EVALUATION OF THE RELATIONSHIP BETWEEN MEDICAL NUTRITION TREATMENT, PENTRAXIN-3, HSCRP AND BODY COMPOSITION ANALYSIS IN TYPE 2 DIABETIC PATIENTS.

Objective: Medical Nutrition Therapy (MNT) is important in the treatment and regulation of diabetic patients. In this study, it was aimed to evaluate the effects of medical nutrition therapy on Pentraxin-3, hsCRP and body composition analysis in Type 2 diabetes patients (DM). Methods: This study included 160 individuals who were admitted and diagnosed with Type 2 DM. Laboratory, clinical, anthropometric and body composition parameters were obtained 3 months after baseline evaluation of the patients and the MNT was given by the dietitian. Results: After 3 months MNT, weight, body mass index, waist circumference, body fat weight, body fat ratio and visceral fat area (p<0.001), glucose (p<0.001), insulin (p=0.033), HOMA index (p=0.004), HbA1c (p<0.001), total cholesterol (p=0.001), LDL (p=0.008), ALT (p<0.001) and hsCRP (p<0.001) levels were significantly lower than they were before MNT. There wasn't significant difference in triglyceride (p=0.509), HDL (p=0.079), Pentraxin-3 (p=0.706) levels and waist-to-hip ratio (p=0.802). The level of Framingham risk score after MNT was significantly lower (p<0.001). Conclusion: In this study, it was cocluded that MNT, applied to patients with Type 2 DM decreased cardiovascular risk and inflammation, contributed to the maintenance of glycemic control, and a significantly improved the body composition.

Evaluation of fractalkine (FKN) and secreted frizzled-related protein 4 (SFRP-4) serum levels in patients with prediabetes and type 2 diabetes.

OBJECTIVE: The objective of this study is to compare serum levels of FKN and SFRP-4 in patients with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and type 2 diabetes mellitus (T2DM). METHODS: A total of 152 patients presented to the endocrinology outpatient clinic of our hospital were included in the study. Eighty-two patients with a history of T2DM were assigned to the T2DM group. IGT (n = 34) and NGT (n = 36) groups included the patients who received oral glucose tolerance test outcomes. RESULTS: Serum FKN levels were significantly higher in the IGT and T2DM groups compared to the NGT group (p < 0.001 and p < 0.001, respectively). Serum SFRP-4 levels were significantly higher in the T2DM group compared to the IGT and NGT groups (p = 0.001 and p = 0.004, respectively). A significant correlation was observed between FKN and fasting glucose levels. SFRP-4 was significantly correlated with fasting glucose, HbA1c, and triglyceride levels. CONCLUSION: To our knowledge, increased FKN levels in patients with IGT were demonstrated for the first time in this study. The results of our study support the opinion that FKN and SFRP-4 may contribute to the pathogenesis of T2DM (Tab. 1, Fig. 3, Ref. 23).

Pantoprazole may improve beta cell function and diabetes mellitus.

BACKGROUND: Proton pump inhibitors induce hypergastrinemia by suppressing gastric acidity. Gastrin has incretin-like stimulating actions on beta cells. Proton pump inhibitors have been shown to decrease glycosylated hemoglobin. AIM: We aimed to observe changes in beta cell function in diabetic and non-diabetic subjects given pantoprazole for an acid-related ailment. METHODS: Seventy-nine male patients (38 non-diabetic and 41 type-2 diabetic receiving only metformin therapy) were followed for 12 weeks after pantoprazole 40 mg/day was given. Fasting plasma glucose, HbA1c, fasting insulin, Pancreatic B cell function (HOMA-B), proinsulin and c-peptide levels were measured before and after the treatment. RESULTS: In non-diabetic patients (n = 38), FPG decreased, whereas c-peptide, log-HOMA-B, increased significantly (p = 0.002, p = 0.03, p = 0.042, respectively) after 12 weeks of pantoprazole administration. In type 2 diabetic patients, FPG, HbA1c and weight decreased, whereas log-HOMA-B, c-peptide and log-proinsulin levels increased significantly after pantoprazole treatment (p = 0.003, p = 0.007, p < 0.001; p < 0.001; p = 0.017, p = 0.05, respectively). After pantoprazole treatment, pancreatic B-cell function was correlated with c-peptide and insulin and inversely with FBG and HbA1c levels in the whole group (r = 0.37, p = 0.001; r = 0.60, p < 0.001, r = -0.29, p = 0.011 and r = -0.28, p = 0.013, respectively). After pantoprazole treatment, HbA1c was correlated with FBG (r = 0.75, p < 0.001) and inversely with only log-HOMA-B level (r = -0.28, p = 0.013). CONCLUSIONS: Pantoprazole administration seems to correlate with increased beta cell function. Pantoprazole administration improves HbA1c, HOMA-B, c-peptide and proinsulin levels. Since beta cell loss plays a significant role in the pathogenesis of type 2 diabetes, PPI-based therapies may be useful in the treatment of diabetes.

