Thyrotoxic hypokalemic periodic paralysis as the first manifestation of interferon-alpha-induced Graves disease.
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Biomedical subjects
Publications and source records attributed to Murat Faik Erdogan.
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BACKGROUND: Elevated levels of basal and stimulated calcitonin are commonly seen in hereditary and sporadic medullary thyroid cancer (MTC) following total thyroidectomy. The cause of these high levels can be residual thyroid tissue, possibly with C-cell hyperplasia, and/or residual micro-MTC foci. MTC does not have the ability to concentrate radioactive iodine. However, radioactive iodine trapped by thyroid follicular cells may affect the neighbouring parafollicular cells. AIM: To investigate the effect of radioactive iodine treatment as adjuvant therapy to surgery in seven patients with persistent elevation of basal and stimulated calcitonin levels. METHODS: Pentagastrin testing was performed in each case immediately before surgery and at intervals of 6 months over a maximum period of 5 years (range, 44-60 months) after surgery. RESULTS: A significant decrease in basal and stimulated calcitonin levels was observed in three patients whose disease was localized to the thyroid gland at the final visit. In the remaining four patients, who initially had lymph node involvement at surgery, basal and stimulated calcitonin levels were decreased significantly in only one. At follow-up, of the three patients who showed no decrease in basal and stimulated calcitonin levels, two developed further regional lymph node and distant metastases. CONCLUSIONS: In patients with persistently elevated basal and stimulated calcitonin levels, radioactive iodine treatment may be the therapy of choice for C-cell hyperplasia and/or micro-MTC after optimal thyroid surgery, especially if the disease has not spread beyond the thyroid gland.
OBJECTIVE: Few studies using ultrasonographic evaluation have addressed the natural course of benign thyroid nodules. In this study, we present the long-term analysis of benign, untreated thyroid nodules in a moderately iodine-deficient area. DESIGN: We collected the retrospective data for 531 nodules in 420 patients followed by ultrasonography for a mean time period of 39.7 +/- 27.8 months (range 12-168 months). RESULTS: When we considered significant nodule size decrease criteria as decreases in nodule volume of at least 15% and 30%, we found that 33.1% and 20.7% of thyroid nodules decreased in size, respectively. Using the criteria of a greater than 15% and 30% increase in volume showed that 32% and 24.1% increased in size, respectively. A logistic regression analysis using mixed models to predict thyroid nodule growth (volume change > or = 15%), including age, TSH, sex and time between evaluations, failed to predict nodule growth. Only hypoechoic echo pattern remained as a statistically significant predictor of growth. CONCLUSION: In 40 months' follow-up, we found that benign thyroid nodules exhibited a mostly favourable clinical natural course. One-third of benign thyroid nodules showed continuous growth, one-third remained unchanged, and the other third decreased in size.
INTRODUCTION: Erectile dysfunction (ED) is a common complication of diabetes mellitus (DM). However, efficacy and/or long-term satisfaction with most of those ED treatment options have been suboptimal. AIM: In this study we try to evaluate the effect of aggressive treatment and DM regulation on the erectile function in men with DM-induced ED (DMED). METHODS: Eight type 1 and 17 type 2 diabetic subjects were included into the study. All patients had a measurement of fasting plasma glucose (FPG) and glycosylated hemoglobin (HbA1(c)) levels, and completed three sessions of consecutive nights using the RigiScan Plus monitoring device before and after blood sugar control. Also International Index of Erectile Function (IIEF) questionnaire scores were obtained before and after blood sugar control. RESULTS: Significant improvement was noted in FPG and HbA1(c) levels throughout the treatment period (P < 0.001). However, no statistically significant difference was observed in both IIEF scores and nocturnal penile tumescence and rigidity (nptr) parameters after the dm regulation (p > 0.05). CONCLUSION: We suggest that there are probably other factors than aggressive treatment and DM regulation for treating DMED, and probably we must consider preventive strategies with pharmacological agents to prevent progressive decrease in erectile function in diabetic patients.
A 53-yr-old previously healthy man was admitted to our hospital for thyrotoxicosis without ophthalmopathy. Initial therapy with propylthiouracil caused an acute elevation of liver enzymes. Then, he received a first course of 131I therapy (20 mCi). At the end of 6-mo follow-up after 131I, he was still thyrotoxic and developed moderately severe ophthalmopathy. The patient refused thyroid surgery and decided to undergo second course of 131I therapy (30 mCi). Concomitantly with the 131I, we opted to give high-dose pulse glucocorticoid therapy (PGT) to prevent further deterioration of GO. The patient was started on intravenous methylprednisolone pulse therapy 1 g daily in a cycle (one cycle every 2 wk, each cycle comprising two infusions on alternate days). After the end of the second day of PGT administration, he suddenly developed onset of acute pulmonary edema and hypertension. There was no previous history of cardiac disorder or conditions predisposing to cardiac failure other than thyrotoxicosis. A presumptive diagnosis of fluid overload and/or hypertension- induced acute heart failure was made. After prompt investigations excluding cardiogenic causes, we thought that this condition was triggered by PGT that was superimposed on thyrotoxicosis-related hemodynamic instability. Graves' patients with uncontrolled thyrotoxicosis should be under careful surveillance when PGT is planned. To our knowledge, this is the first reported case of life-threatening acute pulmonary edema caused by PGT in GO.
