Propylthiouracil and thiamazole do not alter in vitro neutrophil oxidative burst

Russo, Elisa Maria de Sousa; Azzolini, Ana Elisa Caleiro Seixas; Polizello, Ana Cristina Morseli; Assis-Pandochi, Ana Isabel de; Lucisano-Valim, Yara Maria

doi:10.1016/j.metabol.2004.09.009

Cited by 7 publications

(6 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…D1 could also potentially be a source of iodide for the cells; however, blocking D1 activity by PTU was shown to have no effect on the neutrophil respiratory burst, which is in contrast to the observation that TH raises neutrophil ROS production (Mezosi et al 2005, Russo-Carbolante et al 2005a). …”

Section: Role Of Intracellular Thyroid Hormone Metabolism In Neutrophmentioning

confidence: 72%

Thyroid hormone metabolism in innate immune cells

Spek

Fliers

Boelen

2017

Journal of Endocrinology

View full text Add to dashboard Cite

Thyroid hormone (TH) metabolism and thyroid status have been linked to various aspects of the immune response. There is extensive literature available on the effects of thyroid hormone on innate immune cells. However, only recently have authors begun to study the mechanisms behind these effects and the role of intracellular TH metabolism in innate immune cell function during inflammation. This review provides an overview of the molecular machinery of intracellular TH metabolism present in neutrophils, macrophages and dendritic cells and the role and effects of intracellular TH metabolism in these cells. Circulating TH levels have a profound effect on neutrophil, macrophage and dendritic cell function. In general, increased TH levels result in an amplification of the pro-inflammatory response of these cells. The mechanisms behind these effects include both genomic and non-genomic effects of TH. Besides a pro-inflammatory effect induced by extracellular TH, the cellular response to pro-inflammatory stimuli appears to be dependent on functional intracellular TH metabolism. This is illustrated by the fact that the deiodinase enzymes and in some cell types also thyroid hormone receptors appear to be crucial for adequate innate immune cell function. This overview of the literature suggests that TH metabolism plays an important role in the host defence against infection through the modulation of innate immune cell function.

show abstract

Section: Role Of Intracellular Thyroid Hormone Metabolism In Neutrophmentioning

confidence: 72%

Thyroid hormone metabolism in innate immune cells

Spek

Fliers

Boelen

2017

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…Amiodarone and Iodide overload may produce thyrotoxicosis (Chiovato et al, 1997, Table 11). Russo‐Carbolante et al (2005) found that propylthiouracil and thiamazole are thionamides used in the treatment of hyperthyroidism. These drugs are thyrostatic and are used in the treatment of hyperthyroidism to inhibit the iodine organification that is one of the main steps in the formation of thyroid hormones, T3 and T4.…”

Section: Hyperthyroidism and Brain Development Interactionsmentioning

confidence: 99%

Thyroid hormones states and brain development interactions

Ahmed

El-Gareib

El-Bakry

et al. 2007

Intl J of Devlp Neuroscience

279

254

View full text Add to dashboard Cite

The action of thyroid hormones (THs) in the brain is strictly regulated, since these hormones play a crucial role in the development and physiological functioning of the central nervous system (CNS). Disorders of the thyroid gland are among the most common endocrine maladies. Therefore, the objective of this study was to identify in broad terms the interactions between thyroid hormone states or actions and brain development. THs regulate the neuronal cytoarchitecture, neuronal growth and synaptogenesis, and their receptors are widely distributed in the CNS. Any deficiency or increase of them (hypo- or hyperthyroidism) during these periods may result in an irreversible impairment, morphological and cytoarchitecture abnormalities, disorganization, maldevelopment and physical retardation. This includes abnormal neuronal proliferation, migration, decreased dendritic densities and dendritic arborizations. This drastic effect may be responsible for the loss of neurons vital functions and may lead, in turn, to the biochemical dysfunctions. This could explain the physiological and behavioral changes observed in the animals or human during thyroid dysfunction. It can be hypothesized that the sensitive to the thyroid hormones is not only remarked in the neonatal period but also prior to birth, and THs change during the development may lead to the brain damage if not corrected shortly after the birth. Thus, the hypothesis that neurodevelopmental abnormalities might be related to the thyroid hormones is plausible. Taken together, the alterations of neurotransmitters and disturbance in the GABA, adenosine and pro/antioxidant systems in CNS due to the thyroid dysfunction may retard the neurogenesis and CNS growth and the reverse is true. In general, THs disorder during early life may lead to distortions rather than synchronized shifts in the relative development of several central transmitter systems that leads to a multitude of irreversible morphological and biochemical abnormalities (pathophysiology). Thus, further studies need to be done to emphasize this concept.

