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Hyperthyroidism
Kinds of Hyperthyroidism Selected AbstractsEffect of di(n -butyl) phthalate on testicular oxidative damage and antioxidant enzymes in hyperthyroid ratsENVIRONMENTAL TOXICOLOGY, Issue 3 2007Ena Lee Abstract This study compared the effects of di(n-butyl) phthalate (DBP) on the oxidative damage and antioxidant enzymes activity in testes of hyperthyroid rats. Hyperthyroidism was induced in pubertal male rats by intraperitoneal injection of triiodothyronine (T3, 10 ,g/kg body weight) for 30 days. An oral dose of DBP (750 mg/kg) was administered simultaneously to normal or hyperthyroid (T3) rats over a 30-day period. No changes in body weight were observed in the hyperthyroid groups (T3, T3 + DBP) compared with controls. There were significantly higher serum T3 levels observed in the hyperthyroid rats than in the control, but the serum thyroid stimulating hormone levels were markedly lower in the hyperthyroid rats. DBP significantly decreased the weight of the testes in the normal (DBP) and hyperthyroid (T3 + DBP) groups. The serum testosterone concentrations were significantly lower in only DBP group. DBP significantly increased the 8-hydroxy-2-deoxyguanosine (8-OHdG) level in the testes, whereas the DBP-induced 8-OHdG levels were slightly higher in T3 + DBP group. Superoxide dismutase and glutathione peroxidase activities were significantly higher in the testes of the DBP or T3 + DBP groups. Catalase (CAT) activity was significantly higher in the DBP treatment group, but the T3 + DBP group showed slightly lower DBP-induced CAT activity. The testicular expression of thyroid hormone receptor ,-1 (TR,-1) was significantly higher in the DBP groups, and androgen receptor (AR) expression was not detected in the DBP treatment group. In addition, DBP significantly increased the peroxisome proliferator-activated receptor-r (PPAR-r) levels in the testis. These results suggest that hyperthyroidism can cause a change in the expression level of PPAR-r in testes, and may increase the levels of oxidative damage induced by the metabolic activation of DBP. © 2007 Wiley Periodicals, Inc. Environ Toxicol 22: 245,255, 2007. [source] Differential effect of hyperthyroidism on rat epididymal glycosidasesINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 4 2001R. R. M. Maran The impact of hyperthyroidism on epididymal glycosidases was studied in albino rats. Hyperthyroidism was induced in Wistar rats aged 30 days by daily injection of T4 (25 ,g/100 g body weight/day intramuscularly) for 30 or 60 days; control rats were injected with vehicle (alkaline saline, pH 7.8). One set of hyperthyroid rats was reverted to euthyroid status by withdrawing T4 treatment after 30 days of hyperthyroidism. To asses the direct effect of thyroid hormone on epididymal hexosaminidases, caput, corpus and cauda tissues were stimulated with 25, 50 or 100 ng/mL T3 for 24 h, after an initial culture of 24 h. The activity of ,-glucosidase decreased in caput, corpus and cauda epididymis of hyperthyroid rats. ,-Galactosidase activity increased in the caput epididymis irrespective of the duration of hyperthyroidism. While a similar decrease occurred in the corpus and cauda epididymis in the 30 day hyperthyroid group, an opposite trend was observed in 60 day hyperthyroid rats. Caput ,- N -acetylglucosaminidase activities increased at both time points, whereas activity decreased in the corpus and cauda in 30 day, but increased in 60 day hyperthyroid rats. Hyperthyroidism consistently increased caput and corpus ,- N -acetylgalactosaminidase activity irrespective of the duration. Cauda epididymal ,- N -acetylgalactosaminidase activity was decreased in 30 day and increased in 60 day hyperthyroid rats. Hyperthyroidism induced changes in caput ,-galactosidase, ,- N -acetylgalactosaminidases, corpus ,-N-acetylglucosaminidase and cauda ,- N -acetylgalactosaminidase which were irreversible while the remaining actvities were brought back to normal when T4 treatment was withdrawn. In vitro studies showed that T3 stimulates epididymal hexosaminidases (,- N -acetylglucosaminidase and ,- N -acetylgalactosaminidase) irrespective of the dose. These data suggest that thyroid hormones have a specific and direct influence on glycosidases in specific regions of the epididymis. [source] Prevalence and clinical significance of antineutrophil cytoplasmic antibody in Graves' patients treated with propylthiouracilINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 2 2009M.Ozduman Cin Summary Development of antineutrophil cytoplasmic antibody (ANCA) during therapy with propylthiouracil (PTU) is not uncommon and PTU-induced ANCA-positive vasculitis is also reported. The aim of this study was to assess the presence and clinical significance of ANCA positivity in Graves' patients treated with PTU. Newly diagnosed Graves' disease patients (prospective group, n = 58) were evaluated before and during therapy with PTU to investigate the development of ANCA positivity. ANCA positivity is also investigated in previously diagnosed Graves' patients who had already been receiving PTU treatment (cross-sectional group, n = 51). Comparisons with Hashimoto thyroiditis (n = 55) and toxic nodular goitre (n = 20) patients, and healthy control subjects (n = 20) were carried out to define the possible influence of hyperthyroidism and/or thyroid autoimmunity on ANCA positivity. At baseline evaluation, ANCA was negative in all newly diagnosed Graves' patients. Only 28 of the 58 patients in prospective group completed 2 years of follow-up which occurred at 3-month intervals. ANCA positivity was detected 32.1% (n = 9) in a mean period of 11.7 ± 6.1 months in prospective group. Only two (3.9%) patients in a cross-sectional group had ANCA positivity in a mean treatment period of 7.6 ± 4.6 months. None of the patients with ANCA positivity developed symptoms and signs related to vasculitis. None of the patients with Hashimoto thyroiditis and toxic nodular goitre, and healthy control subjects had ANCA positivity. PTU therapy is associated with asymptomatic production of ANCA in a time-dependent manner, which mostly disappears after discontinuation of therapy. Hyperthyroidism or autoimmunity per se does not appear to have effect on development of ANCA positivity. [source] Hyperthyroidism: A Secondary Cause of Isolated Systolic HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 8 2006L. Michael Prisant MD Isolated systolic hypertension is the most common form of hypertension, especially among patients 50 years or older. What is not appreciated is that there are secondary causes of isolated systolic hypertension. Hyperthyroidism increases systolic blood pressure by decreasing systemic vascular resistance, increasing heart rate, and raising cardiac output. Potential cardiovascular consequences of hyperthyroidism include atrial arrhythmias (especially atrial fibrillation), pulmonary hypertension, left ventricular hypertrophy, and heart failure. The prevalence of hypertension is greater among hyperthyroid patients than euthyroid patients. Whether there is a blunted nocturnal decline in ambulatory blood pressure among hyperthyroid patients is more controversial. Treatment is associated with a reduction in systolic blood pressure, heart rate, and cardiac output. [source] Evaluation and Treatment of Hyperthyroidism and HypothyroidismJOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS, Issue 10 2004ANP-C, FAANP, Mary Jo Goolsby EdD ABSTRACT This month's clinical practice guideline (CPG) review is on the diagnosis and treatment of hyperthyroidism and hypothyroidism as provided by the American Association of Clinical Endocrinologists. An estimated 27 million Americans have thyroid disease, and about 13 million of them are undiagnosed. The risk of thyroid disease increases with age, and women are seven times more likely than men to develop thyroid problems. Unfortunately, thyroid symptoms are usually very nonspecific and should be kept in the differential diagnosis of many clinical complaints. The format of this month's column is a little different because we received two independent manuscripts, each of which had merit. We made a decision to present both points of view and deleted repetitive material. This is an example of variable approaches one can take with reviewing and critiquing CPGs. [source] Survival and the Development of Azotemia after Treatment of Hyperthyroid CatsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2010T.L. Williams Background: Hyperthyroidism complicates the diagnosis of chronic kidney disease (CKD) as it increases glomerular filtration rate. No practical and reliable means for identifying those cats that will develop azotemia after treatment for hyperthyroidism has been identified. Hyperthyroidism is associated with proteinuria. Proteinuria has been correlated with decreased survival of cats with CKD and with progression of CKD. Hypothesis: Proteinuria and other clinical parameters measured at diagnosis of hyperthyroidism will be associated with the development of azotemia and survival time. Animals: Three hundred client owned hyperthyroid cats treated in first opinion practice. Methods: Retrospective, cohort study relating clinical parameters in hyperthyroid cats at diagnosis to the development of azotemia within 240 days of diagnosis and survival time (all cause mortality). Multivariable logistic regression analysis was used to identify factors that were predictive of the development of azotemia. Multivariable Cox regression analysis was used to identify factors associated with survival. Results: Three hundred cats were eligible for survival analysis and 216 cats for analysis of factors associated with the development of azotemia. The median survival time was 417 days, and 15.3% (41/268) cats developed azotemia within 240 days of diagnosis of hyperthyroidism. Plasma concentrations of urea and creatinine were positively correlated with the development of azotemia. Plasma globulin concentration was negatively correlated with the development of azotemia. Age, urine protein : creatinine ratio, and the presence of hypertension were significantly correlated with decreased survival time. Urine specific gravity and PCV were significantly correlated with increased survival time. Conclusions and Clinical Importance: The proteinuria associated with hyperthyroidism is not a mediator of progression of CKD; however, it does correlate with all cause mortality. [source] Recombinant Human Thyrotropin Administration Enhances Thyroid Uptake of Radioactive Iodine in Hyperthyroid CatsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2008I. Van Hoek Background: Hyperthyroidism is the most diagnosed endocrine disorder in cats and radioiodine (131I) is the treatment of choice. The dose emission rate and radioactivity in urine, saliva, and on hair and paws are determined by the dose of administered 131I. A dose reduction of therapeutic 131I could possibly be achieved after recombinant human thyrotropin (rhTSH) administration as in humans with nodular goiter. Hypothesis: rhTSH will increase radioiodine uptake in hyperthyroid cats. Animals: Five hyperthyroid cats. Methods: Twenty-five micrograms rhTSH (day 1) or 2 mL 0.9% sodium chloride (NaCl) (day 9) was injected IV. One hour later, 11.4 ± 4.1 (mean ± SD) MBq 123I was injected IV. Radioactive iodine uptake (RAIU) was measured 6, 12, and 24 hours after rhTSH (RAIU-rhTSH) or NaCl (RAIU-blanco) injection. Blood samples for measurement of TT4 were taken before injection of rhTSH or NaCl (TT40) and at the time of imaging. Results: Percentages of RAIU-rhTSH (and RAIU-blanco) at 6, 12, and 24 hours after administration of rhTSH were 34 ± 18 (31 ± 21), 46 ± 20 (38 ± 18), and 47 ± 15 (36 ± 14). There was a statistically significant effect of rhTSH administration on RAIU (P= .043) but not on serum TT4 concentration. Baseline serum TT40 concentration influenced RAIU-rhTSH significantly at 6 hours (P= .037). Conclusion and Clinical Importance: The increased RAIU observed after rhTSH administration in hyperthyroid cats could lead to a lower therapeutic dose of 131I after rhTSH administration in hyperthyroid cats and decreased risk of environmental and owner contamination during and after hospitalization. [source] Thyrotropin-Releasing Hormone Stimulation Test to Assess Thyroid Function in Severely Sick CatsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2001Kamil Tomsa Basal serum thyroxine (T4) concentration and the thyrotropin-releasing hormone (TRH) stimulation test were used to assess thyroid function in 36 critically ill cats examined between July 1996 and October 1998. Of the 36 cats, hyperthyroidism (as underlying or complicating disease) was suspected in 22 based on clinical signs, palpable thyroid nodules, and abnormal thyroid gland histology (study group). Hyperthyroidism was not suspected in the remaining 14 cats, which served as the control group. Based on serum T4 concentrations, suppression of thyroid function was documented in 14 (64%) cats of the study group and in 10 (71%) cats of the control group. The TRH stimulation test revealed an increase in serum T4 of less than 50% of the baseline concentration in 18 (82%) cats of the study group, and in 6 (43%) cats of the control group. In conclusion, based on the results of serum T4 determinations and the TRH stimulation tests, it was not possible to differentiate between cats with clinical and histologic evidence of thyroid dysfunction (hyperthyroidism) and cats with severe nonthyroidal illnesses. [source] Attenuation of Oxidative Stress in Plasma and Tissues of Rats with Experimentally Induced Hyperthyroidism by Caffeic Acid Phenylethyl EsterBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2007Ahmed M. Mohamadin