Multiple endocrine neoplasia type 2B (MEN 2B) is a rare syndrome characterized by medullary thyroid carcinoma (MTC), pheochromocytoma and typical phenotypic features, such as marfanoid habitus, multiple mucosal ganglioneuromas and thickened corneal nerves. Individuals with MEN 2B may develop megacolon and pseudo-obstruction due to intestinal ganglioneuromatosis simulating Hirschsprung's (HSCR) disease. We hereby describe the clinical and genetic features of a 21-year-old male patient with MEN 2B associated with pseudo-HSCR disease. The patient had MTC, pheochromocytoma, marfanoid habitus, multiple mucosal ganglioneuromas, thickened corneal nerves and severe gastrointestinal involvement. Emergent laparotomy was performed when he was presented with acute bowel obstruction. The myenteric and submucosal nerve plexuses in the small and large intestines were composed of diffusely hyperplasic, disorganized, mature ganglion cells. Genetic testing revealed a de novo ret proto-oncogene germline mutation in codon 918 in exon 16. Megacolon and pseudo-obstruction similar to the HSCR disease may develop in patients with MEN 2B. However, the observed dysmotility is the result of an abnormal proliferation of intramural ganglion cells in contrast to the absence of enteric ganglia which were present in the HSCR disease. Attentiveness about the phenotypic characteristics and unusual findings might lead to early and correct diagnosis of the MEN 2B syndrome. This approach improves the survival rate and quality of life considerably.
OBJECTIVE: There is controversy about hormonal dysfunction in the hypothalamic-pituitary-adrenal (HPA) axis that is supposed to contribute to the development or persistence of rheumatoid arthritis (RA). We investigated whether there is an altered and blunted response of the HPA axis when stimulated by exercise stress in patients with RA. METHODS: Twenty women with RA and 15 matched healthy controls were included in the study. All subjects took an ergospirometric exercise test on the treadmill to determine anaerobic threshold (AT). On another day, blood was collected for basal plasma levels of growth hormone (GH), insulin-like growth factor-I, cortisol, and adrenocorticotrophic hormone (ACTH); and subjects exercised on treadmill at an intensity above their AT. Blood was collected again to measure hormone levels just after the exercise stopped and 60 minutes later. RESULTS: Two subjects left the study, so 19 patients and 14 controls were evaluated. Peak oxygen consumption (VO(2)), VO(2) at AT, exercise test duration, and basal hormone levels were similar in groups. In both groups, GH slightly increased just after the exercise (0 min), and decreased at 60 min compared to baseline, but the change was not different between groups. Cortisol levels decreased significantly at 0 and 60 min in both groups, ACTH levels did not change in time, and there was no difference between groups. CONCLUSION: There was no perturbation in HPA axis stimulated by exercise stress test in patients with RA and all the variables measured were similar to those of the control group.
BACKGROUND: Hyperthyroidism is a major cause of paroxysmal atrial fibrillation (AF). The purpose of this study was to evaluate the predictors of AF in the patients with clinical and subclinical hyperthyroidism. METHODS AND RESULTS: The study population consisted of four groups: group I (57 euthyroid healthy persons), group II (33 patients with subclinical hyperthyroidism), group III (69 patients with overt hyperthyroidism) and group IV (31 patients with overt hyperthyroidism and documented paroxysmal AF). The maximum P wave duration (P maximum) in group IV (114 +/- 8 ms) was significantly higher than group I (102 +/- 7 ms, p < 0.001), group II (106 +/- 7 ms, p < 0.001) and group III (108 +/- 9 ms, p0.005). The P wave dispersion (PWD) was measured as 46 +/- 9 ms in group IV and this was significantly higher than group I (29 +/- 8 ms, p < 0.001), group II (36 +/- 9 ms, p < 0.001) and grup III (38 +/- 8 ms, p = 0.001). The P maximum and PWD were higher in the patients with subclinical hyperthyroidism compared to healthy individuals. Univariate regression analysis revealed that age, P maximum and PWD, multivariate analysis showed that P maximum and PWD were significant predictors of paroxysmal AF. A PWD value of 37.5 ms separated group IV from others with a sensitivity of 90%, specificity of 85%, and positive predictive accuracy of 77%. CONCLUSION: Simply measuring P maximum and PWD values, we could identify the patients with high risk for the development of AF and these simple ECG parameters may help in clinical judgement to determine the requirement for treatment in the patients with subclinical hyperthyroidism.