Oxidative and antioxidative status after anthracyclinebased chemotherapy in breast cancer patients.

PURPOSE: The present study was undertaken to evaluate the effects of adjuvant anthracycline-based chemotherapy on thiobarbituric acid reactive substances (TBARS) and superoxide dismutase (SOD) levels in patients with breast cancer who had undergone surgery. METHODS: Body mass index (BMI), serum lipids (total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides), serum TBARS and SOD values were assessed in 30 patients with stage III breast cancer receiving adjuvant anthracycline- based chemotherapy. RESULTS: Anthracycline-based chemotherapy had no effect on BMI, blood pressure and lipid profile. A significant elevation was noted in TBARS (5.5±0.6 vs 5.9±0.9 µmol/L; p=0.038) and a significant reduction to baseline values in SOD levels (226.5±61.0 vs 203.1±48.3 U/mL; p=0.03) in patients following 6 cycles of adjuvant chemotherapy. CONCLUSION: The TBARS levels increased, whereas the SOD levels descreased after anthracycline-based chemotherapy. We suggest that oxidative stress is not always detrimental, as it can be beneficial in cancer treatment.

Increased risk of unfavorable metabolic outcome during short-term follow-up in subjects with nonfunctioning adrenal adenomas.

OBJECTIVE: To demonstrate long-term changes in the prevalence of several types of metabolic derangements in subjects with nonfunctioning adrenal adenomas. SUBJECTS AND METHODS: 273 subjects with adrenal adenomas, including 231 with nonfunctioning adenoma and 42 with subclinical Cushing's syndrome (sCS), were evaluated with respect to anthropometric and laboratory characteristics and prevalence of type 2 diabetes mellitus (T2DM), hypertension, dyslipidemia, metabolic syndrome (MS), prediabetes and cardiovascular disease (CVD). Median duration was 24 months. Follow-up data of 114 participants with nonfunctioning adrenal adenomas are also presented while those of 117 were missing. Follow-up data regarding changes in anthropometric and laboratory parameters and prevalence rates of metabolic disturbances were obtained from the medical records. RESULTS: The prevalence rates for both patients with nonfunctioning adenoma and sCS were: dyslipidemia: 161 (59%), hypertension: 147 (54%), MS: 128 (47%), prediabetes: 62 (23%), T2DM: 49 (18%), and CVD: 21 (8%). Hypertension and CVD were prevalent in subjects with sCS compared to participants with nonfunctioning adenoma. In follow-up, body mass index (p = 0.005), systolic blood pressure (p < 0.001), waist circumference (p = 0.005), homeostasis model assessment (p = 0.046), high-sensitivity C-reactive protein (p = 0.023), total cholesterol (p < 0.001) and low-density lipoprotein cholesterol (p < 0.001) and prevalence of hypertension (p < 0.001), dyslipidemia (p < 0.001), prediabetes (p < 0.001) and MS (p < 0.01) significantly increased in subjects with nonfunctioning adenoma. CONCLUSION: The data showed that nonfunctioning adrenal adenomas were associated with the development or deterioration of atherosclerotic risk factors. Therefore, follow-up and management strategies should be developed to decrease atherosclerotic morbidity in those individuals.

