Relationship of immature granulocytes with disease activity in rheumatoid arthritis.

AIM: To determine whether the IG count (#) and IG percentage (%) are associated with disease activity in rheumatoid arthritis (RA). METHODS: This retrospective study included 65 RA patients and 65 healthy controls. Clinical and demographic characteristics of controls and RA patients (at active period and when the patients achieved remission) were obtained from medical records. Disease activity was defined by disease activity score 28 (DAS28). Furthermore, the clinical disease activity index (CDAI), and simple disease activity index (SDAI) were calculated. For the differential diagnosis of RA patients from healthy controls, the cut-off value was estimated by making receiver-operator curves (ROC). RESULTS: In active RA patients, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), IG#, and IG% levels were significantly higher compared to the healthy controls (p < .001, for all). When the patients achieved remission, DAS28, CDAI, SDAI, ESR, CRP, IG#, and IG% values were significantly decreased (p < .001, for all). IG# and IG% were significantly positively correlated with DAS28, CDAI, SDAI, ESR, and CRP (p = .024, p = .008, p = .003, p < .001, p < .001, respectively). According to ROC curve analysis, IG% and IG# were the biomarkers to have a significant diagnostic value for RA with the area under the curve of 0.853 and 0.865 (p < .001, for all). CONCLUSION: The present study demonstrated that two novel inflammatory markers, IG# and IG%, can be useful for monitoring RA patients' disease activity. Furthermore, IG# and IG% can also be used as fast, inexpensive, and easily available complementary diagnostic markers to diagnose RA patients.

Mimic or coincidentally? TAFRO syndrome and systemic lupus erythematosus: A case-based review.

Castleman's disease (CD) is a rare, systemic disease with histopathological features of angiofollicular lymph node hyperplasia. In the literature, there are case-level reports that mimic or coexist with systemic lupus erythematosus (SLE) clinically and in the laboratory. Is this condition two separate diseases or is it an imitation of each other? A 73-year-old female patient was admitted to our clinic with arthritis, lymphadenopathy, fever, weight loss, and malar rash. He had a history of idiopathic thrombocytopenic purpura and thrombosis in the right leg tibialis posterior and dorsalis pedis arteries. Excisional lymphadenopathy biopsy indicated a diagnosis of hyaline-vascular-type CD. She had anti-nuclear antibody >1/80 homogeneous pattern, anti-double stranded DNA (anti-dsDNA), Anti-Smith (Sm) antibody positivity, hypocomplementemia (C3 and C4), pleural effusion, and pericardial effusion. For this reason, the classification criteria of the European League Against Rheumatism/American College of Rheumatology were studied. Clinical findings, idiopathic thrombocytopenic purpura history, antibody positivity, malar rash, and arthritis led us to the diagnosis of SLE. She was treated with 1 mg/kg/day prednisolone and hydroxychloroquine 200 mg 2 × 1. Azathioprine 2.5 mg/kg daily was added to the patient whose complaints did not improve. In the follow-ups, she completely recovered clinically and laboratory. SLE and CD are systemic diseases that overlap in many ways. The literature review shows that these two diseases may mimic each other or may coexist. This situation may be a reflection of a pathophysiological process that has not yet been clarified. This confusing process also affects the treatment decision. This confusing process also affects the treatment decision.

A rare syndrome mimicking scleroderma: Werner syndrome.

Werner syndrome (WS), also known as adult progeria, is a premature ageing syndrome that can manifest itself with grey hair, hair loss, diabetes mellitus, hyperlipidaemia, hypertension, skin disorders, ocular cataracts, myocardial infarction, osteoporosis, and stroke, especially after puberty. Physical examination findings similar to systemic sclerosis may be seen. Therefore, it may mimic this disease as misleading. A 43-year-old female patient was admitted to our clinic with a pre-diagnosis of systemic sclerosis complaint of skin hardening up to the ankle. In the first physical examination, there were wrinkles and thinning of the lip, suggesting systemic sclerosis in the facial appearance. On her capillaroscopy, there was tortuosity and an old focus of microhemorrhage. She had a history of diabetes mellitus and chronic osteomyelitis. When all symptoms, clinical findings, and antibody results were combined, it was thought that the patient might have WS. WS was diagnosed with homozygous c.2221 C>P p.R741*(rs763089663) positive in genetic analysis. It is known that WS creates a predisposition to malignancies, and most patients die secondary to malignancies. Therefore, early diagnosis becomes essential. Early diagnosis is of vital importance both to prevent complications and to delay treatment. In particular, systemic sclerosis-like findings of this syndrome may cause delays in diagnosis. For this reason, small clues suggesting WS in the clinic should be well known and well defined.