Hashitoxicosis: A clinical perspective

Unnikrishnan, AG

doi:10.4103/0973-0354.106803

Cited by 16 publications

(16 citation statements)

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“…of thyroid cells causing release of thyroid-stimulating hormone (TSH) into the blood circulation [Johnstone et al 2004;Unnikrishnan, 2014;Leyhe and Müssig, 2014;Harsch et al 2008]. This clinical feature is known as hashitoxicosis (HTX) [Leyhe and Müssig 2014].…”

Section: Introductionmentioning

confidence: 99%

Lipid peroxidation, proteins modifications, anti-oxidant enzymes activities and selenium deficiency in the plasma of hashitoxicosis patients

Mseddi

Mansour

Mnif

et al. 2015

Therapeutic Advances in Endocrinology

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Objectives: The aim of this study was to explore the oxidative stress profile in hashitoxicosis (HTX) and to compare it with that of healthy subjects. Patients and methods: Spectrophotometric methods were used to evaluate the oxidative stress markers. The selenium level was investigated by atomic absorption. Results: High levels of thiobarbituric acid reactive species (TBARS) and conjugated dienes were found in HTX patients (p = 0.034 and p = 0.043, respectively) compared with healthy controls. For antioxidant enzymes, superoxide dismutase (SOD) and catalase activities increased, whereas that of glutathione peroxidase (GPx) decreased (p = 0.000, p = 0.014, p = 0.000, respectively) compared with controls. A reduction in the level of selenium (p = 0.029) and thiol groups (p = 0.008) were shown in patients; however, levels of carbonyl group and malondialdehyde (MDA) protein adducts decreased (p = 0.000) compared with controls. Positive correlation was shown between levels of free thyroxine (FT4) and TBARS (r = 0.711, p = 0.048) and between FT4 level and SOD activity (r = 0.713, p = 0.047). Conversely, GPx activity presented a negative correlation with FT4 and free triiodothyronine (FT3) levels (r = -0.934, p = 0.001; r = -0.993, p = 0.000, respectively). In addition, GPx activity showed positive correlation with selenium level (r = 0.981, p = 0.019) and the FT3 level correlated negatively with the level of thiol groups (r = -0.892, p = 0.017). Conclusions: This study shows the presence of an oxidative stress and selenium deficiency in HTX patients and suggests that the hyperthyroid state is strongly implicated in the establishment of this disturbed oxidative profile.

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Section: Introductionmentioning

confidence: 99%

Lipid peroxidation, proteins modifications, anti-oxidant enzymes activities and selenium deficiency in the plasma of hashitoxicosis patients

Mseddi

Mansour

Mnif

et al. 2015

Therapeutic Advances in Endocrinology

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“…The TSH level in our patient was markedly low. Hashitoxicosis, unlike our patient, is characterized by a transient initial phase of hyperthyroidism followed by hypothyroidism (9,10). Hashitoxicosis is a possibility.…”

Section: Discussionmentioning

confidence: 49%

From Famine to a Feast: Little Endogenous Thyroxine to Overproduction

Lal

Trivedi

Abraham

2018

AACE Clinical Case Reports

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Objective: Spontaneous conversion of autoimmune hypothyroidism to Graves disease is a rare occurrence. We present a case of antibody-confirmed autoimmune hypothyroidism, in which the patient was on replacement therapy with levothyroxine for 8 years and had spontaneous conversion to Graves disease with positive thyroid-stimulating hormone receptor antibodies (TRAbs). Methods: A 79-year-old woman was evaluated for persistent fatigue following acute dermatomal herpes zoster. She had developed progressive tremor of the extremities and heat intolerance. Her other problems included Hashimoto thyroiditis and vitiligo, diabetes mellitus, cerebrovascular disease, coronary artery disease, osteoporosis, and hypercholesterolemia. Her medications included metformin, aspirin, lisinopril, atorvastatin, zoledronic acid, and levothyroxine. Clinical examination was notable for healed lesions of herpes zoster and hand tremors. Results: Laboratory evaluation revealed triiodothyronine level of 1.83 ng/mL (normal range, 0.80 to 2.00 ng/ mL), free thyroxine level of 1.53 ng/dL (normal range, 0.93 to 1.70 ng/dL), and thyroid-stimulating hormone (TSH) level of 0.007 μIU/mL (normal range, 0.27 to 4.20 μIU/ mL). Of note, TRAb was positive at 5.37 IU/L (normal range, 0.00 to 1.75 IU/L). Radioactive iodine uptake scan was normal. Conclusion: TSH-stimulation blocking antibodies cause hypothyroidism, whereas thyroid-stimulating antibodies are responsible for Graves hyperthyroidism resulting from overactivation of TSH receptors. Our patient was on stable dose of levothyroxine for 8 years without any complications. We hypothesize that the conversion of blocking to stimulating antibodies was induced by the stress of the herpes zoster infection. Factors that possibly increased her odds for this phenomenon included her gender, thyroid replacement therapy, advanced age, and a background of autoimmune hypothyroidism. This case highlights the critical need to recognize that this transition can occur, since it requires a reversal of treatment plans.

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“…Thyroid antibodies both the microsomal and the thyroglobulin were only available in the last decade, though done, were not uniformly done due to the prohibitive cost factor. Hashitoxicosis, the transient form of hyperthyroidism was only seen in three of our patients, a prevalence of 1.12%, which fits in with the relative rarity (<5%) of the disease 6 . Our results feature a highly significant increase in secondary toxicity, post iodination, an increase in the percentage of toxicity in MNG specially seen in the elderly, This possible "Jod-Basedow" effect is attributed to the sudden availability of iodine to iodine starved endemic goiter, which is autonomously active 7,8 .…”

Section: Discussionmentioning

confidence: 63%

“…Another point that should be emphasized is that, secondary toxicity on MNG's is the commonest cause of toxicity at present in Sri Lanka and as such should be given due consideration. As it is a mild form of toxicity, giving the patient Lugol's iodine pre surgery to evoke the Wolfe -Chaikoff effect and reduce the "vascularity", as is done in Graves' disease is both unnecessary 6,7 and maybe downright risky by provoking enhanced toxicity.…”

Section: Discussionmentioning

confidence: 99%

Iodination and its effect on hyperthyroidism

et al. 2017

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_____________________________________________________________________________ Abstract BackgroundIodine supplementation with salt as a carrier was introduced in Sri Lanka in 1995. Literature from elsewhere suggest that there is an increase in hyperthyroidism after the initiation of such programmes. Objectives To identify weather iodination precipitated an exacerbation of hyperthyroidism in the Central Province of Sri Lanka Methods Four-hundred-and-eight consecutive patients with hyperthyroidism seen over a period of thirty one years in a General Surgical Clinic at Teaching Hospital, Peradeniya were reviewed. ResultsThe prevalence of secondary hyperthyroidism increased after iodination. No change in the demography and presentation of simple diffuse toxic goiter was observed. Conclusions Physicians must be aware of this increased incidence of hyperthyroidism after iodination and need to be vigilant of the need to control it, in view of its complications.

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Hashitoxicosis: A clinical perspective

Cited by 16 publications

References 1 publication

Lipid peroxidation, proteins modifications, anti-oxidant enzymes activities and selenium deficiency in the plasma of hashitoxicosis patients

Lipid peroxidation, proteins modifications, anti-oxidant enzymes activities and selenium deficiency in the plasma of hashitoxicosis patients

From Famine to a Feast: Little Endogenous Thyroxine to Overproduction

Iodination and its effect on hyperthyroidism

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