Impaired hypothalamo-pituitary-adrenal axis in patients with ankylosing spondylitis.

BACKGROUND: To investigate the hypothalamic-pituitary- adrenal (HPA) axis in patients with ankylosing spondylitis (AS) and healthy controls. METHODS: Forty-nine AS patients and 20 healthy controls were included. Lowdose ACTH test (LDST) was used to assess the HPA axis. Basal cortisol, stimulated peak cortisol levels, and acutephase reactants [C-reactive protein (CRP), erythrocyte sedimentation rate, and fibrinogen] were studied. Bath Ankylosing Spondylitis Functional Index, Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and Bath Ankylosing Spondylitis Metrology Index were also evaluated. RESULTS: Patient and control groups were not different regarding age, sex, body mass index and waist circumference (WC). Basal cortisol levels did not show a significant difference between groups. However, cortisol increment after low-dose ACTH was significantly impaired in AS subjects with respect to controls (20.0+/-4.4 vs 24+/-2.2 microg/dl, p<0.001). Eleven AS patients had impaired cortisol peak after LDST when a cortisol cut-off is accepted as 500 nmol/l (18 microg/dl) and none of the controls exhibited a peak cortisol responses to LDST<500 nmol/l. Comparison of AS subjects who were receiving anti-tumor necrosis factor (TNF) (no.=23), and conventional therapy (no.=26) yielded similar basal and peak cortisol concentrations. Peak cortisol concentrations were associated with basal cortisol, impaired cortisol response, CRP, and fibrinogen. Impaired cortisol response (subjects with peak cortisol levels <18 microg/dl) was significantly correlated with basal and peak cortisol concentrations and BASDAI. CONCLUSION: Our results indicate an increased prevalence of subclinical glucocorticoid deficiency in AS patients. Anti-TNF treatment seems not to have effect on HPA axis.

Prospective evaluation of tumor size and hormonal status in adrenal incidentalomas.

BACKGROUND: Because of the increased use of imaging interventions, more subjects have been diagnosed with adrenal incidentaloma in recent years. AIM: To evaluate the risk of mass enlargement, hormone hypersecretion and development of adrenal carcinomas during short-term followup. SUBJECTS AND METHODS: There were 317 subjects with incidentally discovered adrenal tumors in the registry. Forty subjects were excluded because of clinically overt hormone secretion at diagnosis and subjects with complete data were included in radiological (no.=150) and hormonal (no.=150) follow- up. Radiological evaluation was performed with computed tomography (CT) and/or magnetic resonance imaging (MRI). There were 143 subjects with adrenal adenomas and 7 subjects with other tumor types (cyst or myelolipoma). Median follow-up duration was 24 months. RESULTS: Increase in tumor size was detected in 25 subjects (17.4%) with adenomas and 1 subject with adrenal myelolipoma (14.3%). Decrease in tumor size was found in 7 subjects (4.8%) with adrenal adenomas. One patient was diagnosed with adrenocortical carcinoma during follow-up. In subjects with non-functioning adrenal adenoma (NFA, no.=120) or subclinical Cushing syndrome (sCS) (no.=30), no subject developed clinically overt hormone hypersecretion, while 8 (6%) subjects in the NFA group developed sCS. Tumor diameter and follow-up duration were significantly higher in subjects who developed sCS. CONCLUSION: In conclusion, we demonstrated that, despite being infrequent, adrenal tumors may increase in size, develop overt or subclinical hormone secretion or feature malignant transformation. Therefore, radiological and hormonal follow-up should be recommended to the patients. More investigations are needed for the establishment of long-term follow-up protocols.

Is there any relationship between imatinib mesylate medication and hypothalamic-pituitary-adrenal axis dysfunction?

