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HCV Infection Enhances Th17 Commitment, Which Could Affect the Pathogenesis of Autoimmune Diseases  [PDF]
Yasuteru Kondo, Masashi Ninomiya, Osamu Kimura, Keigo Machida, Ryo Funayama, Takeshi Nagashima, Koju Kobayashi, Eiji Kakazu, Takanobu Kato, Keiko Nakayama, Michael M. C. Lai, Tooru Shimosegawa
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0098521
Abstract: Background Various kinds of autoimmune diseases have been reported to have a significant relationship with persistent hepatitis c virus (HCV) infection and Th17 cells. Previously, our group reported that the existence of HCV in T lymphocytes could affect the development of CD4+ helper T cells and their proliferation, in addition to the induction of immunoglobulin hyper-mutation. Methods Therefore, we analyzed the relationship between persistent infection of HCV and the mechanism of Th17 cell induction ex vivo and in vitro. Results The prevalence of autoimmune-related diseases in chronic hepatitis c patients (CH-C) was significantly higher than in other types of chronic hepatitis (hepatitis B and NASH). A significantly higher frequency of IL6 and TGF-β double-high patients was detected in CH-C than in other liver diseases. Moreover, these double-high patients had significantly higher positivity of anti-nuclear antibody, cryoglobulinemia, and lymphotropic HCV and higher amounts of IL1-β, IL21, IL23. In addition to the previously reported lymphotropic SB-HCV strain, we found a novel, genotype 1b lymphotropic HCV (Ly-HCV), by deep sequencing analysis. Lymphotropic-HCV replication could be detected in the lymphoid cells with various kinds of cytokine-conditions including IL1β, IL23, IL6 and TGF-β in vitro. Infection by HCV could significantly enhance the development of Th17 cells. The HCV protein responsible for inducing the Th17 cells was HCV-Core protein, which could enhance the STAT-3 signaling and up-regulate the expression of RORγt as a Th17 master gene. Conclusion Infection by lymphotropic HCV might enhance the Th17 development and contribute to understanding the pathogenesis of autoimmune-related diseases.
2D MR Spectroscopy Combined with Prior-Knowledge Fitting Is Sensitive to HCV-Associated Cerebral Metabolic Abnormalities  [PDF]
Rajakumar Nagarajan,Manoj K. Sarma,April D. Thames,Steven A. Castellon,Charles H. Hinkin,M. Albert Thomas
International Journal of Hepatology , 2012, DOI: 10.1155/2012/179365
Abstract: There is an evidence of neurocognitive dysfunction even in the absence of advanced liver disease in chronic hepatitis C virus (HCV) infection. Brain metabolism has been investigated non-invasively using one-dimensional (1D) in vivo Magnetic Resonance Spectroscopy (MRS) over three decades. Even though highly concentrated cerebral metabolites (N-acetylaspartate, creatine, choline, glutamate/glutamine, myo-inositol) have been detected using MRS, other metabolites at low concentrations (~1–3?mM or less) including glutathione, aspartate and GABA are quite difficult to observe using 1D MRS. In order to resolve overlapping resonances from a number of metabolites, a remedy is to add a second spectral dimension to the existing 1D MRS. Localized two-dimensional correlated spectroscopy (L-COSY) has been developed over the last decade to enhance the spectral dispersion by using the second spectral dimension. We have evaluated this L-COSY technique in the frontal white/gray matter regions of 14 HCV+ (mean age of 56.2 years) and 14 HCV? (mean age of 46.6 years) subjects. Our preliminary results showed significantly increased myo-inositol and glutathione in the HCV+ compared to the HCV? subjects. Hence, glutathione and myo-inositol should be considered along with other metabolites as important markers of inflammation. 1. Introduction The natural course of Hepatitis C virus (HCV) infection, which is transmitted via parenteral route, is modulated by both host and viral factors and typically tends to evolve towards chronicity, which will ensue in approximately 85% of cases following acute infection [1]. Given that this virus affects approximately 3% of the world’s population [2], HCV infection represents a leading cause of chronic hepatitis, cirrhosis, end-stage liver failure, and hepatocellular carcinoma. More recently, evidence suggests that HCV is capable of crossing the blood-brain barrier and that the brain serves as an important reservoir for subsequent viral replication [3–5]. There is evidence that chronic HCV infection results in neurocognitive dysfunction even in the absence of advanced liver disease [6, 7]. In most cases, subtle cognitive complaints are reported that include difficulties in concentration and slowed processing speed. These observations sparked a number of investigations that sought to characterize neuropathological changes in patients with HCV with mild (noncirrhotic) liver disease. In vivo proton (1H) magnetic resonance spectroscopy (MRS) is a noninvasive technique that gives information on brain metabolism at the end of a standard brain
