Biomedical subjects

M A Gundogan

Publications and source records attributed to M A Gundogan.

14 recordsLinked to original sources

PubMed1998

The effects of thyroid status on plasma leptin levels in women.

Leptin, the product of the adipose specific ob gene, regulates food intake and energy expenditure. However, little is known about the effects of thyroid status on plasma leptin levels in women. We determined fasting plasma leptin levels before and 1 month after restoration of euthyroidism in 20 female patients with hypothyroidism, 20 female patients with hyperthyroidism and 20 age and BMI-matched female controls. To restore the normal thyroid function patients with hypothyroidism were treated with levothyroxine, whereas patients with hyperthyroidism were treated with propylthiouracil. Plasma leptin levels were measured by a RIA method with a sensitivity of 0.5 microgram/l. Leptin levels were significantly lower in patients with hypothyroidism before treatment (4.17 +/- 2.58 micrograms/l) than in patients with hyperthyroidism (6.80 +/- 4.3 micrograms/l; z = -2.06, p = 0.037). Leptin levels were significantly higher in hyperthyroid patients than in the control group (3.71 +/- 1.69 micrograms/l, z = -2.44, p = 0.014) whereas leptin levels in the hypothyroid patients were not significantly different from those in control subjects (z = -0.16, p = 0.87). Restoration of euthyroid state was not associated with a significant change in leptin levels either in the hypothyroid (from 4.17 +/- 2.58 to 5.22 +/- 3.4 micrograms/l; z = -1.74, p = 0.08) or in the hyperthyroid group (from 6.80 +/- 4.37 micrograms/l to 7.93 +/- 6.25 micrograms/l z = -0.89, p = 0.37), although a tendency for leptin to increase was observed in both groups. There was no correlation between plasma leptin and FT3, FT4, TSH, or BMI either before or after therapy in both groups. Leptin levels were significantly correlated with BMI in the control group (r = -0.53, p = 0.018). We conclude that plasma leptin levels are increased in hyperthyroidism and unchanged in hypothyroidism. Furthermore, our study demonstrates that mean plasma leptin levels are not influenced by short term restoration of euthyroidism in both hypothyroidism and hyperthyroidism, although an effect of long-term treatment may not be excluded.

Adult↗

PubMed1998

The effects of thyroid status on serum apolipoprotein A-I-containing lipoprotein particles.

Alterations of lipid profile are a well-known phenomenon in thyroid dysfunction. However, little is known about the influence of thyroid hormone on Lp A-I and LpA-I:A-II particles. We have, therefore, studied LpA-I and LpAI:A-II concentrations in a group of 20 patients with hyperthyroidism and in a group of 15 patients with hypothyroidism before and one month after attainment of euthyroidism. In hypothyroid patients, LDL-cholesterol and apo B concentrations decrease significantly after L-T4 replacement treatment (from 4.49+/-2.51 to 2.76+/-0.70 mmol/ L, P=0.036 and from 89.4+/-16.1 to 78.3+/-13.3 mg/dL, P=0.05, respectively), whereas no significant change was observed in the total cholesterol, HDL-C, LpA-I, LpA-I:A-II and apo A-I concentrations. In hyperthyroid patients, total cholesterol (from 3.58+/-0.72 to 4.74+/-1.39mmol/L, P=0.0025), HDL-C (from 1.19+/-0.23 to 1.41+/-0.27mmol/L, P=0.0084), LDL-C (from 1.83+/-0.69 to 2.96+/-1.20 mmol/l, P=0.0025), apo A-I (from 85.6+/-12.5 to 91.7+/-18.1 mg/dL, P=0.05) and apo B (from 52.7+/-8.2 to 65.6+/-16.5 mg/dL, P=0.0013) increased after restoration of euthyroidism while triglycerides, LpA-I and LpA-I: A-II concentrations were unchanged. LpA-I and LpA-I:A-II concentrations were not related to thyroid hormones in both groups. Our study suggests that LpA-I and LpA-I:A-II particles are not under the direct control of thyroid hormones.

Adult↗

PubMed1997

Biochemical composition of benign thyroid cyst fluid.