BACKGROUND: Imatinib mesylate [tyrosine kinase (TK) inhibitor] is a novel medication in the treatment of chronic myelogenous leukaemia (CML). TK is also essential in hypothalamo-pituitary-adrenal (HPA) axis. PURPOSE: The aim of this study was to evaluate HPA axis in patients treated with imatinib. Twenty-five patients were included in this study. METHODS: Glucagon stimulation test (GST) and low-dose (1 microg) adrenocorticotropin test (LDSST) were used to assess the HPA gland axis. RESULTS: Seventeen (68%) subjects had impaired peak response when a cortisol cut-off value is accepted as 500 nmol/L. Twelve (48%) out of 17 subjects also failed to show a response to LDSST. Therefore, 12 patients (48%) were defined as HPA deficient. Only two of these 25 patients had morning serum cortisol < 200 nmol/l (7.22 microg/dl), and failed the GST and/or LDSST, indicating that the majority had partial glucocorticoid deficiency. If the cut-off presume for LDSST is from 500 to 600 nmol/l, 16 patients (64%) would have failed both the GST and LDSST. CONCLUSION: Our results indicate an increased prevalence of subclinical glucocorticoid deficiency in patients receiving imatinib mesylate for CML. Therefore under stressed conditions, such as intercurrent illness state, overt and untreated partial glucocorticoid deficiency in CML patients become life threatening.

Taxane-based adjuvant chemotherapy reduces endothelin-1 and symmetric dimethylarginine levels in patients with breast cancer.

PURPOSE: To evaluate the levels of asymmetric dimethylarginine (ADMA), an endothelin and nitric oxide (NO) synthase inhibitor, in patients with node-positive breast cancer who had undergone surgery and in a control group including healthy individuals. The effects of taxane-based chemotherapy on endothelin-1 (ET-1) and ADMA levels in the patient group were also studied. METHODS: Body mass index (BMI), serum lipids (total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides), ADMA and ET-1 were studied in 19 healthy individuals and in 19 patients with stage II and III, lymph node-positive breast cancer receiving taxane-based chemotherapy. RESULTS: ET-1 (34.3±12.8 vs. 13.8±4.5 pg/mL; p<0.001) and ADMA (0.87±0.18 vs. 0.68±0.24 µmol/L; p=0.024) levels were significantly higher in the breast cancer group compared to the control group. A significant reduction was noted in ET-1 (34.3±12.8 vs. 27.3±4.3 pg/mL; p=0.021) and ADMA (0.87±0.18 vs. 0.73±0.15 µmol/L; p=0.014) levels in patients following 6 cycles of adjuvant chemotherapy to baseline values. CONCLUSION: The present study demonstrated significantly higher levels of ET-1 and ADMA in the breast cancer group compared to the control group, which were reduced significantly with adjuvant taxane-based chemotherapy. It is apparent that prospective studies are needed to understand the effect of reducing ET-1 and ADMA levels on patient survival. We believe that the present study will provide guidance to relevant future studies.

Systolic pulmonary artery pressure and echocardiographic measurements in patients with euthyroid Hashimoto's thyroiditis.

BACKGROUND: The aim of this study was to investigate systolic pulmonary artery pressure (SPAP) and echocardiographic findings in patients with euthyroid Hashimoto's thyroiditis (HT). METHODS: Thirty (8 male, 22 female, mean age 47.4+/-10.5 yr) consecutive patients with euthyroid HT and 30 (9 male, 21 female, mean age 46.4+/-10.7 yr) healthy controls were included in the study. Transthoracic echocardiography was performed for all patients and levels of thyroid hormones, thyroid autoantibodies, glucose, insulin, urea, and creatinine were compared. RESULTS: There were no significant differences in sex, age, body mass index, serum free T4, serum TSH, lipid profiles between patients and controls. Mean SPAP in patients with euthyroid HT were significantly higher than in controls (31.6+/-5.0 vs 25.6+/-4.5 mmHg, p=0.005). Late diastolic transmitral velocity and isovolumic relaxation time were also significantly higher in patients in comparison to controls. In addition, euthyroid HT patients with tricuspid or mitral regurgitation had a higher grade. Correlation between SPAP and antithyroid antibodies and TSH, however, was not significant in this population. CONCLUSIONS: Pulmonary arterial pressure is higher in patients with euthyroid HT. There may be a relationship between elevated pulmonary arterial pressure and autoimmune thyroid disease independent from thyroid function status. However, further investigations are needed to determine the exact mechanism of association between autoimmune thyroid diseases and pulmonary hypertension.