BACKGROUND: One of the candidate genes for susceptibility to Graves' disease (GD) is cytotoxic T lymphocyte-associated molecule-4 (CTLA-4), a negative regulator of T-cell activation. In order to elucidate the relationship of GD with the A/G polymorphism in exon 1 and the C/T polymorphism in the promoter region of the CTLA-4 gene, the frequency of these two polymorphisms was identified in 98 healthy individuals and 77 patients with GD. METHODS: Polymorphisms were analyzed using a PCR-RFLP method. We also examined the relationship between the A/G polymorphism and various clinical and laboratory variables among patients with GD. All patients were treated with an initial dose of propranolol (40-60 mg /day) and PTU (300-400 mg/day). Subjects remained on this treatment for a minimum of 6 months and were followed in our clinic for 1 year after cessation of treatment. RESULTS: The frequency of the GG genotype was significantly higher among patients with GD than among controls of both sexes (P<0.05; odds ratio=3.145, 95% CI=1.212-8.161). There was no difference between patients and controls with regard to the C/T polymorphism. There was no statistical difference in age, sex, cigarette smoking, initial serum thyroid hormone levels, initial goiter size, initial TSH-receptor antibodies, or NOSPECS classification for orbitopathy among the patients with the three different genotypes (GG, AG, and AA). Of the patients with the AA genotype, 17 of 29 (58.6%) were in remission 1 year after PTU withdrawal, while 18 of 33 patients (54.4%) with the AG genotype were in remission 1 year later. However, only 3 of 15 patients (20%) with the GG genotype were in remission 1 year after withdrawal of antithyroid drug therapy (P=0.016 GG/AA, P=0.025 GG/AG). Using 1 year after discontinuation of antithyroid drug therapy as the cut-off point for multivariate logistic regression analysis, we found that the GG genotype, TSH at the end of therapy, and age were independent risk factors for recurrence. CONCLUSION: We conclude that the occurrence of GD is linked to the A/G polymorphism of the CTLA molecule in the Turkish population and is associated with a lower chance of remission after discontinuation of PTU treatment.
Thiocyanate [SCN-] is a complex anion which is a potent inhibitor of iodide transport. It is the detoxification product of cyanide and can easily be measured in body fluids. Consumption of naturally occurring goitrogens, certain environmental toxins and cigarette smoke can significantly increase SCN- concentrations to levels potentially capable of affecting the thyroid gland. Goiter endemics were reported to develop when the critical urinary iodine/ SCN- ratio decreases below 3 microg iodine per mg SCN-. Iodine supplementation completely reverses the goitrogenic influence of SCN-. SCN- is also generated from cigarette smoking as a detoxifying product of cyanide. During the past two decades many reports dealt with the possible effects of cigarette smoking on thyroid hormone synthesis, thyroid gland size and thyroid autoimmunity including infiltrative ophtalmopathy of Graves' disease. In this mini-review, issues regarding thiocyanate overload and thyroid disease will be summarized.
Amiodarone-induced thyrotoxicosis (AIT) is a complex therapeutic challenge. Two major forms have been described: type I and type II. Methimazole (MMI) and potassium perchlorate (KCLO(4)) is the treatment of choice for the former, whereas corticosteroids are used for the latter. However, mixed forms appear frequently and it is not easy to prescribe corticosteroids because of side effects. The present study investigated the validity of a stepwise therapeutic approach to AIT. Twenty patients with AIT were given 30-50 mg/d of MMI and 1000 mg/d of KCLO(4) initially for a month. Euthyroidism or a significant decrease in serum thyroid hormone levels could be achieved in 12 of the patients (7 with type I, 5 type II). Prednisolone, 40-48 mg/d was added for the 8 nonresponding patients (7 type I, 1 type II) and euthyroidism was achieved in all. The prednisolone dose was decreased when free thyroxine (T(4)) levels normalized, and MMI was titrated, maintaining euthyroidism until urinary iodine excretion normalized. Mixed forms of AIT may prevail in iodine-deficient areas. Initial classification of the patients may cause unnecessary corticosteroid use in a substantial number of patients with AIT. A stepwise approach is feasible; however, when the patient is gravely ill, MMI, KCLO(4), and prednisolone could be prescribed simultaneously.
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