The present study was designed to investigate the protective effects of caffeic acid phenylethyl ester (CAPE) on oxidative damage in rats with experimentally induced hyperthyroidism. The study was conducted on 32 male Sprague-Dawley rats. The experimental animals were divided into four groups (control, CAPE alone, hyperthyroidism, and hyperthyroidism + CAPE). Hyperthyroidism was induced by intraperitoneal administration of 0.3 mg/kg/day l -thyroxine for 4 weeks. CAPE (10 µg/kg) was administered intraperitoneally for 4 weeks. At the end of the experimental period, blood samples and various organs (liver, heart and brain) of rats were taken for the determination of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), oxidized glutathione, vitamin C and superoxide dismutase (SOD) levels and concentrations of triiodothyronine (T3), thyroxine (T4) and thyroxine-stimulating hormone (TSH). Our results indicate that TBARS, oxidized glutathione, SOD levels and concentrations of T3 and T4 were higher in plasma and tissues of the hyperthyroid group compared to controls. Vitamin C, GSH and TSH levels were decreased significantly in the hyperthyroid group when compared to the control group. CAPE treatment decreased the elevated TBARS, SOD, T3 and T4 levels and increased the lowered GSH, vitamin C and TSH levels to control levels in rats with hyperthyroidism. In conclusion, our results indicate that CAPE is beneficial as a protective agent against oxidative stress induced by hyperthyroidism in rats. The protection is probably due to multiple mechanisms involving free radical scavenger properties, attenuating lipid peroxidation and increasing the antioxidant status. [source] Hyperthyroidism is characterized by both increased sympathetic and decreased vagal modulation of heart rate: evidence from spectral analysis of heart rate variabilityCLINICAL ENDOCRINOLOGY, Issue 6 2006Jin-Long Chen Summary Objective, The clinical manifestations of hyperthyroidism resemble those of the hyperadrenergic state. This study was designed to evaluate the impact of hyperthyroidism on the autonomic nervous system (ANS) and to investigate the relationship between serum thyroid hormone concentrations and parameters of spectral heart rate variability (HRV) analysis in hyperthyroidism. Design and patients, Thirty-two hyperthyroid Graves' disease patients (mean age 31 years) and 32 sex-, age-, and body mass index (BMI)-matched normal control subjects were recruited to receive one-channel electrocardiogram (ECG) recording. Measurements, The cardiac autonomic nervous function was evaluated by the spectral analysis of HRV, which indicates the autonomic modulation of the sinus node. The correlation coefficients between serum thyroid hormone concentrations and parameters of the spectral HRV analysis were also computed. Results, The hyperthyroid patients revealed significant differences (P < 0·001) compared with the controls in the following HRV parameters: a decrease in total power (TP), very low frequency power (VLF), low frequency power (LF), high frequency power (HF), and HF in normalized units (HF%); and an increase in LF in normalized units (LF%) and in the ratio of LF to HF (LF/HF). After correction of hyperthyroidism in 28 patients, all of the above parameters were restored to levels comparable to those of the controls. In addition, serum thyroid hormone concentrations showed significant correlations with spectral HRV parameters. Conclusions, Hyperthyroidism is in a sympathovagal imbalanced state, characterized by both increased sympathetic and decreased vagal modulation of the heart rate. These autonomic dysfunctions can be detected simultaneously by spectral analysis of HRV, and the spectral HRV parameters could reflect the disease severity in hyperthyroid patients. [source] Necrotizing vasculitis in a patient affected by autoimmune hyperthyroidism treated with propylthiouracilDERMATOLOGIC THERAPY, Issue 2010Angela Antonucci ABSTRACT Necrotizing vasculitis is a complex phenomenon because of an inflammation of small and larger vessels with polymorph infiltration within the vessel walls and leukocytoclasis, occurring in several autoimmune diseases. Propylthiouracil (PTU) is a medication commonly used to treat hyperthyroidism, but it is associated with various rare side effects, such as antineutrophil cytoplasm antibody-positive vasculitis. In the last decades, multiple cases of PTU causing antineutrophilic cytoplasmic antibody have been reported, some of them fatal. The present authors report the case of a 34-year-old Caucasian female affected by autoimmune hyperthyroidism treated with PTU, presenting an antineutrophil cytoplasm antibody-positive necrotizing vasculitis, with high levels of anticardiolipin antibodies that involved the upper arms and buttocks. The clinical manifestations improved after discontinuing of PTU and immunosuppressant treatment. [source] Subnormal energy expenditure: a putative causal factor in the weight gain induced by treatment of hyperthyroidismDIABETES OBESITY & METABOLISM, Issue 2 2006R. Jacobsen Aims:, To examine the causes of weight gain occurring as an adverse effect of treatment of hyperthyroidism. Methods:, We measured 24-h energy expenditure (EE), body composition and spontaneous physical activity (SPA) in eight patients before and 1 year after treatment of hyperthyroidism was initiated, and eight controls. Results:, One year after initiation of treatment thyrotropin was normalized, thyroid hormones had fallen to the lower end of the reference range and fat mass had increased by 3.5 kg (p < 0.001). Twenty-four hour EE adjusted for fat-free mass (FFM) was 15% higher in hyperthyroid patients before treatment than in controls (p = 0.003), and treatment decreased 24-h EE by 1.9 MJ/day (p = 0.001). After treatment, 24-h EE, adjusted for FFM, was similar to the controls. Multiple regression analyses showed that the suppressed EE could partly be attributed to an iatrogenic suppression of thyroid hormones, resulting in lower sleeping EE. Twenty-four hour SPA was normal in the hyperthyroid state, but decreased after treatment by 21% (p = 0.045), to a level not significantly different, but still below that of the controls. Conclusions:, The study suggests that weight gain during treatment of hyperthyroidism might be due to subnormal levels of EE and SPA caused by a suppression of the thyroid hormone to a level in the lower end of the normal range. [source] Role of Transthoracic Echocardiography in Atrial FibrillationECHOCARDIOGRAPHY, Issue 4 2000RICHARD W. ASINGER M.D. Atrial fibrillation is a major clinical problem that is predicted to be encountered more frequently as the population ages. The clinical management of atrial fibrillation has become increasingly complex as new therapies and strategies have become available for ventricular rate control, conversion to sinus rhythm, maintenance of sinus