Although the availability of thyroid cyst fluid is easy by fine-needle aspiration, less is known about the biochemical composition of thyroid cyst fluid. The authors have, therefore, determined the biochemical composition of 18 benign thyroid cyst fluid specimens. They found that the activities of aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and the concentrations of total protein, total bilirubin, and uric acid were highly increased in thyroid cyst fluid specimens when compared with normal human serum specimens. The concentrations of glucose, cholesterol, and triglycerides in cyst fluid were within normal serum limits. Selenium (Se) concentrations in most cyst fluids were low. Moreover, there was no correlation between Se and other biochemical parameters. Protein electrophoresis of cyst fluid specimens yielded high concentrations of alpha 1 and especially alpha 2 globulin fractions indicating an inflammation. The concentrations or activities of biochemical analytes were not significantly different in pure and mixed cysts. Those parameters were also not significantly different between cyst fluids of different colors. The gross appearance of the fluid and the presence of certain biochemical analytes were consistent with a hemorrhagic origin of most of the cyst fluid specimens. However, some biochemical markers indicate that autolysis or necrosis of thyroid tissue may also contribute the composition of thyroid cyst fluid. The reason for lower Se concentration in the thyroid cyst fluid may be the lower Se concentration in the Turkish population. These results also suggest that the fluid color or nature of cyst, e.g., pure or mixed cyst, is not a main determinant of biochemical composition of benign thyroid cyst fluid.

Alanine Transaminase↗

PubMed1997

A case of Addison's disease associated with the Lambert-Eaton myasthenic syndrome.

Nonneoplastic Lambert-Eaton Myasthenic Syndrome (LEMS) is rare. A 27-year-old man as initially having the diagnosis of Addison's disease was admitted to the hospital because of fatigue, dry-mouthness and proximal limb weakness for 1 year. A diagnosis of LEMS was made from electrophysiological studies. Clinical and laboratory studies revealed no malignancy. We report the first case of Addison's disease associated with non-neoplastic LEMS. It is possible that subclinical LEMS might be present in patients with Addison's disease more frequently than currently believed, since the prominent symptoms of LEMS may be confused with symptoms of Addison's disease.

Addison Disease↗

PubMed1997

Auditory even-related brain potentials in hyperthyroidism.

Several studies based on psychometric tests have demonstrated an impairment of cognitive functions in hyperthyroid patients. Long-latency auditory event related potentials (ERPs) allow the measurement of a kind of cerebral reaction time that is unavailable to psychometric tests. However, ERPs alterations in hyperthyroidism have been investigated only in experimentally induced hyperthyroidism in healthy subjects, but no study has reported on thyrotoxic patients so far. Therefore, we investigated alterations of P300 wave latency in hyperthyroid patients before and after antithyroid treatment. ERPs were elicited in 20 untreated patients with hyperthyroidism (mean age: 27.40 +/- 2.10 years) and in 30 sex-, age- and education-matched controls. ERPs recordings were repeated 4 months after attainment of euthyroidism. Untreated patients had longer mean P300 latencies when compared to those in controls (338.3 +/- 26.6) vs 320.7 +/- 16.2 msec, P = 0.020). Slowing of P300 latency was marked in 4 of 20 patients and its normalization was observed after treatment. The mean P300 latencies also returned to normal (320.5 +/- 15.5 msec) 4 months after achievement of euthyroidism. Our study shows that P300 is normal in most cases, while we have found in a subgroup of patients a small but statistically significant slowing. However, these alterations are reversed 4 months after attainment of euthyroidism.

Adult↗

PubMed1996

Evaluation of central motor conduction in hypothyroid and hyperthyroid patients.

