Vasculitis and anti-thyroid medication

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Vasculitis and anti-thyroid medication

As for IgA vasculitis with nephritis, glucocorticoid administration had successfully reduced proteinuria, with peak elevation observed at 0.66 g/gCr on day 3, which reduced to 0.26 g/gCr on day 5, and was finally absent by day 10. After prednisolone was tapered to 60 mg/day, she was transferred to another hospital to undergo cholecystectomy for cholecystitis. After 1 year, she regularly visits our hospital for follow-up and medical treatment. Initially, 636 AAV patients with renal injury were screened from November 2011 to December 2020.

Vasculitis and anti-thyroid medication

  • Certainly, urticarial vasculitis is an underdiagnosed disease, to the extent that its incidence may vary from 3 to 20% 1.
  • Figure 1 Images of the lower legs, chest X-ray, chest computed tomography, electrocardiogram, and echocardiogram.
  • These statistics give us reasonable confidence that recall was not a major issue in our study.

Triamcinolone ointments, bleach baths, ivermectin, butenafine, and H1 and H2 blockers did not provide relief from symptoms. He underwent multiple skin biopsies with nonspecific findings until his most recent biopsy, which showed subtle signs of vasculitis (Figure1B, C). Over a period of several years, the patient tried different thyroid replacement medications with different excipients, starting with Armour Thyroid, branded Synthroid, and Tirosint, under the direction of his endocrinologist. Upon exposure to levothyroxine in each formula, the patient developed the same type of rash a few months into the treatment plan, leading to levothyroxine synthroid dizzy discontinuation and the use of systemic steroids for resolution. Subsequently, his thyroid replacement was discontinued for four months, but he deteriorated significantly with poor clinical status and was restarted on branded Synthroid. He was advised to try oral antihistamines, which did not improve the course of his rash.

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Hence, clinicians should be aware of the risks of dynamic exacerbations in patients with hypothyroidism. Furthermore, our study suggested that combination therapy with thyroxine and liothyronine might prove effective for patients with myxedema coma, especially for those who require high-dose glucocorticoid administration. In addition, the thyroid hormone also regulates neutrophil respiratory burst by regulating gp91phox, the catalytic core of NADPH oxidase, which is an important part of the pathogenesis of AAV 8,9. Thyroid dysfunction can disrupt the delicate balance of the immune system, leading to an unbalanced inflammatory response 10.

3. Relationship between Thyroid Hormone and Clinical Parameters in AAV Patients with Renal Injury

The differential diagnosis between drug-induced and idiopathic vasculitic conditions may be difficult in the individual patient. Withdrawal of the offending agent alone is often sufficient to induce prompt resolution of clinical manifestations, obviating the need for immunosuppressive and anti-inflammatory drugs. Increasing understanding of the pathophysiological characteristics of all inflammatory vasculitides should lead to better diagnostic and therapeutic approaches to drug-induced vasculitis. Previous study revealed an increased risk of thyroid dysfunction in AAV patients 13,14,15.

  • This is due to the lack of a consensus in medical literature upon a disease that manifests diversely, with a definite diagnosis that relies on a high-tech procedure such as biopsy.
  • Moreover, the clinical and prognostic relevance of thyroid dysfunction in AAV patients with renal injury is also unclear.
  • After 1 year, she regularly visits our hospital for follow-up and medical treatment.
  • HI, KF, KA, SH, AN, TS, KM, MK, SY, SI, NH, SH, TA, and MN interpreted the data and provided input in the preparation of the manuscript.

We carried out a retrospective analysis from 2005 to 2016 involving 98 patients diagnosed with either chronic spontaneous urticaria or urticarial vasculitis at Respiralab Urticaria Center, Guayaquil-Ecuador. Demographic and clinical variables such as age, sex, years with the disease, type of urticaria, thyroid function tests and antithyroid antibodies were collected using medical records from the institution. The diagnostic definitions used for chronic spontaneous urticaria and urticarial vasculitis are summarized in Table1 5,6,7,8.

A two-tailed p-value of less than 0.05 was considered statistically significant. Statistical analyses were performed using SPSS Statistics for Windows Version 25.0 (SPSS Inc., Chicago, IL, USA). Although the pathogenic mechanism of immunoglobulin A (IgA) vasculitis has yet to be elucidated, it has been suggested that immune complexes deposit mainly on arterial walls and activate the complement system (9). Blood vessel wall destruction by neutrophils causes IgA vasculitis with nephritis (10), the symptoms of which include tactile purpura on the lower legs, arthritis, abdominal pain, and nephropathy. Systemic inflammation caused by autoimmune mechanisms may cause severe hypothyroidism resulting in the development of myxedema coma by disrupting the compensatory mechanism for downregulated T3 expression. In addition, proteinuria related to IgA vasculitis with nephritis may contribute to thyroid hormone deficiency (11–13).

Figure 1.

This report describes a patient with UV triggered by thyroid replacement, necessitated by Hashimoto’s thyroiditis, which can itself cause UV. There were no significant differences in thyroid hormone levels among groups of patients with different ANCA positivity status. Clinicians should be aware of this critical condition that would be masked by the trigger disorders.

However, whether IgA vasculitis causes deterioration of hypothyroidism into myxedema coma requires further clarification. In addition, it remains unclear whether liothyronine (LT3) should be administered in addition to levothyroxine (LT4) to treat myxedema coma, although the efficacy of combination therapy with LT3 and LT4 has been demonstrated previously (14–16). Drug-induced vasculitis is an inflammation of blood vessels caused by the use of various pharmaceutical agents. Vasculitis causes changes in the walls of blood vessels, including thickening, weakening, narrowing and scarring. Inflammation can be short-term (acute) or long-term (chronic) and can be so severe that the tissues and organs supplied by the affected vessels do not get enough blood.

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In clinical practice, a subset of AAV patients with renal involvement exhibiting thyroid dysfunction were observed. However, the clinical and prognostic relevance of thyroid dysfunction in AAV patients with renal injury remained unclear. The present study analyzed the thyroid function in the cohort of AAV patients with renal injury. Woywodt et al. also question our method of collecting medical and treatment history via telephone interviews. We concur that recall bias is a concern in any case-control study and can lead to spurious associations. The best defense against recall bias is the confirmation of information through a separate source.

Although combination therapy with LT3 and LT4 is not common (14–16), it has reportedly been effective in improving the prognosis in certain cases of myxedema coma (27). Additionally, rapid thyroid hormone replacement is generally avoided because it carries the risk of inducing myocardial infarction and arrhythmias (28). In this context, administration of LT3 was hesitated; however, recovery of serum free T3 levels were delayed in comparison with normal to high levels of serum free T4 levels (Figure 3) (16). The potential for exacerbation of hypothyroidism in response to a pharmacological dose of glucocorticoid should also be noted. Combination therapy with both LT4 and LT3 may prove effective, especially for myxedema coma patients with diseases requiring glucocorticoid administration.

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