Background: Mönckeberg Medial Calcific Sclerosis (MMCS) is a rare condition that can mimic giant cell arteritis (GCA). It may be misinterpreted as giant cell arteritis by the clinician and cause unnecessary treatments. Therefore, it is a disease that should be differentiated from giant cell arteritis with its clinical, radiological, and pathological findings. Case Presentation: A 56-year-old female patient was admitted to our clinic with sudden unilateral vision loss on the right, pain in the right temporal artery trace, scalp sensitivity in the section corresponding to that area, difficulty chewing, and temporal artery sensitivity. He had a history of hemodialysis for 13 years due to hypertension, osteoporosis, a history of renal stones, and end-stage renal failure. In routine blood tests, White Blood Cell: 7.86X109/L, Hemoglobulin: 10.9 g/dL, C-reactive protein: 3.03 mg/L, Erythrocyte sedimentation rate: 53 mm/hour came. As a result of temporal artery biopsy performed for GCA, absence of giant cells, absence of epithelioid histiocytes, absence of pathological findings in the internal elastic lamina, diffuse calcification in the tunica media, and sclerosis was diagnosed as MMCS. Conclusions: In the literature, 4 case reports resemble giant cell arteritis and are diagnosed as MMCS. This case report is a rare case report showing that MMCS can completely mimic GCA findings.

Werner syndrome (WS), also known as adult progeria, is a premature aging syndrome that can manifest itself with gray hair, hair loss, diabetes mellitus, hyperlipidemia, 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 prediagnosis 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 Werner syndrome. Werner Syndrome was diagnosed with homozygous c.2221 C > P p.R741*(rs763089663) positive in genetic analysis. It is known that Werner syndrome 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. Especially, systemic sclerosis-like findings of this syndrome may cause delays in diagnosis. For this reason, small clues suggesting Werner syndrome in the clinic should be well known and well defined.

Behçet syndrome(BS), also known as Behçet disease (BD), is characterized by recurrent oral aphthae and any of several systemic manifestations including genital aphthae, ocular disease, skin lesions, gastrointestinal involvement, neurologic disease, vascular disease or arthritis. Sarcoidosis is a multisystem granulomatous disorder of unknown etiology that affects individuals worldwide and is characterized pathologically by the presence of noncaseating granulomas in involved organs. BD may be confused with sarcoidosis because they are both multisystem inflammatory disorders presenting with uveitis, polyarthritis, meningitis, cardiovascular disease, erythema nodosum, and other cutaneous lesions, and abnormal chest radiographs.

Introduction 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 laboratoryly. Is this condition two separate diseases or is it an imitation of each other? Case Presentation A 73-year-old female patient was admitted to our clinic with arthritis, lymphadenopathy (LAP), fever, weight loss and malar rash. He had a history of idiopathic thrombocytopenic purpura (ITP) and thrombosis in the right leg tibialis posterior and dorsalis pedis arteries. Excisional LAP biopsy indicated a diagnosis of hyaline vascular type CD. She had antinuclear antibody >1/80 homogeneous pattern, anti-dsDNA, anti-Sm positivity, hypocomplementemia (C3 and C4), pleural and pericardial effusion. For this reason, the classification criteria of the European League Against Rheumatism/American College of Rheumatology (2019 EULAR/ACR) were studied. Clinical findings, ITP 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 2x1. 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. Conclusions 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.