Deficiency or excess of thyroid hormones is associated with central nervous system (CNS) disturbances. Although the CNS involvement either in hypothyroidism or in hyperthyroidism have previously been shown on the basis of visual, auditory and somatosensory evoked potentials studies, less is known about the function of central motor pathways in both disorders. We studied the motor evoked potentials (MEPs) following the magnetic stimulation of the motor cortex and spinal roots in 20 patients with hypothyroidism and in 19 patients with hyperthyroidism both before treatment and after they became euthyroid and compared with findings in 20 age-, sex- and height-matched control subjects. Disease duration (expressed as time from diagnosis of diseases to the time of neurological testing) is less than one month in both disorders. Central motor conduction time (CMCT) was determined as the differences between MEPs latencies after cortical and spinal stimulation. The mean CMCTs before treatment in hypothyroid patients (8.31 +/- 1.52 msec.) and in hyperthyroid patients (7.92 +/- 1.06 msec.) were significantly prolonged as compared to those in normal controls (6.82 +/- 0.83 msec. p = 0.002 and p = 0.004, respectively). Four of the 20 (20.0%) hypothyroid patients and 2 of 19 (10.5%) hyperthyroid patients had abnormal CMCT (values exceeding mean +2.5 SD of normal control). The mean CMCT values in both groups were not significantly decreased after euthyroidism was achieved, although a tendency of the decrease in CMCT was observed. Improvement of CMCT abnormalities was observed in 1 of 4 hypothyroid patients and in one of 2 patients with hyperthyroidism, who had CMCT abnormalities before treatments, after they became euthyroid. No correlation was found between CMCT and free T3, free T4, or TSH levels as well as the onset age, the severity of the diseases or the disease duration in both disorders. We conclude that abnormal CMCT could be documented in few patients in both disorders. However, these alterations could not be improved completely after restoration of euthyrodism. Thus, it remains to be determined if long-term treatment would completely improve CMCT abnormalities in both disorders. Since abnormal CMCT values in both disorders were observed only in few patients, our results also suggest that CMCT measurement does not have, at present time, a clinical usefulness to assess the peripheral action of thyroid hormones. Thus, the data obtained need a more extensive evaluation.

Adult↗

PubMed1996

Acute hypothyroidism leads to reversible alterations in central nervous system as revealed by somatosensory evoked potentials.

Although functional alterations in the central nervous system (CNS) and peripheral nerves are well documented in overt hypothyroidism, little is known about alterations of CNS in acute hypothyroidism. Sixteen patients with differentiated thyroid carcinoma were studied when prepared for radioiodine scanning after stopping levothyroxine (L-T4) therapy for 6 weeks to determine whether acute hypothyroidism leads to alteration in somatosensory evoked potentials (SSEPs). Repeat SSEPs were performed on the same patients at 6 months following L-T4 therapy when patients were euthyroid. Neurophysiological findings were compared with a group of 20 normal controls with no history of thyroid disease. Peripheral and central conduction in the median and tibial nerve stimulated SSEPs studied. A significant prolongation of central conduction time in SSEPs was found in patients with acute hypothyroidism when compared to those in control subjects. Abnormal latencies were not correlated with thyroid hormone levels. These neurophysiologic abnormalities were completely restored to normal at 6 months after L-T4 therapy. We conclude that acute hypothyroidism leads to reversible alterations in CNS as determined by SSEP recordings. Our results also suggest that SSEPs could be useful tests to monitor functional alteration of the CNS in acute hypothyroidism.

Acute Disease↗

PubMed1996

Effects of octreotide treatment on Graves' ophthalmopathy and circulating sICAM-1 levels.

Efficacy of octreotide treatment for Graves' ophthalmopathy (GO) and the effects of this treatment on the serum levels of the circulating intercellular adhesion molecule-1 (sICAM-1) were evaluated. Ten patients with GO were treated with octreotide three daily SC injections of 100 micrograms, for 3 months. Octreotide treatment was initiated after restoration of euthyroidism with antithyroid drugs. All patients were treated with methimazole to maintain euthyroidism during the study. Sera were collected from all patients before and 3 months after initiation of the study, and from 20 age- and sex-matched healthy subjects for sICAM-1 measurement. sICAM-1 was measured by a sandwich ELISA method. Proptosis in all patients was evaluated by orbital CT scan before and 3 months after initiation of the study. Two of 10 patients did not respond to octreotide therapy, while the remaining eight patients showed regression or improvement after therapy. Octreotide therapy was particularly successful in patients with soft tissue involvement of GO (class II or III disease). Mean proptosis and ophthalmopathy index scores were significantly decreased after 3 months of octreotide therapy. Mean sICAM-1 levels were significantly higher in patients before octreotide therapy (470.5 +/- 52.6 ng/mL, p < 0.0001) when compared to normal subjects (186.5 +/- 53.3 ng/mL). Mean sICAM-1 levels were significantly decreased 3 months after octreotide therapy (from 478.7 +/- 52.6 to 415 +/- 42.8 ng/mL, p = 0.012) in the 8 patients who responded to therapy. In contrast, sICAM-1 levels remained unchanged or increased in two patients with poor response to octreotide therapy. Our results suggest that octreotide therapy could be a treatment modality in patients with GO. The mechanism by which octreotide acts on GO is not clear. The observed decrease in sICAM-1 levels during octreotide therapy suggests that octreotide may have immunomodulatory properties. Further investigation is needed to determine the optimal dose and duration of octreotide therapy.

