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NMDAR, Hu and Ma2-antibodies were the most prevalent ANA in this first antibody screening study in a Turkish cohort. Antibody type was determined to be the foremost prognostic factor in ANA seropositive cases.

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BackgroundDeep vein thrombosis (DVT) is the most common form of vascular involvement in Behçet’s disease (BD). Post-thrombotic syndrome (PTS) refers to the symptoms and signs of chronic venous insufficiency following DVT. It develops within the first 2 years in more than half of the patients after acute DVT [1].ObjectivesIn this prospective study, we aimed to evaluate the risk of PTS development after DVT and the factors affecting the development and severity of PTS in BD patients.MethodsBD patients (n=18) with acute DVT and were followed in 3 tertiary rheumatology centers were included in the study. Patients are evaluated for PTS presence during acute DVT, 6-12. months and then annually. Villalta scoring with a total score of >4 or presence of venous ulcer was defined as PTS. PTS was classified as mild if the score was between 5-9, moderate between 10-14, and presence of >14/venous ulcers as severe. Venous Damage Score (VDS) was used to evaluate the effect of venous disease on work productivity and Venous Clinical Severity Score (VCSS) for symptom severity.ResultsThe clinical features of the 18 patients included in the study are shown in Table 1. Major-organ involvement was present in 12 patients (pulmonary involvement in 7 (39%), ocular involvement in 5 (28%), arthritis in 3 (13%), neurobehçet and enterobehçet each in 1 patient). Steroid and IS treatment was given to all patients after an acute DVT attack. Additional anticoagulant (AC) treatment was chosen in 16 of the patients. Patients were followed up for a median 23.2 (6-40) months after DVT. The number of patients followed for at least 1 year after an acute DVT attack was 15, and the median follow-up period was 26 (12-40) months. The median duration of AC use in patients who received AC treatment in the follow-up was 6 (0-12) months. PTS developed in 5 (33%) of 15 patients during follow-up. The baseline, 6th and 12th month course of Villalta, VCSS, and VDS scores are shown in figure 1.ConclusionIn this prospective follow-up after an acute DVT attack 33% of BD patients developed PTS within 1 year. In our previous retrospective study, 62% of 205 patients, half of whom received AK, developed PTS during follow-up [2]. Despite the limitations of our study, such as the low number of patients and the short follow-up period, AC treatment in all patients (except 1) may have influenced a lower PTS development in the prospective follow-up compared to the retrospective data.References[1]Baldwin MJ et al. J Thromb Haemost. 2013 May;11(5):795-805.[2]Aksoy Aet al. J Vasc Surg Venous Lymphat Disord 2021; 9:1451.Table 1.Characteristics of Study PatientsClinical manifestationsSS/StdAge, average33.56 (9.62)Female/male, n(%)4/14 (%22.2)Family history (BD)3 (%16.7)Oral ulcers16 (%88.9)Genital ulcers9 (%50)Papulopustular lesions(%61.1)erythema nodosum6 (%33.3)Pulmonary involvement7 (%38.9)Articular involvement3 (%16.6)Neurological involvement1 (%5.6)Ocular disease5 (%27.8)Gastrointestinal involvement1 (%5.6)Figure 1.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

Dear Editor,A 63-year-old woman was evaluated in the emergency department for generalized tonic clonic seizure lasting 2-3 minutes, which was accompanied by contractions in her body and urinary incontinence. She gave a history of similar convulsions for the last 15 years, eight of which were clustered in the last year. She also reported that she sometimes had numbness, a tingling sensation in her hands and face, and cramps and weakness in her legs. She had a history of thyroidectomy for multinodular goiter 32 years ago, after which she had only rare health checks and used her medications irregularly. She had no neuropsychiatric signs, gait disturbance, or family history for any disease. Her physical examination and neurologic examination were normal. Her laboratory examination revealed normal blood count, hepatic and renal functions. She had hypocalcemia (4.3 mg/ dL), hyperphosphatemia (5.4 mg/dL), a low parathormone level (2.7 pg/mL), normal thyroid-stimulating hormone (3.3 uIU/mL), free T3 (2.9 pg/mL), free T4 (1.1 ng/dL), and vitamin D (23.9 ng/mL) levels. An electroencephalograph study was normal. Computerized brain tomography (CT) revealed diffuse symmetrical areas of calcification bilaterally in the centrum semiovale, corona radiata, periventricular white matter, caudate nucleus, putamen, globus pallidus, thalamus, and cerebellum (Figure 1, 2). On brain magnetic resonance imaging (MRI), T1A sequences showed peripheral hyperintense heterogeneous areas in the caudate nucleus, putamen, and globus pallidus, and hyperintense areas in the posterior thalamus ( Figure 3); T2A sequences showed hypointense heterogeneous areas in the caudate nucleus, putamen, and globus pallidus, and hyperintense heterogeneous lesions in the centrum semiovale and corona radiata (Figure 4). The patient was administered parenteral calcium replacement in the acute period, and calcium 1000 mg/day and calcitriol 0.5 mcg/day were begun as maintenance therapy. Her calcium level was normalized at follow-up, and she experienced no recurrent seizure attacks.Cerebral calcification is a common condition in neurologic practice, with 0.3% to 1.5% of cases being physiologic (1). The differential diagnosis includes hereditary disorders (Fahr disease, tuberosclerosis, Cockayne syndrome, mitochondrial disorders), endocrinologic disorders, metabolic disorders (disorders of calcium, vitamin D, and iron metabolism), infections (brucella, toxoplasmosis, rubella, cytomegalovirus), and toxins (2). Hypoparathyroidism following thyroid gland surgery is one of the most common pathologic causes of cerebral calcification. As well as general symptoms such as tingling sensation, cramps, spasm, weakness, bronchospasm, and cardiac arrhythmias, the disorder may also manifest itself with seizure, altered consciousness, psychiatric, extrapyramidal, and cognitive symptoms (3). MRI is the most sensitive method for demonstrating brain lesions. However, CT is superior to MRI in detecting calcifications and determining their location. The diffuseness of calcifications depen...