13 research outputs found

    The Role of Endoscopic Ultrasonography for Localization of Insulinomas without a Pancreatic Lesion on Magnetic Resonance Imaging: A Short Series and Literature Review

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    Insulinoma is a rare neuroendocrine tumor of the pancreas and is the most common cause of endogenous hyperinsulinemic hypoglycemia. Although 90% of insulinomas are benign tumors, recurrent episodes of hypoglycemia may lead to life-threatening consequences. Since surgery is the only curative method for patients with insulinomas, the preoperative localization of these tumors by appropriate imaging methods is important. In this case series, we report 5 patients with endogenous hyperinsulinemic hypoglycemia, including one with MEN-1 syndrome, who were diagnosed with insulinoma according to the prolonged fasting test. All patients had normal pancreas on upper abdominal magnetic resonance imaging (MRI), therefore, they underwent endoscopic ultrasonography (EUS) for localization of the insulinomas and were operated according to the EUS results. EUS demonstrated well-demarcated tumors in the tail of the pancreas in 4 subjects and in the head of the pancreas in one patient. However, in contrast to EUS results, one patient with MEN-1 syndrome had a glucagonoma and two insulinomas and one patient had not any tumor on histopathological evaluation of the distal pancreas after surgery. In this case series, we aimed to present the diagnostic performance of EUS and the treatment outcomes in a cluster of patients with insulinomas who had not a pancreatic lesion on upper abdominal MRI and to briefly review the currently available imaging methods for localization of insulinomas. Turk Jem 2015; 19: 93-9

    Is Biochemical Assessment of Pheochromocytoma Necessary in Adrenal Incidentalomas with Magnetic Resonance Imaging Features Not Suggestive of Pheochromocytoma?

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    Objective: Currently, it is unclear whether pheochromocytomas can be ruled out based on low intensity on T2-weighted sequences and signal loss on out-of-phase magnetic resonance imaging (MRI) sequences. Hence, in this study, we investigated whether biochemical screening for pheochromocytoma in patients with adrenal incidentalomas (AIs) showing MRI features not suggesting pheochromocytoma would prove beneficial. Methods: We performed MRI for 300 AIs in 278 consecutive patients. All patients were screened for pheochromocytoma with plasma metanephrine and normetanephrine. Patients with high plasma levels of metanephrine and/or normetanephrine were also assessed for pheochromocytoma by urinary metanephrines. Results: Hyperintensity was detected on T2-weighted MRI sequences in 28 (9.3%) of the 300 AIs. Among these 28 incidentalomas, pheochromocytoma was diagnosed in 13 (46.4%) of the cases by histopathologic analysis. Hyperintensity on T2-weighted MRI was significantly higher in pheochromocytomas compared to the remaining AIs (P<.001). All 13 pheochromocytomas were characterized by hyperintensity on T2-weighted sequences and the absence of signal loss on out-of-phase MRI sequences. Pheochromocytoma was not detected in any of the 272 AIs that appeared hypointense or isointense on T2-weighted MRI sequences or in the 250 cases with signal loss on outof- phase sequences. Conclusion: The results of this study suggest that AIs that appear hypointense or isointense on T2-weighted MRI sequences and those with signal loss on out-of-phase sequences may not require routine biochemical screening for pheochromocytoma. Further studies including a higher number of pheochromocytomas are required to confirm our results

    The Role of Endoscopic Ultrasonography for Localization of Insulinomas without a Pancreatic Lesion on Magnetic Resonance Imaging: A Short Series and Literature Review

    No full text
    Insulinoma is a rare neuroendocrine tumor of the pancreas and is the most common cause of endogenous hyperinsulinemic hypoglycemia. Although 90% of insulinomas are benign tumors, recurrent episodes of hypoglycemia may lead to life-threatening consequences. Since surgery is the only curative method for patients with insulinomas, the preoperative localization of these tumors by appropriate imaging methods is important. In this case series, we report 5 patients with endogenous hyperinsulinemic hypoglycemia, including one with MEN-1 syndrome, who were diagnosed with insulinoma according to the prolonged fasting test. All patients had normal pancreas on upper abdominal magnetic resonance imaging (MRI), therefore, they underwent endoscopic ultrasonography (EUS) for localization of the insulinomas and were operated according to the EUS results. EUS demonstrated well-demarcated tumors in the tail of the pancreas in 4 subjects and in the head of the pancreas in one patient. However, in contrast to EUS results, one patient with MEN-1 syndrome had a glucagonoma and two insulinomas and one patient had not any tumor on histopathological evaluation of the distal pancreas after surgery. In this case series, we aimed to present the diagnostic performance of EUS and the treatment outcomes in a cluster of patients with insulinomas who had not a pancreatic lesion on upper abdominal MRI and to briefly review the currently available imaging methods for localization of insulinomas. Turk Jem 2015; 19: 93-9

    The diagnostic value of late-night salivary cortisol for diagnosis of subclinical Cushing's syndrome