Adult↗

PubMed1996

Daytime plasma melatonin levels in male hypogonadism.

It has previously been shown that increased nocturnal melatonin (MT) secretion exists in male patients with hypogonadotropic hypogonadism. However, little is known about the effects of gonadotropin and testosterone (T) treatment on early morning plasma MT levels in male hypogonadism. Also, the impact of gonadal steroids on plasma MT levels is an open question. We, therefore, determined early morning plasma MT levels at the same hour before and 3 months after treatment in 21 patients with idiopathic hypogonadotropic hypogonadism (IHH), 10 patients with primary hypogonadism, and 11 male controls. Plasma FSH, LH, PRL, T, and estradiol levels were also determined before and 3 months after treatment. Patients with IHH were treated with hCG/human menopausal gonadotropin, whereas patients with primary hypogonadism received T treatment. Short term treatments did not achieve normal T levels, although significant increases in T were observed in both groups. Plasma MT levels were measured by a RIA with a sensitivity of 10.7 pmol/L. Mean plasma MT levels before treatment were significantly higher in IHH (41.8 +/- 24.4 pmol/L) compared with those in the controls (21.7 +/- 10.8 pmol/L; P < 0.05). However, a slight, but not significant, increase in MT (34.2 +/- 21.1 pmol/L) was found in primary hypogonadism. Mean MT levels did not change significantly 3 months after the initiation of gonadotropin (41.7 +/- 22.8 pmol/L) or T (28.4 +/- 12.6 pmol/L) treatment in either IHH or primary hypogonadism, although a tendency for MT to decrease was observed in both groups. No correlation was found between MT and circulating FSH, LH, PRL, and gonadal steroids either before or after therapy. We conclude that male patients with IHH have increased early morning MT levels, although the pathophysiological mechanism is not clear. Furthermore, our study demonstrated that mean plasma MT levels are not influenced by short term gonadotropin or T treatment in male hypogonadism, although a longer time effect of gonadotropins or T treatment may not be excluded. The lack of correlation between plasma MT and circulating gonadal steroids before and after treatment suggests that there is no classic feedback regulation between the pineal gland and the testes.

Adult↗

PubMed1996

Effects of gonadotropin and testosterone treatments on Lipoprotein(a), high density lipoprotein particles, and other lipoprotein levels in male hypogonadism.