rhythm, and prevention of thromboembolism. Clinical and transthoracic echocardiographic features are important in determining etiology and directing therapy for atrial fibrillation. Left atrial size, left ventricular wall thickness, and left ventricular function have independent predictive value for determining the risk of developing atrial fibrillation. Left atrial size may have predictive value in determining the success of cardioversion and maintaining sinus rhythm in selected clinical settings but has less value in the most frequently encountered group, patients with nonvalvular atrial fibrillation, in whom the duration of atrial fibrillation is the most important feature. When selecting pharmacological agents to control ventricular rate, convert to sinus rhythm, and maintain normal sinus rhythm, transthoracic echocardiography (TTE) allows noninvasive evaluation of left ventricular function and hence guides management. The combination of clinical and transthoracic echocardiographic features also allows risk stratification for thromboembolism and hemorrhagic complications in atrial fibrillation. High-risk clinical features for thromboembolism supported by epidemiological observations, results of randomized clinical trials, and meta-analyses include rheumatic valvular heart disease, prior thromboembolism, congestive heart failure, hypertension, older (> 75 years old) women, and diabetes. Small series of cases also suggest those with hyperthyroidism and hypertrophic cardiomyopathy are at high risk. TTE plays a unique role in confirming or discovering high-risk features such as rheumatic valvular disease, hypertrophic cardiomyopathy, and decreased left ventricular function. Validation of the risk stratification scheme used in the Stroke Prevention in Atrial Fibrillation-III trial is welcomed by clinicians who are faced daily with balancing the benefit and risks of anticoagulation to prevent thromboembolism inpatients with atrial fibrillation. [source] Effect of di(n -butyl) phthalate on testicular oxidative damage and antioxidant enzymes in hyperthyroid ratsENVIRONMENTAL TOXICOLOGY, Issue 3 2007Ena Lee Abstract This study compared the effects of di(n-butyl) phthalate (DBP) on the oxidative damage and antioxidant enzymes activity in testes of hyperthyroid rats. Hyperthyroidism was induced in pubertal male rats by intraperitoneal injection of triiodothyronine (T3, 10 ,g/kg body weight) for 30 days. An oral dose of DBP (750 mg/kg) was administered simultaneously to normal or hyperthyroid (T3) rats over a 30-day period. No changes in body weight were observed in the hyperthyroid groups (T3, T3 + DBP) compared with controls. There were significantly higher serum T3 levels observed in the hyperthyroid rats than in the control, but the serum thyroid stimulating hormone levels were markedly lower in the hyperthyroid rats. DBP significantly decreased the weight of the testes in the normal (DBP) and hyperthyroid (T3 + DBP) groups. The serum testosterone concentrations were significantly lower in only DBP group. DBP significantly increased the 8-hydroxy-2-deoxyguanosine (8-OHdG) level in the testes, whereas the DBP-induced 8-OHdG levels were slightly higher in T3 + DBP group. Superoxide dismutase and glutathione peroxidase activities were significantly higher in the testes of the DBP or T3 + DBP groups. Catalase (CAT) activity was significantly higher in the DBP treatment group, but the T3 + DBP group showed slightly lower DBP-induced CAT activity. The testicular expression of thyroid hormone receptor ,-1 (TR,-1) was significantly higher in the DBP groups, and androgen receptor (AR) expression was not detected in the DBP treatment group. In addition, DBP significantly increased the peroxisome proliferator-activated receptor-r (PPAR-r) levels in the testis. These results suggest that hyperthyroidism can cause a change in the expression level of PPAR-r in testes, and may increase the levels of oxidative damage induced by the metabolic activation of DBP. © 2007 Wiley Periodicals, Inc. Environ Toxicol 22: 245,255, 2007. [source] Basal TSH levels compared with TRH-stimulated TSH levels to diagnose different degrees of TSH suppression: diagnostic and therapeutic impact of assay performanceEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2002M. Christ-Crain Abstract Background The estimated prevalence of endogenous subclinical hyperthyroidism varies from 4% to 6% and a basal thyroid stimulating hormone (TSH) level < 0·5 mU L,1 may be associated with increased mortality in subjects over 60 years of age who are not on thyroid medication. Exogenous TSH suppression is a mainstay in the treatment of thyroid cancer. Because of recent concerns about potential adverse effects, especially of endogenous TSH suppression on bone, the cardiovascular system and cognitive functions, subclinical hyperthyroidism obtained new clinical importance. We therefore re-evaluated the diagnostic value of basal and thyrotrop in TRH-stimulated serum TSH measurements using TSH assays with different sensitivities. Materials and methods A total of 805 oral and nasal TRH stimulation tests were performed on 409 ambulatory subjects with low basal serum TSH concentrations of less than 0·1 mIU L,1. Basal serum TSH was measured either using a second generation assay (functional sensitivity > 0·03 mIU L,1) or two third generation assays (functional sensitivity 0·01 mIU L,1 and 0·007 mU L,1, respectively). Serum TSH concentration was determined before and 3 h after oral administration of 40 mg of TRH and before and 30 min after nasal administration of 2 mg of TRH. Results In the oral testing group, the basal TSH levels measured by the different TSH assays were 0·06 ± 0·03, 0·04 ± 0·02 and 0·03 ± 0·02, respectively, whereas the peak TSH levels were 0·4 ± 0·6, 0·4 ± 0·6 and 0·3 ± 0·5 in the patients with subclinical hyperthyroidism. In overt hyperthyroidism, the basal TSH levels were 0·06 ± 0·02, 0·03 ± 0·02 and 0·03 ± 0·02, whereas the peak TSH levels were 0·19 ± 0·3, 0·16 ± 0·3 and 0·15 ± 0·2, respectively. Basal TSH values could discriminate between different degrees of TSH suppression if measured with a third generation assay (P < 0·001), but not with a second generation assay. There was only a weak correlation between basal TSH and peak TSH when measured by a second generation assay (n = 126; r = 0·3; P < 0·001) in contrast to the strong correlation found using the third generation assays (n = 128; r = 0·7; P < 0·001 and n = 69; r = 0·8; P < 0·001, respectively). Conclusions In view of the recent concerns about potential adverse effects in TSH suppression and based on our data, it is mandatory to select a TSH assay with a functional sensitivity of , 0·01 mIU L,1 for optimal titration of L-T4 suppressive therapy, especially in patients with thyroid cancer. If, however, only a second generation TSH assay is available, additional TRH testing allows a