Vasculitis and anti-thyroid medication PMC

In the same study, among 426 patients followed in their thyroid clinic, a 30% incidence of systemic autoimmune disease was observed 6. Serum FT4 and FT3 levels are denoted by closed triangles and circles, respectively. FT4 levels increased and reached above the normal range following levothyroxine administration after 20th day. The shadows represent the normal ranges of serum free T4 and free T3 levels. We appreciate the opportunity to respond to the comments made by Woywodt et al., regarding our evaluation of the association of thyroid disease and vasculitis 1.

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.

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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.

Drug-induced vasculitis: a clinical and pathological review

After careful and precise consideration, we screened out and excluded two patients with primary hyperthyroidism and 460 patients with a lack of thyroid-related laboratory tests or medical record integrity, and 174 AAV patients were finally included in the study. In this cohort of 174 AAV patients, the mean age was 56.9 ± 16.5 years, 102 patients were females (58.6%), and the mean BVAS score was 16.97 ± 6.22. Table 1 summarized the baseline demographic and clinical characteristics of enrolled patients. Severe and long-term hypothyroidism reduces intracellular triiodothyronine (T3) levels, thus leading to lessened sensitivity to high carbon dioxide and low oxygen concentrations, decreased thermogenesis, diminished cardiac output, and increased fluid retention. Respiratory failure (due to hypoventilation), hypothermia, circulatory failure, and central nervous system dysfunction are considered the major clinical symptoms of myxedema coma. Continuous data with normal distribution were presented as means ± standard deviations (SDs).

Rapid aggravation of the patient’s condition after admission led us to diagnose her with myxedema coma. Myxedema coma is an endocrine emergency with a high fatality rate that necessitates thyroid preparations as soon as possible (2). Nevertheless, because myxedema coma occurs suddenly, it is necessary to grasp the dynamic pathological condition during the course. Furthermore, delays resulting from failure to diagnose or wait for confirmation by blood tests have contributed to the high mortality of this disease (7).

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).

Vasculitis and anti-thyroid medication

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 synthroid alendronate 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.

4. Survival Analysis

• A 59-year-old Japanese woman presented with bilateral painful purpura on her lower legs.
• 3 It has been well documented that propylthiouracil could induce antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis, which predominantly affects small vessels.
• 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.
• Thyroid dysfunction can disrupt the delicate balance of the immune system, leading to an unbalanced inflammatory response 10.

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.

• The patient successfully completed the desensitization protocol; however, his levothyroxine dose remained subtherapeutic.
• All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.
• However, when a cause is found, specific treatment of the underlying problem or removal of an offending agent will resolve the symptoms.
• He was advised to try oral antihistamines, which did not improve the course of his rash.

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 (Figure 1B, 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 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.

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.