Anti-cyclic citrullinated peptide antibody (anti-CCP) is a specific marker for the diagnosis of rheumatoid arthritis. However, this antibody can be detected in other rheumatic diseases and even in healthy people. This study aims to determine the prevalence and the clinical significance of anti-CCP in patients with primary Sjögren syndrome (pSS). We analyzed the clinical and laboratory data of 95 patients with pSS by retrospective review of their medical records. Anti-CCP was measured by ELISA kit. Anti-CCP, rheumatoid factor (RF), anti-nuclear antibody, anti-Ro and anti-La antibodies, and clinical data were investigated. We analyzed clinical and serologic characteristics of anti-CCP-positive patients. Twenty-one patients (22.1%) had positive anti-CCP (mean titer 61.6 ± 15.6 U/ml) and 40 patients (42.1%) had positive RF (mean titer 98.8 ± 22.7 IU/ml). Seventy-nine patients (83.1%) had arthralgia, and 31 patients (32.6%) had non-erosive arthritis on physical examination and radiologic images. Anti-CCP-positive patients had more frequently positive RF (71.4% vs. 41.8%, P = 0.01) and anti-Ro antibody (85.7% vs. 60.8%, P = 0.03). Anti-CCP-positive patients had non-erosive arthritis more frequently than anti-CCP-negative patients (76.1% vs. 21.6%, P < 0.01). The prevalence of anti-CCP was 22.1% in pSS, and anti-CCP was associated with non-erosive arthritis, and positivity of RF and anti-Ro antibody.

We investigated whether taurine chloramine (TauCl), which is -endogenously produced by immune cells such as macrophages that infiltrate adipose tissue, affects the differentiation of preadipocytes into adipocytes or modulates the expression of adipokines in adipocytes. To study the physiological effects of TauCl on human adipocyte differentiation and adipokine expression, preadipocytes were cultured under differentiation conditions for 14 days in the presence or the absence of TauCl. Differentiated adipocytes were also treated with TauCl in the presence or the absence of IL-1β (1 ng/ml) for 7 days. The culture supernatants were analyzed for adipokines such as adiponectin, leptin, IL-6, and IL-8. At concentrations of 400-600 μM, TauCl significantly inhibited the differentiation of human preadipocytes into adipocytes in a dose-dependent manner. It did not induce the dedifferentiation of adipocytes or inhibit fat accumulation in adipocytes. Expression of major transcription factors of adipogenesis and adipocyte marker genes was decreased after treatment with TauCl, in agreement with its inhibition of -differentiation. These results suggest that TauCl may inhibit the differentiation of -preadipocytes into adipocytes. Thus, TauCl or more stable derivatives of TauCl could potentially be a safe drug therapy for obesity-related diseases.

Type 1 myotonic dystrophy (DM1) is an autosomal-dominant inherited disorder with a multisystem involvement, caused by an abnormal expansion of the CTG sequence of the dystrophic myotonia protein kinase (DMPK) gene. DM1 is a variable multisystem disorder with muscular and nonmuscular abnormalities. Increasingly, endocrine abnormalities, such as gonadal, pancreatic, and adrenal dysfunction are being reported. But, Electrolytes imbalance is a very rare condition in patients with DM1 yet. Herein we present a 42-yr-old Korean male of DM1 with abnormally elevated serum sodium and potassium. The patient had minimum volume of maximally concentrated urine without water loss. It was only cured by normal saline hydration. The cause of hypernatremia was considered by primary hypodipsia. Hyperkalemic conditions such as renal failure, pseudohyperkalemia, cortisol deficiency and hyperkalemic periodic paralysis were excluded. Further endocrine evaluation suggested selective hyperreninemic hypoaldosteronism as a cause of hyperkalemia.

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