Utility of serum complement factors C3 and C4 as biomarkers during therapeutic management of giant cell arteritis.

OBJECTIVE: There is a strong unmet need for biomarkers in giant cell arteritis (GCA), as C-reactive protein (CRP) may be unreliable in patients treated with Tocilizumab (TCZ). We aimed to assess whether C3 and C4 are useful biomarkers in GCA patients, particularly in those treated with TCZ. METHOD: We retrospectively enrolled all patients who underwent C3 and C4 measurement at baseline. All patients were evaluated at 3, 6, 12, and 24 months after diagnosis, as part of routine follow-up. Two assessments after the end of the observational period, in case of further relapses, were also included. RESULTS: At baseline, mean ± sd levels (mg/dL) of C3 (133 ± 28.99) and C4 (25.9 ± 9.04) were within normal ranges. During follow-up, C3 and C4 decreased in patients attaining remission (107.07 ± 19.86, p = 0.0006; 19.86 ± 10.27, p = 0.01, respectively) and sustained remission (95.85 ± 18.04, p = 0.001; 15.61 ± 9.75, p = 0.006). In TCZ-treated patients, even stronger decreases in C3 (83.11 ± 19.66, p = 0.001) and C4 (8.26 ± 3.83, p < 0.0001) were observed, and their values were not correlated with CRP or erythrocyte sedimentation rate. CONCLUSION: C3 and C4 do not seem useful in the diagnosis of GCA, as normal values do not rule out active vasculitis. However, C3 and C4 correlate with disease activity. As the low C4 levels found in TCZ-treated patients are not correlated with CRP, C4 should be evaluated as a potential biomarker of disease activity and treatment response.

Adhesive capsulitis and ultrasound diagnosis, an inseparable pair: a novel review.

PURPOSE: Adhesive Capsulitis (AC) is a musculoskeletal disorder initially described by Codman in 1934. The disease is characterized by pain-limited restriction in active and passive glenohumeral range of motion (ROM) despite the lack of a structural deficit. In the last decades, arthroscopy and magnetic resonance imaging (MRI) has been the only diagnostic tools able to highlight the characteristic alterations of the glenohumeral capsular-ligament apparatus in AC; nevertheless, both arthroscopy and MRI are burdened by intrinsic limitations. The aim of this narrative review is to summarize the most significant evidence supporting the use of ultrasound (US) for the diagnosis of AC. METHODS: We extensively searched via PubMed library the terms "frozen-shoulder" and "adhesive capsulitis" each combined with "ultrasound". RESULTS: We found 3723 papers on PubMed and selected those inherent to AC diagnosis, US imaging, correlation with arthroscopic and MRI findings. Forty papers which were strictly related to the topic of this narrative review were initially chosen, then 20 studies which described and exploited US for AC diagnosis were finally included. Coracohumeral ligament (2.65 ± 0.4 mm) and axillary pouch thickening (3.34 ± 0.8 mm), as well as an increase in vascularity at rotator interval (78/214, 36.44%), represented the commonest US signs useful for AC diagnosis and for which the most significant cut-off values were reported. CONCLUSIONS: The evidence collected in this review testify that musculoskeletal US is as reliable as MRI for AC diagnosis, therefore we believe that in this context US should be considered a first-line imaging technique.

Observations about subcalcaneal adventitial bursitis (heel fat pad inflammatory lesion) in rheumatoid arthritis. Comment on the article of Suzuki and Shirai.

Not available.

Gitelman syndrome associated with chondrocalcinosis and severe neuropathy: a novel heterozygous mutation in SLC12A3 gene.

Gitelman syndrome (GS) is an inherited salt-wasting tubulopathy characterized by hypocalciuria, hypokalemia, hypomagnesemia and metabolic alkalosis, due to inactivating mutations in the SLC12A3 gene. Symptoms may be systemic, neurological, cardiovascular, ophthalmological or musculoskeletal. We describe a 70 year-old patient affected by recurrent arthralgias, hypoesthesia and hyposthenia in all 4 limbs and severe hypokalemia, complicated by atrial flutter. Moreover, our patient reported eating large amounts of licorice, and was treated with medium-high dosages of furosemide, thus making diagnosis very challenging. Genetic analysis demonstrated a novel heterozygous mutation in the SLC12A3 gene; therefore, we diagnosed GS and started potassium and magnesium replacement. GS combined with chondrocalcinosis and neurological involvement is quite common, but this is the first case of an EMG-proven severe neuropathy associated with GS. Herein, we underline the close correlation between hypomagnesemia, chondrocalcinosis and neurological involvement. Moreover, we report a new heterozygous mutation in exon 23 (2738G>A), supporting evidence of a large genetic heterogeneity in this late-onset congenital tubulopathy.