Introduction Arteriovenous fistulas (AVFs) are a form of arteriovenous malformations clinically characterized by anomalous communications between arterial and venous systems that bypass the normal anatomic capillary beds (1). Broadly it can be divided into two forms based on the cause: acquired or congenital. Surgery, penetrating trauma, and percutaneous catheterization are the most common causes of acquired AVFs. Rarely AVFs can be formed in the absence of a clear cause and are called spontaneous AVFs which are rare with very few case reports in the literature (2-4). The anatomy of the fistula depends on the location in the body and where the causative factor was applied. Greater than 50% of traumatic AVFs happen in the lower extremity, and about one-third occur in the femoral vessels, while 15% take place in the popliteal vessels but AVF can occur at any site (5-8).AVFs present clinically with progressively growing pulsatile mass on each respective site associated with or without complications including infection, thrombosis, aneurysm, hypertension, and heart failure demanding timely intervention (9).

IntroductionThe term overlap syndrome includes a large group of conditions characterized by the coexistence of signs, symptoms, and immunological features of two or more connective tissue diseases occurring simultaneously in the same patient.1 It is very rare to see an overlap of inflammatory myositis and SLE and it has not been well studied.2 With variable epidemiological data, most often diagnosed concurrently with SLE.3 In contrast to myalgia which can affect nearly half of patients with SLE, true myositis is relatively rare as shown by some studies.11Myositis can occur before, after SLE, or sporadically both diseases can be present simultaneously.10Myositis associated with overlap syndromes is usually of paroxysmal variety and has been associated with one or another of connective tissue disorders.1 Raised serum creatine kinase is found to correspond with underlying myositis in patients with SLE.12 Furthermore, the presence of myositis-specific antibodies such as anti-U1RNP, anti-Ro/SSA, anti-La/SSB, anti-Sm or anti-PM-Scl is suggestive of an overlap myositis.13,12

Tittle Page:Myocardial bridging, unusual cause of myocardial infarction; case report and review of literatures.1Merga Daba, 1Dawit Bineyam,1Ibraist Yohannes, 1Beniam Yohannes,2Rabirra Waktola, 3Eshetu Bedada1Department of Internal Medicine, College of Health Sciences, Addis Ababa University, Addis Ababa, Ethiopia.2Department of Radiology and MRT, St. Paul Hospital Millennium Medical College, Addis Ababa, Ethiopia.3Cardiology unit, Department of Internal medicine, College of Health Sciences , Addis Ababa University , Addis Ababa , EthiopiaCorrespondence : Merga Daba, Department of Internal medicine, College of Health Sciences, Addis Ababa University, Addis Ababa, Ethiopia. Tel: +251912684411, Email: [email protected]

Introduction Nearly 25% of systemic symptoms of autoimmune disorders are misdiagnosed and mismanaged and often come with flare-ups or complications. The coexistence of multiple rheumatic diseases makes it more challenging regarding both management and diagnosis. Several types of overlap syndrome are documented in the literature. While two or more rheumatic diseases coexist, one disease often is clinically predominant. Rhupus syndrome, which combines the clinical and laboratory aspects of rheumatic arthritis (RA) and systemic lupus erythematosus (SLE), is one of the uncommon and sporadically documented overlaps. SLE and RA are systemic autoimmune rheumatic illnesses that affect multiple organs and systems and have unique clinical and serological traits.  (1)“ Rhupus” was first coined in 1971 to describe patients who satisfy the criteria for both systemic lupus erythematosus(SLE) and rheumatoid arthritis(RA). (2) it has been defined as a deforming and symmetric polyarthritis accompanied by symptoms of SLE and the presence of antibodies such as ant-ds-DNA, anti-smith, and rheumatoid factor with or without ant-CCP antibody. (a)  because of the rarity of the disease the prevalence, pathophysiology, natural history, and radiological and immunological profiles profile of rhupus are poorly described.There is no known etiology causing the disease but there are limited studies suggesting the combined role of genetic, immunological, hormonal, and environmental factors in the progression of the disease. (3) identification of rhupus is very essential owing that their therapy and outcome differ from those patients having RA or SLE alone. (4)We report one such rare case below.Case presentation :