show abstract

“…13,14 Although it has been postulated that propylthiouracil directly increases neutrophil cytotoxicity, this remains controversial. 17,[23][24][25] Propylthiouracil may enhance a predisposition to antibody formation in patients with Graves disease. ANCAs with or without other triggers such as infection 26 can trigger neutrophil activation and subsequent release of lytic enzymes, including ANCA antigens and oxygen radicals that cause endothelial injury in a cascade.…”

Section: Discussionmentioning

confidence: 99%

Atypical Antineutrophil???Cytoplasmic Antibodies and Vasculitis-Like Syndrome With Aphthous Ulcer and Violaceous Pinnae after Retreatment With Propylthiouracil for Graves Disease

Koller

Svoboda

Jones

et al. 2006

The Endocrinologist

View full text Add to dashboard Cite

Rash with thioamides is not uncommon, but vasculitis is rare. The vasculitis is thought to be mediated by antibodies directed against proteins in the cytoplasmic granules of myeloid cells (antineutrophil-cytoplasmic antibodies ͓ANCAs͔). We report the case of a 47-year-old white male with a vasculitis-like syndrome after propylthiouracil for recurrent Graves disease. He was initially treated with propylthiouracil (150 mg every 6 hours) for approximately 18 months with clinical remission. Two months after propylthiouracil discontinuation, he had recurrence (T4-free 5.56 ng/mL ͓normal, 0.75-1.54 ng/mL͔, antithyroglobulin antibodies Ͼ90 IU/mL ͓normal, 0 -2 IU/mL͔, antithyroperoxidase antibodies 13.6 IU/mL ͓nor-mal, 0 -2 IU/mL͔, anti-TSH-receptor antibodies 74% ͓normal, Ͻ10%͔), and propylthiouracil was restarted with rapid titration to 200 mg every 4 to 6 hours. After 1 month, skin and mouth lesions appeared in the setting of neutropenia (700/L). Propylthiouracil was stopped for 1 week with improvement. Physical examination revealed proptosis, purple pinnae with lobe sparing, hoarse voice, 1-cm aphthous ulcer, 80-g goiter, erythematous skin lesions with dark centers, and joint effusions limiting hand, knee, and ankle mobility. Labs revealed C-reactive protein of 3.2 mg/dL (normal, Ͻ0.7 mg/dL), rheumatoid factor of Ͻ0.9 IU/mL (normal, Ͻ40 IU/mL), antinuclear antibody: negative, and ANCAs 1:1024 (normal, Ͻ1:16) with a perinuclear pattern. Symptoms abated with propylthiouracil cessation and thyroidectomy. P-ANCA levels declined over 8 months. Despite the extensive exposure to propylthiouracil, our patient did not experience symptoms until rechallenged at high doses. He had prompt recovery on withdrawal. Although some clinical findings were consistent with relapsing polychondritis, type II collagen antibody levels were unremarkable. His antineutrophil-cytoplasmic antibodies were atypical; antimyeloperoxidase and antiserine proteinase 3 antibodies were not the primary antibody types. Future investigation may identify the causative antibodies for the vasculitis variant expressed by our patient.

show abstract

Propylthiouracil and thiamazole do not alter in vitro neutrophil oxidative burst

Cited by 7 publications

References 36 publications

Thyroid hormone metabolism in innate immune cells

Thyroid hormone metabolism in innate immune cells

Thyroid hormones states and brain development interactions

Atypical Antineutrophil???Cytoplasmic Antibodies and Vasculitis-Like Syndrome With Aphthous Ulcer and Violaceous Pinnae after Retreatment With Propylthiouracil for Graves Disease

Contact Info

Product

Resources

About