more careful titration of suppressive thyroxine therapy. [source] Elderly patient presenting with severe thyrotoxic hypercalcemiaGERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 4 2006Reiko Kikuchi An 81-year-old woman with Graves' disease and osteoporosis was referred to the hospital because of anorexia over one month and impaired consciousness. She also presented with low-grade fever and emaciation. Laboratory tests revealed marked hypercalcemia (corrected serum calcium level of 12.4 mg/dL), which was initially suspected to result from vitamin D toxicity, because she had been taking vitamin D3 (alphacalcidol of 0.5 µg/day) for the treatment of osteoporosis. However, discontinuation of vitamin D3 and fluid infusion did not ameliorate hypercalcemia one week later. After excluding hyperparathyroidism and malignancy-related hypercalcemia, hypercalcemia was considered to be attributable to the exacerbation of hyperthyroidism (free T4 of 6.69 ng/dL, free T3 of 13.27 pg/mL and thyroid stimulating hormone (TSH) <0.015 µIU/mL) with increased bone resorption. Finally, the increased dose of thiamazole (30 mg/day) normalized serum calcium level and thyroid function three months later. Laboratory tests suggested that normal bone formation in spite of increased bone resorption contributed to hypercalcemia in hyperthyroid state. [source] Differential effect of hyperthyroidism on rat epididymal glycosidasesINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 4 2001R. R. M. Maran The impact of hyperthyroidism on epididymal glycosidases was studied in albino rats. Hyperthyroidism was induced in Wistar rats aged 30 days by daily injection of T4 (25 ,g/100 g body weight/day intramuscularly) for 30 or 60 days; control rats were injected with vehicle (alkaline saline, pH 7.8). One set of hyperthyroid rats was reverted to euthyroid status by withdrawing T4 treatment after 30 days of hyperthyroidism. To asses the direct effect of thyroid hormone on epididymal hexosaminidases, caput, corpus and cauda tissues were stimulated with 25, 50 or 100 ng/mL T3 for 24 h, after an initial culture of 24 h. The activity of ,-glucosidase decreased in caput, corpus and cauda epididymis of hyperthyroid rats. ,-Galactosidase activity increased in the caput epididymis irrespective of the duration of hyperthyroidism. While a similar decrease occurred in the corpus and cauda epididymis in the 30 day hyperthyroid group, an opposite trend was observed in 60 day hyperthyroid rats. Caput ,- N -acetylglucosaminidase activities increased at both time points, whereas activity decreased in the corpus and cauda in 30 day, but increased in 60 day hyperthyroid rats. Hyperthyroidism consistently increased caput and corpus ,- N -acetylgalactosaminidase activity irrespective of the duration. Cauda epididymal ,- N -acetylgalactosaminidase activity was decreased in 30 day and increased in 60 day hyperthyroid rats. Hyperthyroidism induced changes in caput ,-galactosidase, ,- N -acetylgalactosaminidases, corpus ,-N-acetylglucosaminidase and cauda ,- N -acetylgalactosaminidase which were irreversible while the remaining actvities were brought back to normal when T4 treatment was withdrawn. In vitro studies showed that T3 stimulates epididymal hexosaminidases (,- N -acetylglucosaminidase and ,- N -acetylgalactosaminidase) irrespective of the dose. These data suggest that thyroid hormones have a specific and direct influence on glycosidases in specific regions of the epididymis. [source] Prevalence and clinical significance of antineutrophil cytoplasmic antibody in Graves' patients treated with propylthiouracilINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 2 2009M.Ozduman Cin Summary Development of antineutrophil cytoplasmic antibody (ANCA) during therapy with propylthiouracil (PTU) is not uncommon and PTU-induced ANCA-positive vasculitis is also reported. The aim of this study was to assess the presence and clinical significance of ANCA positivity in Graves' patients treated with PTU. Newly diagnosed Graves' disease patients (prospective group, n = 58) were evaluated before and during therapy with PTU to investigate the development of ANCA positivity. ANCA positivity is also investigated in previously diagnosed Graves' patients who had already been receiving PTU treatment (cross-sectional group, n = 51). Comparisons with Hashimoto thyroiditis (n = 55) and toxic nodular goitre (n = 20) patients, and healthy control subjects (n = 20) were carried out to define the possible influence of hyperthyroidism and/or thyroid autoimmunity on ANCA positivity. At baseline evaluation, ANCA was negative in all newly diagnosed Graves' patients. Only 28 of the 58 patients in prospective group completed 2 years of follow-up which occurred at 3-month intervals. ANCA positivity was detected 32.1% (n = 9) in a mean period of 11.7 ± 6.1 months in prospective group. Only two (3.9%) patients in a cross-sectional group had ANCA positivity in a mean treatment period of 7.6 ± 4.6 months. None of the patients with ANCA positivity developed symptoms and signs related to vasculitis. None of the patients with Hashimoto thyroiditis and toxic nodular goitre, and healthy control subjects had ANCA positivity. PTU therapy is associated with asymptomatic production of ANCA in a time-dependent manner, which mostly disappears after discontinuation of therapy. Hyperthyroidism or autoimmunity per se does not appear to have effect on development of ANCA positivity. [source] Willan's itch and other causes of pruritus in the elderlyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 4 2005Jon R. Ward MD Itch in the elderly presents a diagnostic and therapeutic challenge. A thorough history, review of systems, and physical examination are critical to determining its cause. Examination of the skin may be misleading. There are frequently only secondary lesions, eczematous changes, lichenification, and excoriation, which may be misdiagnosed as a primary dermatitis. Xerosis may be the cause, but it is sometimes merely coincidental. If primary lesions are present, a skin biopsy can enable a diagnosis to be made. Systemic causes of itch, such as cholestasis, uremia, hyperthyroidism, medications, or lymphoma, must be considered. If the cause remains elusive, idiopathic itching of the elderly or so-called "senile pruritus" may be considered. However, we propose to discard the term "senile pruritus", which can be offensive and frightening. We propose to replace it with "Willan's itch". Robert Willan (1757,1812) is honored as one of the founders of modern dermatology thanks to his book, On Cutaneous Diseases, and its morphological approach to skin disease. He was probably the first to give a good clinical description of itching in the elderly. The diagnosis of Willan's itch should be reserved for generalized pruritus in the absence of xerosis or other recognizable cause. The pathophysiology