined as having mild-to-severe depressive symptoms) were assessed by the Patient Health Questionnaire-9 (PHQ-9) diagnostic algorithm. The prevalence and the odds ratios (ORs) with 95% confidence intervals (CIs) for having depressive symptoms were estimated using logistic regression analysis. Results The age-adjusted prevalence of depressive symptoms was significantly higher in non-diabetic subjects with waist-to-hip ratio (WHR) ≥0.9 (8.6%, age-adjusted OR 1.51 [95% CI 1.17, 1.95]), total cholesterol (TC)>6.22 mmol/L (8.8%, 1.58 [1.16, 2.15]), and Hemoglobin A1c (HbA1c) ≥6.00 mmol/L (7.7%, 1.69 [1.34, 2.14]), while it was significantly lower in non-diabetic subjects with diastolic blood pressure (DBP) between 80 to 89 mmHg (6.2%, 0.78 [0.64, 0.95]). These relationships remained significant even after controlling for multiple factors (WHR ≥0.9: multivariable-adjusted OR 1.39 [95% CI 1.07, 1.80]; TC>6.22 mmol/L: 1.56 [1.14, 2.12]; HbA1c ≥6.00 mmol/L: 1.64 [1.30, 2.08]; DBP 80-89 mmHg: 0.78 [0.64, 0.95]). However, no significant trend between depressive symptoms and WHC, TC, HbA1c, DBP was observed in diabetic women, and no significant trend relationship between depressive symptoms and BMI, WC, TG, or SBP was observed in both non-diabetic and diabetic women. Moreover, the prevalence of depressive symptoms was significantly higher in previously-diagnosed diabetes, compared with non-diabetic subjects, while no significant differences were observed between newly-diagnosed diabetes and non-diabetic subjects. Conclusion The present study showed a relationship between WHR, TC, HbA1c, DBP and depressive symptoms among non-diabetic women, while no significant relationship between them was observed among diabetic women, even after controlling for multiple confounding factors.