2D MR Spectroscopy Combined with Prior-Knowledge Fitting Is Sensitive to HCV-Associated Cerebral Metabolic Abnormalities  [PDF]
Rajakumar Nagarajan,Manoj K. Sarma,April D. Thames,Steven A. Castellon,Charles H. Hinkin,M. Albert Thomas
International Journal of Hepatology , 2012, DOI: 10.1155/2012/179365
Abstract: There is an evidence of neurocognitive dysfunction even in the absence of advanced liver disease in chronic hepatitis C virus (HCV) infection. Brain metabolism has been investigated non-invasively using one-dimensional (1D) in vivo Magnetic Resonance Spectroscopy (MRS) over three decades. Even though highly concentrated cerebral metabolites (N-acetylaspartate, creatine, choline, glutamate/glutamine, myo-inositol) have been detected using MRS, other metabolites at low concentrations (~1–3 mM or less) including glutathione, aspartate and GABA are quite difficult to observe using 1D MRS. In order to resolve overlapping resonances from a number of metabolites, a remedy is to add a second spectral dimension to the existing 1D MRS. Localized two-dimensional correlated spectroscopy (L-COSY) has been developed over the last decade to enhance the spectral dispersion by using the second spectral dimension. We have evaluated this L-COSY technique in the frontal white/gray matter regions of 14 HCV
Electroneuromyography and neuromuscular findings in 16 primary hypothyroidism patients
Cruz, Márcia W.;Tendrich, Mauro;Vaisman, Mário;Novis, Sérgio A. P.;
Arquivos de Neuro-Psiquiatria , 1996, DOI: 10.1590/S0004-282X1996000100002
Abstract: there has been few reports on electroneuromyography (enmg) changes in hypothyroidism. the objectives of the present study were to investigate the frequency of enmg abnormalities in hypothyroidism and correlate them with neurological signs and symptoms and muscle enzyme levels; and to compare latency, amplitude and nerve conduction velocity from selected nerves with controls. sixteen patients suffering from primary hypothyroidism were submitted to enmg before treatment. enmg abnormalities were found in 87.5% of the patients; 46.6% had myopathy and 43.7% had carpal tunnel syndrome. there was no case of polyneuropathy. a clear-cut clinical, laboratorial and enmg correlation was observed in patients with myopathy and carpal tunnel syndrome. the patients showed a significant tendency of nerve conduction slowness as compared with controls. the findings are in accordance with the well-known nerve and muscle damage in hypothyroidism.
Congenital hypothyroidism
Maynika V Rastogi, Stephen H LaFranchi
Orphanet Journal of Rare Diseases , 2010, DOI: 10.1186/1750-1172-5-17
Abstract: Congenital hypothyroidism (CH) is defined as thyroid hormone deficiency present at birth. Thyroid hormone deficiency at birth is most commonly caused by a problem with thyroid gland development (dysgenesis) or a disorder of thyroid hormone biosynthesis (dyshormonogenesis). These disorders result in primary hypothyroidism. Secondary or central hypothyroidism at birth results from a deficiency of thyroid stimulating hormone (TSH). Congenital TSH deficiency may rarely be an isolated problem (caused by mutations in the TSH β subunit gene), but most commonly it is associated with other pituitary hormone deficiencies, as part of congenital hypopituitarism. Peripheral hypothyroidism is a separate category resulting from defects of thyroid hormone transport, metabolism, or action.Congenital hypothyroidism is classified into permanent and transient CH. Permanent CH refers to a persistent deficiency of thyroid hormone that requires life-long treatment. Transient CH refers to a temporary deficiency of thyroid hormone, discovered at birth, but then recovering to normal thyroid hormone production. Recovery to euthyroidism typically occurs in the first few months or years of life. Permanent CH can be further classified into permanent primary and secondary (or central) CH; transient primary CH has also been reported. In addition, some forms of CH are associated with defects in other organ systems; these are classified as syndromic hypothyroidism.The underlying etiology of CH typically will determine whether hypothyroidism is permanent or transient, primary, secondary, or peripheral, and whether there is involvement of other organ systems (see section on Etiology for details). The primary emphasis of this review is a discussion of primary CH, but there also will be some discussion of secondary or central CH. It should be borne in mind that an underlying etiology may not be determined for many cases of CH. Further, while the exact cause of some cases of thyroid dysgenesis is known,
SEVER HYPOTHYROIDISM
Akbar Khoja
The Professional Medical Journal , 1998,