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    Introduction: Late-night salivary cortisol is a frequently used and easily implemented diagnostically valuable test for the diagnosis of overt Cushing's syndrome. The use of late-night salivary cortisol in the diagnosis of subclinical Cushing's syndrome is somewhat controversial. In this study, we aimed to determine the diagnostic value of late-night salivary cortisol in diagnosing subclinical Cushing's syndrome and compare it with 24-hour urinary free cortisol levels (UFC). Material and methods: The study consisted of 33 cases of subclinical Cushing's syndrome, 59 cases of non-functioning adrenal adenoma, and 41 control subjects. Late-night salivary cortisol and UFC were measured in all the cases. The diagnosis of subclinical Cushing's syndrome was based on combined results of 1 mg dexamethasone suppression test > 1.8 mu g/dL and ACTH < 10 pg/mL. Results: Mean late-night salivary cortisol levels in subjects with subclinical Cushing's syndrome were significantly higher than in subjects with non-functioning adrenal adenoma and the control group (p < 0.001). Using a cut-off value of 0.18 mu g/dL, the sensitivity and specificity of late-night salivary cortisol for diagnosing subclinical Cushing's syndrome were determined as 82% and 60%, respectively. Using a cut-off value of 137 mu g/day, the sensitivity and specificity of UFC was determined as 18% and 90%, respectively. Conclusions: Because the sensitivity of late-night salivary cortisol for the diagnosis of subclinical Cushing's syndrome is limited, using it as the sole screening test for subclinical Cushing's syndrome may lead to false negative results. However, using it as an adjunct test to other tests may be beneficial in the diagnosis of subclinical Cushing's syndrome

    Relationship between Empty Sella Syndrome and Hashimoto’s Thyroiditis

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    Purpose: It is not clear if Hashimoto’s thyroiditis leads to Empty sella syndrome. In the present study, we aimed to investigate if Hashimoto’s thyroiditis was associated with Empty sella syndrome, and Hashimoto’s thyroiditis was a secondary cause od some cases of primary Empty sella syndrome. Material and Method: Eighty-one patients who were diagnosed with primary Empty sella syndrome were included in the study. All patients underwent thyroid ultrasonography and biochemical tests for thyroid-stimulating hormone, free triiodothyronine, free thyroxine, anti thyroid peroxidase, anti thyroglobulin, follicle stimulating hormone, luteinizing hormone, 17 β estradiol, growth hormone, insulin-like growth factor 1, adrenocorticotropic hormone and total testosterone for Hashimoto’s thyroiditis and pituitary hormone deficiency. Results: Out of 81 patients, thyroid disease was diagnosed in 34 (42%) patients; 18 of them had Hashimoto’s thyroiditis (22.2%) and 16 (19.8%) had central hypothyroidism. Among Hashimoto’s thyroiditis patients, 11 (13.6%) had hypothyroidism and 7 (8.6%) were euthyroid. Discussion: In conclusion, it is possible that some cases of primary Empty sella syndrome are caused by Hashimoto’s thyroiditis. It is recommended that the presence of Hashimoto’s thyroiditis should be investigated in patients with primary Empty sella syndrome. Further studies investigating anti-pituitary antibody in patients with primary Empty sella syndrome, are needed to further declare this relationship

    Relationship between Empty Sella Syndrome and Hashimoto’s Thyroiditis

    No full text
    Purpose: It is not clear if Hashimoto’s thyroiditis leads to Empty sella syndrome. In the present study, we aimed to investigate if Hashimoto’s thyroiditis was associated with Empty sella syndrome, and Hashimoto’s thyroiditis was a secondary cause od some cases of primary Empty sella syndrome.\ud Material and Method: Eighty-one patients who were diagnosed with primary Empty sella syndrome were included in the study. All patients underwent thyroid ultrasonography and biochemical tests for thyroid-stimulating hormone, free triiodothyronine, free thyroxine, anti thyroid peroxidase, anti thyroglobulin, follicle stimulating hormone, luteinizing hormone, 17 β estradiol, growth hormone, insulin-like growth factor 1, adrenocorticotropic hormone and total testosterone for Hashimoto’s thyroiditis and pituitary hormone deficiency.\ud Results: Out of 81 patients, thyroid disease was diagnosed in 34 (42%) patients; 18 of them had Hashimoto’s thyroiditis (22.2%) and 16 (19.8%) had central hypothyroidism. Among Hashimoto’s thyroiditis patients, 11 (13.6%) had hypothyroidism and 7 (8.6%) were euthyroid.\ud Discussion: In conclusion, it is possible that some cases of primary Empty sella syndrome are caused by Hashimoto’s thyroiditis. It is recommended that the presence of Hashimoto’s thyroiditis should be investigated in patients with primary Empty sella syndrome. Further studies investigating anti-pituitary antibody in patients with primary Empty sella syndrome, are needed to further declare this relationship