of this form of pruritus is poorly understood, but it is likely that age-related changes of the skin, cutaneous nerves, and other parts of the nervous system play a role. Anecdotal and limited data suggest that gabapentin, cutaneous field stimulation, serotonin antagonists, and ultraviolet B phototherapy may attenuate itch in some of these patients. [source] Mucous membrane pemphigoid, thymoma, and myasthenia gravisINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 9 2000Haideh Yazdani Sabet In November 1997, approximately 1 year before being evaluated at the Mayo Clinic, Rochester, a 63-year-old woman presented with erosive tongue lesions that were diagnosed by her physician as oral lichen planus. The lesions responded well to 3 months of treatment with systemic and topical corticosteroids and topical antiyeast medication. She stopped taking the medications and had a relapse. A few months after the oral lesions developed, her left eyelid became ptotic. Results of magnetic resonance imaging of her brain were normal, and the ptosis resolved spontaneously after 2 weeks. One year later, her right eyelid began to droop, and the results of edrophonium testing were positive. She was prescribed prednisone, 30 mg daily, and pyridostigmine, as needed. The ptosis improved, but never fully resolved. Radiography revealed a left ,,thyroid nodule,'' but computed tomography did not show a mediastinal mass. She was advised to have the ,,nodule'' removed surgically and came to the Mayo Clinic, Rochester, for a second opinion. Her medical history was significant for the following: tinnitus, glaucoma, early bilateral cataracts, and long-standing hypertension, for which she took losartan, 50 mg twice daily. Other medications included: prednisone, 30 mg daily; pyridostigmine as needed; famotidine, 40 mg daily; and eyedrops for glaucoma. She denied any history of hyperthyroidism or hypothyroidism, head and neck irradiation, family history of thyroid disease, or diplopia. Hepatitis serologic studies revealed hepatitis B exposure and recovery, hepatitis C immunity, and a previous hepatitis A viral infection. On examination at the Mayo Clinic, Rochester, an erosive hypertrophic plaque was noted on the posterior dorsal half of the tongue, and vesicles and erythematous erosions on the hard and soft palates ( Fig. 1a). A lace-like white pattern was seen on the buccal mucosa bilaterally, and a small erosive patch on the left buccal mucosa ( Fig. 1b). Ocular and nasal mucous membranes were normal in appearance, and there were no pertinent skin findings. Dermatopathologic examination of an excisional biopsy specimen from the left dorsum of the tongue demonstrated an ulcer with epitheliomatous hyperplasia and a granulomatous reaction, presumably due to yeast infection. Silver staining showed hyphae and yeast at the base of the tongue ulcer. The results of the direct immunofluorescence study were negative and revealed no lichenoid changes on hematoxylin and eosin staining. Indirect immunofluorescence testing of the serum revealed a 1 : 80 titer of basement membrane zone antibodies, reflecting pemphigoid. This test was positive on repeat study. Salt-split skin on monkey esophagus revealed an epidermal pattern of basement membrane zone antibodies. Treatment included fluocinonide gel applied to the involved areas four times daily and oral antiyeast therapy (fluconazole, 200 mg once daily by mouth) while the rest of the evaluation was being completed. Figure 1(a). Erosive hypertrophic tongue plaque. Figure (b) ,. Erosive patch on the buccal mucosa. As part of the evaluation of the ptosis, a myasthenia gravis antibody panel was performed. It revealed the following abnormalities: striated muscle antibody at 1 : 480 (reference range, <1 : 60), acetylcholine receptor binding antibody at 6.33 nmol/L (reference range, ,,0.02 nmol/L), acetylcholine receptor blocking antibody at 31% (reference range, 0,25%), and acetylcholine receptor modulating antibody at 100% (reference range, 0,20%), suggesting thymoma. Treatment included pyridostigmine, 30,45 mg 3,4 times daily, to control the myasthenia symptoms, while the ill-defined neck mass was being evaluated. A mildly enlarged thyroid was noted on physical examination. Hematology panel revealed thyroid-stimulating hormone (TSH) levels in the low normal range; the thyroid microsomal antibody was normal. Chest radiography showed minor tracheal deviation, and a previous computed tomogram showed what appeared to be a 3-cm enlarged mass in the thyroid. Ultrasonographically guided thyroid biopsy did not show malignancy, but a benign mesenchymal-type tumor was found and surgical excision was planned. Intraoperatively, a thymoma of the left cervical thymic tongue was found. At 6 months' follow-up, the ptosis and oral mucosal lesions had improved significantly, although she continued topical corticosteroid therapy intermittently for minor erosive oral disease. [source] Membrane-bound and cytosolic forms of heterotrimeric G proteins in young and adult rat myocardium: Influence of neonatal hypo- and hyperthyroidismJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2001Jiri Novotny Abstract Membrane and cytosolic fractions prepared from ventricular myocardium of young (21-day-old) hypo- or hyperthyroid rats and adult (84-day-old) previously hypo- or hyperthyroid rats were analyzed by immunoblotting with specific anti-G-protein antibodies for the relative content of Gs,, Gi,/Go,, Gq,/G11,, and G,. All tested G protein subunits were present not only in myocardial membranes but were at least partially distributed in the cytosol, except for Go,2, and G11,. Cytosolic forms of the individual G proteins represented about 5,60% of total cellular amounts of these proteins. The long (Gs,-L) isoform of Gs, prevailed over the short (Gs,-S) isoform in both crude myocardial membranes and cytosol. The Gs,-L/Gs,-S ratio in membranes as well as in cytosol increased during maturation due to a substantial increase in Gs,-L. Interestingly, whereas the amount of membrane-bound Gi,/Go, and Gq,/G11, proteins tend to lower during postnatal development, cytosolic forms of these G proteins mostly rise. Neonatal hypothyroidism reduced the amount of myocardial Gs, and increased that of Gi,/Go, proteins. By contrast, neonatal hyperthyroidism increased expression of Gs, and decreased that of Gi, and G11, in young myocardium. Changes in G protein content induced by neonatal hypo- and hyperthyroidism in young rat myocardium were restored in adulthood. Alterations in the membrane-cytosol balance of G protein subunits associated with maturation or induced by altered thyroid status indicate physiological importance of cytosolic forms of these proteins in the rat myocardium. J. Cell. Biochem. 