Insulin-like growth factor-1 is essential to the increased mortality caused by excess growth hormone: a case of thyroid cancer and non-Hodgkin's lymphoma in a patient with pituitary acromegaly.

The effects of growth hormone are mediated in part by stimulating the production of insulin-like growth factor-1. Insulin-like growth factor-1 has significant effects on cell proliferation and differentiation, it is a potent mitogen, and it is a powerful inhibitor of programmed cell death (apoptosis). Insulin-like growth factor-1 also has a well-established role in the transformation of normal cells to malignant cells. Case reports on a possible association between elevated growth hormone and cancer risk in a variety of patient groups have been published. Here, we describe clinical and laboratory findings for a patient with acromegaly who first developed thyroid cancer, and then, in the follow up period, probably due to poorly controlled insulin-like growth factor-1 levels, developed a large cell non-Hodgkin's lymphoma. A search revealed that a case with these peculiarities had not previously been reported.

Does imatinib mesylate therapy cause growth hormone deficiency?

OBJECTIVE: The purpose of this study was to determine whether or not imatinib mesylate therapy induces growth hormone deficiency (GHD). SUBJECTS AND METHODS: Seventeen patients with chronic myloid leukemia (CML) were enrolled in the study. The glucagon stimulation test (GST), and standard deviation scores (SDSs) of insulin-like growth fac- tor 1 (IGF-I) and insulin-like growth factor binding protein (IGFBP-3) were used to determine GHD. The L-dopa test was performed on those with IGF-I SDSs above the -1.8 cut-off level. RESULTS: Of the 17 patients in the study, 12 (70%) had severe GHD (serum GH level <3 microg/l after GST). IGF-I SDSs and IGFBP-3 SDSs were below -1.8 in 12 patients (70%) and below -0.9 in 10 subjects (58%). Four of the 5 remaining subjects with IGF-I SDS >-1.8 showed insufficient GH response to L-dopa stimulation. Nine subjects (52%) had both severe GHD based on GST response and IGF-I SDS below -1.8. If an IGF-I SDS cut-off value l<-3 were used,5 out of 17 subjects (30%) would be classified as GH deficient. These same patients also showed severe GHD based on GST response. CONCLUSIONS: The data showed that a large number of patients on imatinib mesylate therapy had GH deficiency. A study involving a larger number of patients with a matched control group is needed to confirm the present observations.

Primary thyroid lymphoma: case series with literature review.

Non Hodgkin's lymphomas (NHL) of the thyroid are rare thyroid neoplasms. The majority of histopathologic types are extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) type and, diffuse large B-cell lymphoma (DLBCL). Most of them arise in a background of Hashimoto's thyroiditis and patients mostly present with a rapidly enlarging thyroid mass and with pressure symptoms. Treatment depends on the histological subtype and stage of the disease and includes radiotherapy and chemotherapy. The prognosis usually is favorable with proper treatment. Herein, we discuss the clinical diagnosis and treatment of thyroid lymphoma.

Transforming growth factor-beta 1 levels in women with prior history of gestational diabetes mellitus.

