The relationship between serum calprotectin levels and disease activity in patients with subacute thyroiditis. Original paper
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Autoimmune Diseases
Autoimmune Diseases
Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.
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Karen Pendergrass
What was studied?
This study investigated serum calprotectin (S100A8/A9) as a potential biomarker for the diagnosis and follow-up of subacute thyroiditis, specifically subacute granulomatous (De Quervain) thyroiditis. The focus was on evaluating calprotectin’s utility in differentiating the acute inflammatory phase from the recovery phase of the disease, and whether its levels can predict persistent hypothyroidism. Calprotectin, a cytosolic protein complex primarily produced by neutrophils and monocytes, is known to be elevated in various acute and chronic inflammatory states, but had not previously been evaluated in subacute thyroiditis. Patients were assessed using an array of standard laboratory parameters (e.g., free thyroxine [fT4], thyroid-stimulating hormone [TSH], C-reactive protein [CRP], erythrocyte sedimentation rate [ESR], white blood cell [WBC] count, absolute lymphocyte, and neutrophil counts) during both the acute and recovery phases, with persistent hypothyroidism determined at six months.
Who was studied?
The study included 36 adult patients (mean age 44.1 ± 8.8 years; 80.6% female) with a confirmed diagnosis of subacute granulomatous thyroiditis, presenting to a single tertiary center in Turkey between November 2018 and January 2020. Patients with confounding conditions (other infections, autoimmune or rheumatic disorders, recent steroid use, pregnant, major surgery, chronic hepatic/renal/cardiac diseases, or malignancies) were rigorously excluded to ensure specificity. Diagnosis was based on clinical presentation (fever, neck pain, thyrotoxic symptoms), elevated ESR and CRP, and supportive ultrasonographic findings. All patients provided informed consent, and local ethics approval was granted.
Most important findings
Serum calprotectin levels were significantly higher in the acute inflammatory phase than in the recovery phase (median 96.92 ng/mL [IQR: 24.47–130.37] vs. 37.98 ng/mL [IQR: 14.02–20.52]; p <0.001). Similar trends were observed for other acute phase markers (ESR, CRP, WBC, ANC), all of which decreased upon resolution. However, calprotectin did not correlate with these classical inflammatory markers or with TSH and fT4 in either phase. Logistic regression revealed that neither calprotectin nor any traditional inflammatory marker predicted the development of permanent hypothyroidism at six months. The study concluded that, while calprotectin is a sensitive indicator of acute inflammation in subacute thyroiditis, it is not useful as a prognostic marker for long-term thyroid dysfunction. No significant correlations were identified between calprotectin and other inflammatory or thyroid parameters, pointing to its independence from other markers.
| Marker | Acute Phase (Median/IQR or Mean±SD) | Recovery Phase (Median/IQR or Mean±SD) | p-value |
|---|---|---|---|
| Calprotectin (ng/mL) | 96.92 (24.47–130.37) | 37.98 (14.02–20.52) | <0.001 |
| ESR (mm/h) | 81.17 ± 23.19 | 19.00 (13.0–26.75) | <0.001 |
| CRP (mg/L) | 31.05 (17.62–46.12) | 3.23 (3.23–4.16) | <0.001 |
| WBC (10³/mm³) | 8.27 ± 2.44 | 6.72 ± 1.85 | <0.001 |
| ANC (10³/mm³) | 5.31 ± 2.00 | 3.73 ± 1.44 | <0.001 |
| TSH (μU/L) | 0.010 ([<0.001]-0.037) | 3.51 ± 2.69 | <0.001 |
| fT4 (pmol/L) | 19.13 (15.59–31.37) | 11.33 (10.49–12.41) | <0.001 |
Key implications
The findings support serum calprotectin as a reliable and independent marker for the diagnosis and monitoring of the acute phase of subacute thyroiditis, enhancing clinical discrimination during active disease. However, its lack of association with persistent hypothyroidism restricts its use as a prognostic tool for long-term outcomes. The lack of correlation between calprotectin and classical markers implies mechanistic independence, potentially providing unique insight into innate immune activity in thyroid inflammation. Microbiome researchers and clinicians may consider including calprotectin as part of a broader signature for neutrophil-driven inflammatory processes. Further, larger, controlled studies are needed to clarify the predictive value of calprotectin for tissue-damaging sequelae and to explore therapeutic modulation (e.g., zinc supplementation) in subacute thyroiditis.