82: 215,224, 2001. © 2001 Wiley-Liss, Inc. [source] Hyperthyroidism: A Secondary Cause of Isolated Systolic HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 8 2006L. Michael Prisant MD Isolated systolic hypertension is the most common form of hypertension, especially among patients 50 years or older. What is not appreciated is that there are secondary causes of isolated systolic hypertension. Hyperthyroidism increases systolic blood pressure by decreasing systemic vascular resistance, increasing heart rate, and raising cardiac output. Potential cardiovascular consequences of hyperthyroidism include atrial arrhythmias (especially atrial fibrillation), pulmonary hypertension, left ventricular hypertrophy, and heart failure. The prevalence of hypertension is greater among hyperthyroid patients than euthyroid patients. Whether there is a blunted nocturnal decline in ambulatory blood pressure among hyperthyroid patients is more controversial. Treatment is associated with a reduction in systolic blood pressure, heart rate, and cardiac output. [source] Timing of Thyroid Hormone Action in the Developing Brain: Clinical Observations and Experimental FindingsJOURNAL OF NEUROENDOCRINOLOGY, Issue 10 2004R. T. Zoeller Abstract The original concept of the critical period of thyroid hormone (TH) action on brain development was proposed to identify the postnatal period during which TH supplement must be provided to a child with congenital hypothyroidism to prevent mental retardation. As neuropsychological tools have become more sensitive, it has become apparent that even mild TH insufficiency in humans can produce measurable deficits in very specific neuropsychological functions, and that the specific consequences of TH deficiency depends on the precise developmental timing of the deficiency. Models of maternal hypothyroidism, hypothyroxinaemia and congential hyperthyroidism have provided these insights. If the TH deficiency occurs early in pregnancy, the offspring display problems in visual attention, visual processing (i.e. acuity and strabismus) and gross motor skills. If it occurs later in pregnancy, children are at additional risk of subnormal visual (i.e. contrast sensitivity) and visuospatial skills, as well as slower response speeds and fine motor deficits. Finally, if TH insufficiency occurs after birth, language and memory skills are most predominantly affected. Although the experimental literature lags behind clinical studies in providing a mechanistic explanation for each of these observations, recent studies confirm that the specific action of TH on brain development depends upon developmental timing, and studies informing us about molecular mechanisms of TH action are generating hypotheses concerning possible mechanisms to account for these pleiotropic actions. [source] Thyroxine Modulates Corticotropin-Releasing Factor but not Arginine Vasopressin Gene Expression in the Hypothalamic Paraventricular Nucleus of the Developing RatJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2000N. Dakine Neonatal rats were daily injected with 100 ,g/kg T4 and killed at 4, 8 or 15 days. Circulating corticosterone and corticosteroid binding globulin concentrations increased in 8- and 15-day-old rats after T4 treatment. Plasma adrenocorticotropic hormone (ACTH) concentrations, pituitary ACTH content and pro-opiomelanocortin mRNA expression were unaffected in T4 -treated rats. T4 treatment induced an increase in corticotropin-releasing factor (CRF) mRNA expression in the whole population of CRF synthesizing cells of the paraventricular nucleus (PVN) that became significant at day 8 and disappeared at day 15. Double labelling in situ hybridization revealed that CRF gene expression in the CRF+/arginine vasopressin (AVP)+ subpopulation was increased at days 4 and 8 and decreased at day 15. CRF immunoreactivity in the zona externa of the median eminence increased with age but was not affected by the experimental hyperthyroidism. The degree of CRF and AVP colocalization, the concentration of AVP mRNA in the parvo and magnocellular cell bodies of the PVN and the density of immunoreactive AVP in the zona interna or zona externa of the median eminence did not change after T4 treatment. Our data demonstrate that experimental hyperthyroidism accelerates the maturation of hypothalamic CRF gene expression, including in particular in the CRF+/AVP+ subpopulation, during the stress hyporesponsive period. These observations suggest that the physiological peak of plasma thyroxine that occurs between days 8,12 may participate in the maturation of hypothalamic CRF cells. [source] Clinical efficacy and safety of a once-daily formulation of carbimazole in cats with hyperthyroidismJOURNAL OF SMALL ANIMAL PRACTICE, Issue 10 2009R. Frénais Objective:Evaluation of efficacy and safety of a novel controlled-release formulation of carbimazole in feline hyperthyroidism. Methods:A multicentre, self-controlled study in 44 client-owned cats with history and clinical signs of hyperthyroidism, and total thyroxine concentration greater than or equal to 50 nmol/l. Treatment was started at 15 mg once daily, response assessed after 10 days, and 3, 5, 8, 26 and 53 weeks and dose adjusted as required. Results:The median dose of carbimazole was 10 mg (range 10 to 15 mg) and 15 mg (5 to 25 mg) once daily after 3 and 53 weeks, respectively. Median total thyroxine concentration dropped significantly from 118 nmol/l (50 to 320 nmol/l) at presentation to 33 nmol/l (n=40) after 10 days, 31 nmol/l (n=34) at 3 weeks and 21 nmol/l (n=18) at 53 weeks. Clinical signs improved or resolved in almost all cats within three weeks after starting treatment. Twenty-one adverse reactions possibly (20) or probably (1) related to treatment were reported. During treatment, increased blood urea nitrogen concentration was observed in 25 per cent of the cats, eosinophilia in 20 per cent and lymphopenia in 16 per cent, while liver enzymes tended to improve. Clinical Significance:Once daily administration of controlled-release carbimazole tablets was effective and had expected tolerance in hyperthyroid cats during short- and long-term treatment. [source] Evaluation and Treatment of Hyperthyroidism and HypothyroidismJOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS, Issue 10 2004ANP-C, FAANP, Mary Jo Goolsby EdD ABSTRACT This month's clinical practice guideline (CPG) review is on the diagnosis and treatment of hyperthyroidism and hypothyroidism as provided by the American Association of Clinical Endocrinologists. An estimated 27 million Americans have thyroid disease, and about 13 million of them are undiagnosed. The risk of thyroid disease increases with age, and women are seven times more likely than men to develop thyroid problems. Unfortunately, thyroid symptoms are usually very nonspecific and should be kept in the differential diagnosis of many clinical complaints. The format of this month's column is a little different because we received two independent manuscripts, each of which had merit. We made a