It is known that lipoprotein(a) [Lp(a) is an independent risk factor for developing atherosclerosis, whereas the LpA-I particle of high density lipoprotein (HDL) is an antiatherogenic factor. The effects of androgen replacement therapy on lipid and lipoproteins have previously been reported in male hypogonadism. However, no study reported the effect of gonadotropin or testosterone treatment on Lp(a), LpA-I, or LpA-I;A-II levels in make hypogonadism. We, therefore, determined Lp(a), LpA-I, LpA-I:A-II, and other lipoprotein levels before and 3 months after treatment in 22 patients with idiopathic hypogonadotropic hypogonadism (IHH) and in 9 patients with Klinefelter's syndrome. All patients had been previously untreated for androgen deficiency. Plasma FSH, LH, PRL, testosterone (T), estradiol, and dehydroepiandrosterone sulfate levels were also determined before and 3 months after treatment. Patients with IHH were treated with hCG/human menopausal gonadotropin, whereas patients with Klinefelter's syndrome received T treatment. Three months after treatment, mean T levels role to low normal levels in both groups. Triglyceride, LpA-I:A-II, Lp(a), HDL cholesterol, HDL3 cholesterol, and apolipoprotein (apo) A-I concentrations did not change significantly after treatment, whereas total cholesterol, low density lipoprotein cholesterol, LpA-I, and HDL2 concentrations were significantly increased 3 months after treatment in both groups. The apo B concentration significantly increased in patients with klinefelter's syndrome, whereas no change was observed in the IHH group. Lp(a) concentrations were not related to all hormonal and clinical parameters in both groups. LpA-I concentrations were significantly and negatively correlated with free T (r = -0.80; P = 0.010) in patients with Klinefelter's syndrome and were not correlated with all hormonal and clinical parameters in the IHH group. The LpA-I:A-II concentration was only correlated with body mass index (r = -0.83; P = 0.005) in patients with Klinefelter's syndrome, whereas it was correlated negatively with dehydroepiandrosterone sulfate (r = -0.57; P = 0.005) in the IHH group.2 Overall, our study demonstrates that gonadotropin or T treatment has a complex effect on lipids and lipoproteins. This complexity will be resolved when sufficient large scale androgen treatment data are available for assessment of the long term outcome of androgen treatment. The increases in total cholesterol and low density lipoprotein cholesterol concentrations after treatments are the adverse effects of these treatments, whereas the increases in HDL2 and LpA-I concentrations and the lack of changes in Lp(a) are the beneficial effects. Gonadotropin or T treatment did not modify the Lp(a) concentration, indicating that it is not affected by the hormonal milieu in male hypogonadism. Our study also showed that LpA-I, but not LpA-I:A-II, particles could be modified by androgen replacement therapy.

Adult↗

PubMed1996

Soluble intercellular adhesion molecule-1 concentrations in patients with subacute thyroiditis and in patients with Graves' disease with or without ophthalmopathy.

Increased circulating soluble ICAM-1 (sICAM-1) levels has been previously reported in Graves' disease (GD) patients with or without ophthalmopathy (GO) and in patients with toxic nodular goiter but not in patients with subacute thyroiditis. Conflicting results have also been reported about the usefulness of sICAM-1 levels as a marker for the activity of hyperthyroidism. We have therefore determined sICAM-1 levels by a sandwich enzyme linked immunosorbent assay (ELISA) method in 10 patients with subacute thyroiditis (Group 1), who are at the initial or acute phase of thyroiditis, in 10 hypothyroidic patients with Hashimoto's thyroiditis (Group 2), in 10 patients with euthyroid nodular goiter (Group 3), in 10 patients with untreated GD patients with active ophthalmopathy (Group 4), in 10 hyperthyroid GD patients without clinical ophthalmopathy (Group 5), in 10 patients with GO who are euthyroid and treated with glucocorticoids for 3 months (Group 6) and in 20 normal subjects (Control Group). Groups 1,2,4,5 and 6 (P < 0.00001 for Groups 1,4,5,6 and P < 0.05 for Group 2) but not Group 3 showed increased sICAM-1 levels compared with the control group. However Groups 4 and 6 (patient with GO) showed significantly higher sICAM-1 levels (P = 0.0003 for Group 4 and P = 0.00013 for Group 6) than Group 5. Furthermore Group 4 showed slightly but not significantly higher sICAM-1 levels than Group 6. Mean sICAM levels were significantly decreased 3 months after glucocorticoid treatment (Group 6), but had not returned to normal levels. Three patients did not respond to steroid therapy and their sICAM-1 levels were not decreased. We concluded that patients with GO with or without hyperthyroidism and patients with subacute thyroiditis have elevated sICAM-1 levels. Moreover, sICAM-1 levels reflect the degree of inflammatory activity in the thyroid gland or orbital tissue independent of the thyroidal status, since we found elevated levels in both hyperthyroidism and hypothyroidism.

Adult↗

PubMed1995

Subclinical hypothyroidism does not lead to alterations either in peripheral nerves or in brainstem auditory evoked potentials (BAEPs).