Abstract: Thyroidal status has well known effect on lipid metabolism. Thyroid insufficiency may cause secondaryhyperlopidemia, but effect of short course (£ 12 weeks) L-thyrodoxine therapy on elevated high densitylipoportein cholesterol (HDL-c) is controversial. Particularly the effect of short course of L-thyrodoxine4 therapy on elevated levels of various serum lipoproteins in severely hypothyroid patients. (serum T levels<15 mmol/L and hTSH > 150 mU/L) has not been established . OBJECTIVES: To assess the efficacy ofL-thyrodoxine therapy in normalizing the elevated lipid contents of various serum lipoprotein fractions insevere primary hypothyroidism in the local population. DESIGN: Controlled clinical trial. PATIENTSAND METHODS: 17 male patients referred to Punjab Institute of Nuclear Medicine, Faisalabad, mean age4 (mean age 32 ± 18 years, ranging 23-67 years), having serum levels of T <15 mmol/L and hTSH > 150mU/L were selected. Pre-therapy fasting blood samples was taken at the time of diagnosis. All subjectsbecame euthyroid after 9 weeks of L-thyrodoxine therapy with gradual increase of dosing from 50 to 150μ g/d. Post-therapy fasting blood was taken after 12 weeks of L-thyrodoxine therapy. RESULTS: With Lthyrodoxinetherapy euthyroid state was achieved within 9 weeks and all patients became free from signsand symptoms of hypothyroidism. Serum triacylglycerols, total cholesterol and LDL-c levels were reducedsignificantly (P <0.01) but there was a slight reduction in the serum HDL-c levels. CONCLUSIONS: Lthyrodoxinetherapy is severe hypothyroidism does have a cardioprotective effect by normalizing theelevated levels of TAGs, total cholesterol and LDL-c.
The Association Between Hypothyroidism and Anemia: a Clinical Study
Mitra Kazemi-Jahromi,Ali Shahriari-Ahmadi,Seyed-Hosein Samedanifard,Soraya Doostmohamadian
International Journal of Hematology-Oncology and Stem Cell Research , 2010,
Abstract: "nIntroduction: Hypothyroidism is diagnosed by elevated thyroid stimulating hormone (TSH) and normal or decreased serum levels of T4 or T3, and is associated with a wide range of metabolic abnormalities, including anemia. This clinical study aimed to assess the improvement of anemia in patients with primary hypothyroidism following administration of levothyroxine in Iranian population. "nMaterials & Methods: The effect of levothyroxine in 70 patients with hypothyroidism was examined and the improvement of anemia in patients who had a poor or good response to levothyroxine was assessed during a 3 month follow-up. "nResults: Three months after treatment, the levels of TSH in 64 patients with hypothyroidism (91.4%) significantly decreased to a normal limit (TSH< 2.5 IU/ml). Forty three out of 70 patients (61.4%) had a concurrent anemia. A significant difference was found in the levels of hematologic parameters between those who had a good response (TSH< 2.5 IU/ml) and those with poor responses to the treatment (TSH≤2.5 IU/ml) (p< 0.05). "nConclusions: Current study showed a high rate of association between anemia and hypothyroidism in Iranian population. Improvement in hypothyroidism and its associated anemia was observed in majority of patients (more than 90%), indicating a dual benefit for hypothyroidism treatment. Less than 10% of patients poorly responded to levothyroxine, with no clear reasons.
Hipotiroidismo Hypothyroidism
Judith Parlá Sardi?as
Revista Cubana de Endocrinología , 2012,
Abstract: El hipotiroidismo es el cuadro clínico resultante de la disminución en la producción de hormonas tiroideas. Tiene una incidencia en la población general del 1 al 2 %. Se clasifica desde el punto de vista anatomo-etiológico, y si se acompa a de la presencia de bocio o no. El diagnóstico es clínico (interrogatorio y el examen físico) y humoral (niveles elevados de TSH y disminuidos de T3 y T4 libres). Los objetivos del tratamiento son reemplazar la deficiencia de hormonas tiroideas hasta lograr el eutiroidismo clínico y bioquímico. El tratamiento sustitutivo con hormonas tiroideas es para toda la vida a la dosis de 1,7 μg/kg/día. Se utiliza el nivel de TSH para individualizar la dosis óptima de levotiroxina sódica. Hypothyroidism is the clinical picture resulting from the reduction of thyroid hormone production. It affects 1 to 2 % of the general population. It is classified from the anatomical and etiological viewpoint and the presence or absence of goiter. The diagnosis is clinical (questioning and physical exam) and humoral (high TSH levels and low free T3 and T4 levels). The treatment is aimed at eliminating the deficiency of thyroid hormones until clinical and biochemical euthyroidism is achieved. The replacement treatment with thyroid hormone is lifelong at a dose of 1.7 μg/kg/day. The level of TSH indicates the individual optimal dose of sodium levothyroxine that should be used.