It is known that women with prior history of gestational diabetes mellitus (pGDM) feature obesity, insulin resistance and endothelial dysfunction which cause premature atherosclerosis. Transforming growth factor-beta 1 (TGF-beta1) is a key cytokine in obesity and insulin resistance and also play important roles in the development of atherosclerosis. This study was conducted to demonstrate the serum TGF-beta1 levels of people with pGDM. Thirty women with pGDM, 20 women with type 2 diabetes mellitus (T2DM) and 20 healthy women were enrolled. Serum TGF-beta1 levels of people with pGDM were found to be significantly higher than healthy controls and significantly lower than women with T2DM. TGF-beta1 levels were found to be correlated with postprandial glucose and age and inversely correlated with body mass index (BMI) and waist circumference. On multiple regression analysis postprandial glucose level, age and BMI were determined as the most important factors affecting TGF-beta1 levels. This study demonstrates elevated TGF-beta1 levels in pGDM. The inflammatory response to hyperglycemia and insulin resistance could be the major factors for the increased expression of TGF-beta1.

Low transforming growth factor-beta1 serum levels in idiopathic male osteoporosis.

INTRODUCTION: Although the etiology of osteoporosis is different between men and women, the underlying pathophysiological mechanism is similar, namely an absolute or relative increase in bone resorption, leading to progressive bone loss. Transforming growth factor (TGF)-beta1 is a growth factor in human bone, which is produced by osteoblasts, and which has various effects on osteoclasts and osteoblasts. The aim of our study was to determine serum TGF-beta1 levels in male patients with idiopathic osteoporosis. METHODS: Twenty five males with idiopathic osteoporosis and 25 age-matched controls were studied. Osteoporosis was defined by a T score of <-2.5 in the lumbar spine or at the femoral neck. We measured levels of TGF-beta1, estradiol, total and bioactive testosterone. Various markers of bone remodeling were also measured. RESULTS: TGF-beta1 was significantly lower in osteoporotic patients than in controls (3.706 ng/dl, 25-75 percentiles: 2.81-5.33 vs 8.659 ng/dl, 25-75 percentiles: 4.837-11.835; p=0.000). Moreover, TGF-beta1 levels were positively correlated with bone mineral density (BMD) at the femoral neck (r=0.439, p=0.028), and at the lumbar spine (r=0.41, p=0.042). No correlation was found between serum estradiol, testosterone and TGF-beta1 levels. DISCUSSION: Serum TGF-beta1 levels are depressed in osteoporotic men and are positively correlated with hip and spine BMD. The results of our study suggest that TGF-beta1 may play a role in the pathogenesis of idiopathic male osteoporosis.

Cushing's syndrome due to ectopic CRH secretion by adrenal pheochromocytoma accompanied by renal infarction.

Ectopic production of corticotropin-releasing hormone (CRH) by a pheochromocytoma is an infrequent cause of Cushing's syndrome. We report the case of a 43-year-old man with Cushing's syndrome due to a CRH-producing adrenal pheochromocytoma. The patient had clinical and biochemical evidence of hypercortisolism in conjunction with high ACTH levels and non-suppressible serum cortisol levels on low-dose and high-dose dexamethasone suppression testing. In addition to these clinical features of one month's duration, the patient developed symptoms of pheochromocytoma including headache, hypertension that was resistant to conventional therapy and excessive sweating. Biochemical testing confirmed elevated 24-hour urinary catecholamines and metabolites. Abdominal CT revealed a 4.5 x 4 x 3.5 cm mass in the left adrenal gland. He underwent elective left adrenalectomy. Light microscopic and immunochemical studies revealed a pheochromocytoma that contained immunoreactive CRH and was negative for ACTH. Plasma ACTH and dexamethasone supression tests normalized after surgery. This is an unusual case of a CRH-secreting pheochromocytoma. This was complicated by renal infarction, illustrating further the complexity of Cushing's syndrome in a patient with pheochromocytoma caused by CRH hypersecretion.

Pancrelipase treatment in a patient with the history of Roux-en-Y gastric bypass operation that developed resistant hypocalcemia secondary to total thyroidectomy.