    The Effect of Vitamin-D on the Diabetic Rethinopathy

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    Background: To determine the relationship between grade of diabetic retinopathy and serum vitamin D levels in diabetic patients. Methods: The study included a total of 173 diabetic patients consisting of patients without retinopathy ( n=67), patients with non proliferative diabetic retinopathy (NPDRP group n=47), patients with proliferative diabetic retinopathy (PDRP group n=59). Age and sex-matched 55 healthy subjects was taken as a control group. Patients with type 1 DM, those taking vitamin D, multivitamin including vitamin D, drug affecting vitamin D metabolism like rifampin, phenytoin was excluded from the study. Patients with chronic renal failure was also excluded. Dilated fundoscopic examination of all subject was done and serum creatinine, Hb A1c, 25 hydroxyvitamin D (25 (OH) D) level of all subject were measured between may 2012 and September 2012 Results: There were no statistical difference in age, sex, systolic tension, diastolic tension and body mass index between groups. Serum creatinine level was also not statistically different between groups (p = 0.11). Serum fasting glucose and HbA1c level were significantly lower in the control group than diabetic groups (p <0.001). The mean 25 (OH)D levels of PDRP group, NPDRP group, diabetic patients without retinopathy and control group were 11,9 ± 6,4 ng/ml, 18,8 ± 10,2 ng/ml, 16,6 ± 7,5 ng/ml and 20,1 ± 9,2 ng/ml respectively. There was statistically significant difference between the PDRP group and other groups in univariate analysis (p < 0.001). When 173 diabetic patients, were compared, with control group, 25 (OH) D levels were significantly lower in diabetic patients than control group regardless of retinopathy status (p = 0.004). Conclusions: Diabetic patients especially, patients with proliferative diabetic retinopathy had lower serum vitamin D levels than healthy subjects. Additionally randomized, controlled, prospective studies are necessary to determine whether vitamin D treatment will stop or slow the progression of diabetic retinopathy in diabetic patients. © 2022 A. CARBONE Editore. All rights reserved

    Expression of voltage gated potassium channel ether a go-go in pituitary adenomas of patients with acromegaly: A preliminary study

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    OBJECTIVE: To determine immunohistochemical expression of Eag1 in pituitary adenomas of patients with acromegaly and to assess the correlation between Eag1 expression with cavernous sinus invasion, tumoral Ki-67 labeling index (LI), age and gender of the patients. METHODS: The paraffin embedded pituitary adenoma tissue sections of 28 patients with acromegaly who were diagnosed as monohormonal growth hormone (GH) secreting adenomas were immunostained for Eag1 using the avidin-biotin-peroxidase complex method. Eag1 immunoreactivity was scored according to the extensity of the cytoplasm and cell membrane immunoreactivity for Eag1 (score 1 = 50% of the adenoma cells showed immunoreactivity for Eag1, respectively). RESULTS: Overall, GH secreting pituitary adenomas displayed diverse levels of Eag1 immunoreactivity, however, 64% of the adenomas displayed a strong Eag1 immunoreactivity (score 3 and 4). Five of the tumors displayed Eag1 immunoreactivity score 1, 5 displayed score 2, 10 displayed score 3 and 8 displayed score 4, respectively. No correlation was found between Eag1 immunoreactivity with cavernous sinus invasion, Ki-67 LI, age and gender of the patients. CONCLUSIONS: Our results suggest Eag1 is strongly expressed in the majority of GH secreting pituitary adenomas. However, we could not find any correlation between immunoreactivity of Eag1 with cavernous sinus invasion, Ki-67 LI, age and gender of the patients. Further studies with larger sample sizes are required to demonstrate the role of Eag1 on tumorigenesis, angiogenesis, invasion and response to the treatment in GH secreting pituitary adenomas

    The effect of feto-maternal blood type incompatibility on development of gestational diabetes mellitus

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    Objective. To assess the relation between fetal and maternal blood type (ABO, Rh) incompatibility and development of gestational diabetes mellitus (GDM). Materials and Methods. A total of 500 pregnant women underwent diagnostic test for GDM by a 100-g oral glucose tolerance test (OGTT) after an 8 to 12-h overnight fast participated in this study. OGTT was performed between the 24-28 weeks of gestation, but participants who were at high risk for GDM were tested after the first prenatal visit. In the postpartum period, maternal and infant blood types were determined. Presence of GDM was evaluated in terms of matched and unmatched fetal and maternal ABO and Rh blood types separately. Results. GDM was detected in 235 participants. Unmatched ABO blood types between the mother-infant pairs were present in 44.7% (n=105) of GDM (+) and 35.8 % (n=95) of GDM (-) patients. Incompatible feto-maternal ABO blood type was positively correlated with development of GDM which was marginally significant. (p=0.045; R=1.2;95% CL; 1.004-1.48). However, Rh feto-maternal blood type incompatibility was not related with development of GDM. Conclusions. Feto-maternal ABO blood type incompatibility may be a weak risk factor for the development of GDM
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