Hypothyroidism Induced Severe Rhabdomyolysis in a Hemodialysis Patient  [PDF]
Erhan Tatar,Tolgay Isikyakar,Kezban Pinar Yeniay,Hasan Huseyin Uzuner,Ebru Sevinc Ok
Case Reports in Medicine , 2014, DOI: 10.1155/2014/501890
Abstract: Hypothyroidism occurs relatively common and is a significant cause of morbidity and mortality during the course of chronic kidney disease. Rhabdomyolysis is a potentially life-threatening condition characterised by necrosis of muscular tissue and rarely associates with hypothyroidism. Here we describe a case of rhabdomyolysis due to severe hypothyroidism in a 56-year-old female hemodialysis patient. 1. Introduction Thyroid dysfunction is relatively common in patients with chronic kidney disease (CKD) when compared to general population [1, 2]. Both hormonal changes including alterations in TRH, TSH, and iodine clearance as well as presence of associating autoimmune disorders (type 1 diabetes mellitus or systemic lupus erythematosus) and comorbidities such as HCV infection or treatment with drugs having adverse thyroid effects (e.g., amiodarone) are thought to be responsible for thyroid dysfunction [2–4]. Thyroid dysfunction particularly hypothyroidism is a significant cause of cardiovascular mortality and morbidity in CKD patients [5–10]. In hemodialysis patients, however, the frequency of acute complications and neuromuscular effects of hypothyroidism are not known. Rhabdomyolysis is a rapid breakdown of skeletal muscle tissue leading to release of its contents into systemic circulation [11]. Rhabdomyolysis, a life-threatening condition, may occur due to physical factors including trauma, convulsions, or overexertion as well as to chemical and hormonal causes [11]. Hypothyroidism associated rhabdomyolysis is rare in nonuremic patients. Hypothyroidism induced rhabdomyolysis in dialysis patients has not been reported as far as we know. Here we present a case of rhabdomyolysis in a hemodialysis patient on amiodarone treatment receiving antithyroid therapy for subclinical hyperthyroidism. 2. Case Presentation A 56-year-old female with a past medical history of end stage diabetic nephropathy, interstitial pulmonary disease, congestive heart failure, and atrial fibrillation presented to nephrology outpatient clinics with complaints of nausea and fatigue. She was back on routine hemodialysis 4 times a week for 18 months (she underwent a renal transplantation 10 years ago). She provided a history of subclinical hyperthyroidism detected six months ago for which antithyroid treatment was started because of the diagnosis of a thyroid nodule. She stated that she missed her follow-up appointments. Her medications included warfarin 5?mg, diltiazem 30?mg, amiodarone 400?mg (started for atrial fibrillation with rapid ventricular response), propylthiouracil 300?mg,
HYPOTHYROIDISM FOLLOWING THYROID SURGERY
M. Lankarani,H. Mahmoodzadeh,N. Poorpezeshk,B. Soleimanpour
Acta Medica Iranica , 2008,
Abstract: Postsurgical hypothyroidism and its incidence has not been fully investigated. In this study, the incidence of hypothyroidism and its possible risk factors at Shariati Hospital was assessed. One hundred and two patients with benign thyroid diseases, who had undergone thyroidectomy, were investigated with regards to thyroid function profile during period of one year after the operation every three months with post-operative sample as the baseline. Hypothyroidism was developed in 36 patients (35.2%) on average 5 ± 3.2 months after surgery. Factors such as increased age, operation type, histopathologic type, underlying disease, lymphocytic infiltration and use of levothyroxine before surgery were associated with the increased incidence of hypothyroidism. It seems that use of indicators such as Graves' disease and lymphocytic infiltration in pathologic specimens should be helpful in projecting the potential occurrence of hypothyroidism in patients undergoing thyroidectomy.
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