Functional alterations in the central nervous system and peripheral nerves are well documented in overt hypothyroidism, but not in subclinical hypothyroidism. Twenty-seven patients with subclinical hypothyroidism were compared with a control group of 20 age- and sex-matched subjects to determine whether subclinical hypothyroidism can lead to alterations in peripheral nerves or in the brainstem auditory evoked potentials (BAEPs). None of the patients had carpal tunnel syndrome or any other neurological or metabolic disturbances. Disease duration (expressed as the time from diagnosis of subclinical hypothyroidism to the time of neurological testing) ranged from less than 1 month to 6 months (median 2.5 months). We studied the distal motor latency, nerve conduction velocity (NCV), compound muscle action potentials, and F response in the median and peroneal nerves whereas the sensory nerve conduction velocity and sensory potential amplitude were measured in the sural and median nerves. Electrophysiological parameters and interpeak latencies yielded no significant difference between patient and control groups. The present study indicates that subclinical hypothyroidism of short duration does not lead to abnormalities of peripheral nerves or brainstem auditory evoked potentials.

Action Potentials↗

PubMed1995

Sequential changes in serum thyroid peroxidase following radioiodine therapy of patients with differentiated thyroid carcinoma.

To determine the detectability and the time course of serum thyroid peroxidase (TPO) levels before and 1, 2, 4, and 6 months after 131I administration, we evaluated TPO in 13 selected patients with differentiated thyroid carcinoma (DTC) whose sera did not contain antimicrosomal or antithyroglobulin (Tg) antibodies. All patients received 131I therapy 6 or 8 weeks after thyroid surgery for ablation of the postsurgical thyroid remnant. Serum samples were also collected from 10 normal subjects. Measurement of TPO was carried out by using a new commercially available immunoluminometric assay with a sensitivity of 30 pg/mL. Serum Tg was measured by RIA with a sensitivity of 2.6 micrograms/L before and 6 months after 131I administration. In all patients, a standard total body scan was obtained before and 6 months after 131I administration. TPO was undetectable in all sera from normal subjects. However, serum TPO became detectable in all patients with DTC during the study, whereas rescans were either negative or positive and appeared not to be related to the radioiodine dose given, histology of the thyroid tumor, residual thyroid volume, TSH levels, or age of patients. However, a significant negative correlation was present between TPO levels before 131I administration and the time from surgery (r = -0.82, P < 0.001). Six of 13 patients had increased TPO levels 1 month after 131I administration. Serum TPO levels tended to decrease during follow-up in most patients (7 of 10) with a negative rescan. In 3 patients with positive rescans, TPO levels tended to increase during follow-up. Patients with negative rescans had values of serum TPO overlapping the range of values seen in patients with positive rescans, thus demonstrating the inability of TPO assay as a useful marker for following patients with DTC. We found no correlation between Tg and TPO levels measured before and 6 months after 131I administration, thereby excluding TPO levels as a marker for thyroid cancer. Our results suggest that TPO, unlike Tg, does not appear to be a useful marker for following patients with DTC.

Adult↗

PubMedDate not supplied

Central and peripheral neural responses in males with idiopathic hypogonadotropic hypogonadism.

It has previously been shown that abnormal neurophysiologic responses are associated with Kallmann's syndrome. However, little is known about neurophysiologic responses in idiopathic hypogonadotropic hypogonadism (IHH). Fifty-six untreated male patients with IHH (mean age: 20 +/- 0.7 years) were compared with a control group of 20 age-matched male subjects to determine whether IHH can lead to alterations in somatosensory evoked potentials (SSEPs) and brainstem auditory evoked potentials (BAEPs). We have also investigated the effect of gonadotropin replacement (hCG/hMG) therapy on these tests in 20 randomly selected patients. Significant cervical 7 (N13), Erb (N9) and thoracic 12 (N22) latency prolongation was observed in median and tibial nerve SSEPs in patients with IHH as compared with a matched control group. Other components of SSEPs and interpeak latencies of BAEPs yielded no significant difference between untreated patients and control group. Abnormal components of SSEPs did not correlate with basal hormone levels and did not improve with gonadotropin therapy. We conclude that IHH results abnormalities in peripheral but not central nervous system components of SSEPs and that short term gonadotropin treatment cannot correct these abnormalities.

Adolescent↗