OBJECTIVE: Roux-en-Y gastric bypass (RYGB) is an independent risk factor for moderate hypocalcaemia and may lead to the development of resistant hypocalcaemia following thyroid surgery. Subject and Results. A 35-year old female patient was referred to our hospital by her family physician for treatment of resistant hypocalcaemia. The patient underwent RYGB three years ago and a total thyroidectomy for a benign thyroid nodule one year ago. Calcitriol, calcium carbonate, magnesium oxide, and ergocalciferol therapeutic dosages were incremented. Despite dosage increments, the desired calcium levels were not achieved. In the sixth month after admission to our hospital, pancrelipase was added to patient's treatment scheme. On the following visit, a good calcium increase had been achieved. CONCLUSION: This report presents a case history of RYGB and resistant hypocalcaemia, which developed after thyroid surgery and positively responded to pancrelipase treatment.

A case of hypercalcaemic crisis secondary to coexistence of primary hyperparathyroidism and Graves' disease.

A 46 year-old female patient presented to the hospital with ongoing and progressively increasing fatigue, severe nausea and vomiting, loss of appetite, constipation, palpitations and somnolence. Laboratory evaluation revealed a severe hypercalcaemia and overt hyperthyroidism. She was diagnosed with primary hyperparathyroidism accompanied by Graves' disease. The patient underwent total thyroidectomy and right inferior parathyroid gland adenoma excision on the 24th day of her admission to the hospital after calcium levels and free thyroid hormone levels were brought to normal ranges. We suggest that a possibility of simultaneous thyrotoxicosis and primary hyperparathyroidism in cases presenting with a hypercalcaemic crisis should be considered.

Leptin, insulin and body composition changes during adjuvant taxane based chemotherapy in patients with breast cancer, preliminary study.

BACKGROUND: The objectives of the present study were to compare the effect of adjuvant chemotherapy for breast cancer on serum insulin levels, serum leptin levels, and body composition in early stage breast cancer patients. MATERIALS AND METHODS: 17 breast cancer patients underwent 6 cycles of docetaxel (75 mg), epirubicine (100 mg) and cyclophosphamide (500 mg) (TEC). Anthropometrical and foot-to-foot body fat analyzer BIA, serum glucose, insulin, lipids, HOMA-IR and leptin were compared pre- and post-treatment. RESULTS: There was no statistically significant weight gain after treatment; however, there was an overall trend toward weight gain (69.7 ± 9.8 kg vs 71.03 ± 9.8; P= 0.05). From baseline to the end of the study, percentage of body fat and body fat mass showed an upward trend at the end of chemotherapy (1%; 2 kg P> 0.05). Pre and post-treatment period, leptin was strongly correlated with insulin and HOMA-IR (Spearman's pre-T; r = 0.74; P <0.001, r = 0.66; P = 0.004 post-T; r = 0.549; P =0.022, r = 0.51; P =0.036, respectively). Insulin levels were significantly increased in the post-treatment period (P < 0.05). On correlation analysis, post-T insulin levels were correlated with leptin, weight, fat-mass and fat percentage (Spearman's r = 0.549; P=.022, r = 0.567; P= 0.018, r = 0.498, P= 0.042, r = 0.502; P= 0.040, respectively). DISCUSSION: High insulin and leptin levels, important factors that were previously shown to be related to breast cancer outcome, and insulin resistance may be increased in taxane based chemotherapy regimen. These data may have broad implications for diet and lifestyle strategies for the prevention and treatment of cancers.

Hypokalemic paralysis due to thyrotoxicosis accompanied by Gitelman's syndrome.

A 35-year-old male patient was admitted with fatigue and muscle weakness. He had been on methimazole due to thyrotoxicosis for 2 weeks. Laboratory tests showed overt hyperthyroidism and hypokalemia. Potassium replacement was started with an initial diagnosis of thyrotoxic hypokalemic periodic paralysis. Later on, despite the euthyroid condition and potassium chloride treatment, hypokalemia persisted. Further investigations revealed hyperreninemic hyperaldosteronism. The patient was considered to have Gitelman's syndrome (GS) and all genetic analysis was done. A c. 1145C>T, p. Thr382Met homozygote missense mutation located on solute carrier family 12, member gene 3, exon 9 was detected and GS was confirmed.