Urticarial Vasculitis Associated With Levothyroxine

A Kolmogorov–Smirnov test and P-P diagram were used for the normality test of the included data. Quantitative parameters were assessed with the t-test between groups for normally distributed data, and non-normally distributed data were assessed with the Mann–Whitney U test. Categorical data were compared using the chi-square test or Fisher’s exact test.

Urticarial vasculitis (UV) is identified as a clinicopathologic entity that involves clinical features of urticaria and histopathologic findings compatible with a cutaneous leukocytoclastic vasculitis of small vessels with fibrinoid deposits. UV represents a spectrum of diseases that differ in severity, ranging from an urticaria with minimal vasculitis to a systemic disease that can lead to serious organ-specific complications. Certainly, urticarial vasculitis is an underdiagnosed disease, to the extent that its incidence may vary from 3 to 20% 1. 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.

• Subsequently, his thyroid replacement was discontinued for four months, but he deteriorated significantly with poor clinical status and was restarted on branded Synthroid.
• Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
• ICO, VLM, GDR formulated the study question, EV, MF wrote the manuscript.
• Many AAV patients included in years much further back had no data of thyroid function, which made the sample size small.
• We concur that recall bias is a concern in any case-control study and can lead to spurious associations.

Urticarial Vasculitis Associated With Levothyroxine

• Annually, 1.08 cases per million people in Japan and 0.22 cases per million people in Spain develop myxedema coma (2, 3).
• All authors have read and agreed to the published version of the manuscript.
• Combination therapy with LT4 and LT3 may be useful for patients with myxedema come who require supra-physiological glucocorticoid administration.
• Only this data would, in clinical practice, support the screening of AAbs in UV patients.
• Previous studies also reported an increased risk of thyroid dysfunction in AAV patients 13,14.

All patients with clinical features suggestive of urticarial vasculitis were confirmed by biopsy. Thyroid function tests (T3, T4, TSH) were categorized into normal, below normal or above normal, while AAbs (antithyroperoxidase, antithyroglobulin antibodies) where dichotomized as absent or present. The diagnostic definitions used for chronic spontaneous urticaria and urticarial vasculitis are summarized in Table1 5–8. Firstly, it was a single-center study, and the data were collected retrospectively from clinical databases. bioidentical synthroid There might be a possible bias that the included patients might be suspected of having thyroid dysfunction. However, we checked all the medical records and found that all patients included had no history of previous thyroid disease.

Allergy, Asthma & Clinical Immunology

Their major concern is that our study does not support our statement that the use of anti-thyroid agents does not account for many cases of ANCA-Small Vessel Vasculitis (ANCA-SVV) in the general population, a contention we continue to support. Urticarial vasculitis (UV) is a protean disorder that can be triggered by a myriad of causes although it is often idiopathic. Treatment is often successful with corticosteroids and/or immunosuppressive drugs. However, when a cause is found, specific treatment of the underlying problem or removal of an offending agent will resolve the symptoms. This report describes a patient with UV triggered by thyroid replacement, necessitated by Hashimoto’s thyroiditis, which can itself cause UV. In this unusual presentation, rather than thyroiditis, thyroid replacement was the trigger for the vasculitis.

It can lead to highly critical conditions, such as central nervous system dysfunction, hypothermia, respiratory failure, and circulatory failure (3). Thus, although the incidence of myxedema coma is low, early diagnosis and avoidance of overlooking this disease are required for successful treatment (2). The patient successfully completed the desensitization protocol; however, his levothyroxine dose remained subtherapeutic. As a result, it was deemed clinically necessary to slowly up-titrate levothyroxine further to 150 µg daily; the rash reoccurred at 88 mcg dosage.

1. Patients

4, 5 However, the causal relationship between Henoch–Schönlein purpura (IgA vasculitis) and Grave’s disease or antithyroid drugs has been remained unclear yet 6. The studies involving human participants were reviewed and approved by Shimada Hospital. The patients/participants provided their written informed consent to participate in this study. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article. Myxedema coma is an endocrine emergency and fatal disease that is rarely encountered (1). Annually, 1.08 cases per million people in Japan and 0.22 cases per million people in Spain develop myxedema coma (2, 3).

Patients were followed up from the index date until their date of death or March 2022, whichever came first. Information regarding disease progression to the stage of maintenance dialysis or death was collected through telephone inquiries. The authors would like to thank all medical staffs who worked with us at Shimada Hospital for medical supporting and Enago () for the English language review. The original contributions presented in the study are included in the article/Supplementary Material. This section collects any data citations, data availability statements, or supplementary materials included in this article. Written informed consent was obtained from the patient(s) to publish this paper.

She was diagnosed with coexisting immunoglobulin A (IgA) vasculitis and severe IgA vasculitis with nephritis and was consequently treated with intravenous methylprednisolone (125 mg/day). However, she rapidly developed multiple organ failure due to the exacerbation of severe hypothyroidism, i.e., myxedema. Her condition improved significantly following oral administration of prednisolone along with thyroxine. There was a delayed increase in the serum free triiodothyronine level, while the serum free thyroxine level was quickly restored to normal. Rapid deterioration of the patient’s condition after admission led us to diagnose her as having myxedema coma triggered by IgA vasculitis.

The rash consisted of fixed, non-migratory clusters of wheals and pink papules with hyperpigmented macules along the lower back and lower extremities (Figure 1A). Symptom onset typically occurred one month after starting any thyroid replacement medication but would resolve within two months of medication cessation and the addition of systemic corticosteroids. Kidney survival curve of AAV patients with renal injury in different groups. 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. Figure1 Images of the lower legs, chest X-ray, chest computed tomography, electrocardiogram, and echocardiogram. (C) No abnormalities were found on the electrocardiogram at the time of admission.

1. The General Information of Included AAV Patients with Renal Injury

Disruption of the compensatory mechanism for severe and long-term hypothyroidism by various causes leads to critical conditions, including hypothermia, respiratory failure, circulatory failure, and central nervous system dysfunction. Infectious diseases, stroke, myocardial infarction, sedative drugs, and cold exposure are considered the main triggers for myxedema coma. A 59-year-old Japanese woman presented with bilateral painful purpura on her lower legs.