decision to present both points of view and deleted repetitive material. This is an example of variable approaches one can take with reviewing and critiquing CPGs. [source] Survival and the Development of Azotemia after Treatment of Hyperthyroid CatsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2010T.L. Williams Background: Hyperthyroidism complicates the diagnosis of chronic kidney disease (CKD) as it increases glomerular filtration rate. No practical and reliable means for identifying those cats that will develop azotemia after treatment for hyperthyroidism has been identified. Hyperthyroidism is associated with proteinuria. Proteinuria has been correlated with decreased survival of cats with CKD and with progression of CKD. Hypothesis: Proteinuria and other clinical parameters measured at diagnosis of hyperthyroidism will be associated with the development of azotemia and survival time. Animals: Three hundred client owned hyperthyroid cats treated in first opinion practice. Methods: Retrospective, cohort study relating clinical parameters in hyperthyroid cats at diagnosis to the development of azotemia within 240 days of diagnosis and survival time (all cause mortality). Multivariable logistic regression analysis was used to identify factors that were predictive of the development of azotemia. Multivariable Cox regression analysis was used to identify factors associated with survival. Results: Three hundred cats were eligible for survival analysis and 216 cats for analysis of factors associated with the development of azotemia. The median survival time was 417 days, and 15.3% (41/268) cats developed azotemia within 240 days of diagnosis of hyperthyroidism. Plasma concentrations of urea and creatinine were positively correlated with the development of azotemia. Plasma globulin concentration was negatively correlated with the development of azotemia. Age, urine protein : creatinine ratio, and the presence of hypertension were significantly correlated with decreased survival time. Urine specific gravity and PCV were significantly correlated with increased survival time. Conclusions and Clinical Importance: The proteinuria associated with hyperthyroidism is not a mediator of progression of CKD; however, it does correlate with all cause mortality. [source] Spontaneous Feline Hypertension: Clinical and Echocardiographic Abnormalities, and Survival RateJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2003Valerie Chetboul Systemic hypertension was diagnosed in 58 of 188 untreated cats referred for evaluation of suspected hypertension-associated ocular, neurologic, cardiorespiratory, and urinary disease, or diseases frequently associated with hypertension (hyperthyroidism and chronic renal failure). Hypertensive cats were significantly older than normotensive subjects (13.0 ± 3.5 years versus 9.6 ± 5.0 years; P < .01), and had a greater prevalence of retinal lesions (48 versus 3%; P < .001), gallop rhythm (16 versus 0%; P < .001), and polyuria-polydipsia (53 versus 29%; P < .01). Blood pressure was significantly higher (P < .001) in cats with retinopathies (262 ± 34 mm Hg) than in other hypertensive animals (221 ± 34 mm Hg). Hypertensive cats had a thicker interventricular septum (5.8 ± 1.7 versus 3.7 ± 0.64 mm; P < .001) and left ventricular free wall (6.2 ± 1.6 versus 4.1 ± 0.51 mm; P < .001) and a reduced diastolic left ventricular internal diameter (13.5 ± 3.2 versus 15.8 ± 0.72 mm; P < .001) than control cats. Left ventricular geometry was abnormal in 33 of 39 hypertensive subjects. No significant difference was found in age or blood pressure at the initial visit between cats that died or survived over a 9-month period after initial diagnosis of hypertension. Mean survival times were not significantly different between hypertensive cats with normal and abnormal left ventricular patterns. Further prospective studies are needed to clearly identify the factors involved in survival time in hypertensive cats. [source] Thyrotropin-Releasing Hormone Stimulation Test to Assess Thyroid Function in Severely Sick CatsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2001Kamil Tomsa Basal serum thyroxine (T4) concentration and the thyrotropin-releasing hormone (TRH) stimulation test were used to assess thyroid function in 36 critically ill cats examined between July 1996 and October 1998. Of the 36 cats, hyperthyroidism (as underlying or complicating disease) was suspected in 22 based on clinical signs, palpable thyroid nodules, and abnormal thyroid gland histology (study group). Hyperthyroidism was not suspected in the remaining 14 cats, which served as the control group. Based on serum T4 concentrations, suppression of thyroid function was documented in 14 (64%) cats of the study group and in 10 (71%) cats of the control group. The TRH stimulation test revealed an increase in serum T4 of less than 50% of the baseline concentration in 18 (82%) cats of the study group, and in 6 (43%) cats of the control group. In conclusion, based on the results of serum T4 determinations and the TRH stimulation tests, it was not possible to differentiate between cats with clinical and histologic evidence of thyroid dysfunction (hyperthyroidism) and cats with severe nonthyroidal illnesses. [source] Impact on adherence and sustained virological response of psychiatric side effects during peginterferon and ribavirin therapy for chronic hepatitis CALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2006L. CASTERA Summary Background The psychiatric side effects of interferon, often responsible for dose reduction or treatment discontinuation, represent a major limitation in the treatment of chronic hepatitis C (CHC). Aim To prospectively assess the impact on adherence and sustained virological response (SVR) of the occurrence of psychiatric side effects during peginterferon and ribavirin therapy for CHC. Methods Ninety-eight consecutive treatment-naďve CHC patients receiving a standard course of peginterferon plus ribavirin were systematically screened for psychiatric side effects, using DSM-IV, at baseline and both during and after treatment. Results Psychiatric side effects occurred in 38 patients (39%), mostly within the first 12 weeks (87%), and always consisted of mood disorders. Overall, 68% of patients achieved an SVR (71% of patients with mood disorders and 68% of those without; P = N.S.). Peginterferon and ribavirin dose reductions did not differ between patients with mood disorders and those without (46% vs. 37%, respectively; P = N.S. and 13% vs. 22%, respectively; P = N.S.). Anti-viral therapy had to be discontinued in four patients (nonresponse: two, hyperthyroidism: one, psychiatric event: one). Conclusion Early detection and appropriate management of psychiatric side effects during peginterferon and ribavirin therapy for CHC allow optimizing adherence and virological efficacy. [source] | |||||||||||||