תוצאת חיפוש

אורה שובמן¹, ויטור פורדאוס¹, לריסה גורנדה², אלי קונן²,

¹מח' פנימית ב' והמרכז למחלות אוטואימוניות, מרכז רפואי שיבא, תל-השומר, ²מכון דימות, מרכז הרפואי שיבא, תל השומר

בת 18 שנה אושפזה בשל תלונות על שיעול יצרני וקוצר נשימה שהחל חודש לפני שהתקבלה למחלקה. מתוך הנחה שמדובר בדלקת ריאות ממקור זיהומי טופלה החולה באמצעות אנטיביוטיקה, אך ללא הטבה...

אורה שובמן, בוריס גילבורד, פנינה לנגביץ', יהודה שינפלד

המח' לרפואה פנימית ב' והיחידה לחקר מחלות אוטואימוניות, המרכז הרפואי שיבא תל השומר והפקולטה לרפואה סאקלר, אוניברסיטת תל אביב

מילות מפתח:

נוגדני RA33, RA33, מחלות אוטואימוניות, אורה שובמן, בוריס גילבורד, פנינה לנגביץ', יהודה שינפלד, שובמן, גילבורד, לנגביץ', שינפלד

Primary Subclavian Vein Thrombosis after Intensive Physical Exertion

Ora Shovman, Jacob George, Yehuda Shoenfeld

Dept. of Medicine B and Autoimmune Disease Research Unit, Chaim Sheba Medical Center, Tel Hashomer and Sackler Faculty of Medicine, Tel Aviv University

Subclavian vein thrombosis accounts for approximately 1-2% of recorded deep venous thromboses. It may be primary or secondary, and insertion of a central venous catheter is the most common cause of secondary subclavian vein thrombosis. Traumas, anatomic abnormalities and carcinoma are important additional risk factors for secondary thrombosis. Primary thrombosis of the subclavian veins is known as Paget-Schroetter syndrome. New criteria for its diagnosis include a history of increased upper extremity use prior to onset of symptoms, the presence of a venographically demonstrated thrombus and absence of any definable causes. We describe a 42-year-old woman with a history of intensive physical exertion admitted with swelling, pain and difficulty moving her arm. The diagnosis of primary subclavian vein thrombosis was established from the history of physical effort, results of Doppler ultrasound, and exclusion of other causes of subclavian vein thrombosis. This case suggests that primary subclavian vein thrombosis should be considered in young patients with subclavian vein thrombosis after exclusion of secondary disease.

Q Fever Endocarditis and Bicuspid Aortic Valve

Ora Shovman, Jacob George, Yehuda Shoenfeld

Medial Dept. B and Autoimmune Disease Research Unit, Chaim Sheba Medical Center, Tel Hashomer and Sackler of Medicine, Tel Aviv University

Q fever is caused by the rickettsia Coxiella burnetti, an obligate intracellular bacterium acquired by inhalation of infected dust from subclinically infected animals. Q fever may be acute or chronic; the chronic form mostly presents as endocarditis. Immunocompromised states and underlying heart disease are the most important risk factors. Usually the symptoms of Q fever endocarditis are nonspecific and diagnosis is often established very late. New criteria for diagnosis include a single blood culture positive for Coxiella burnetti, positive Q fever serology and characteristic echocardiographic studies. We describe a 49-year-old man with bicuspid aortic valve admitted with fever, weight loss and a new heart murmur. The diagnosis of Q fever endocarditis was established by positive Q fever serology, and an echocardiogram showing vegetations and valvular dysfunction. This case suggests that Q fever endocarditis should be considered in patients with "sterile" endocarditis.

Ischemic Hepatitis in Congestive Heart Failure after an Episode of Hypotension

Ora Shovman, Jacob George, Yehuda Shoenfeld

Dept. of Medicine B and Autoimmune Disease Clinic Research Unit, Sheba Medical Center, Tel Hashomer and Sackler Faculty of Medicine, Tel Aviv University

Ischemic hepatitis can occur as an acute episode in advanced congestive heart failure (CHF). The mechanism is massive necrosis of the central lobules resulting from acute hypoxia when low cardiac output further reduces oxygen supply, aggravating underlying congestion due to poor venous outflow. We describe a 70-year-old woman with congestive heart failure for 7 years who was admitted with jaundice, vomiting, abdominal pain and oliguria after an episode of hypotension. The diagnosis of ischemic hepatitis was established by a documented episode of severe hypotension, followed by elevation of serum transaminases, a rise in serum bilirubin and LDH levels, prolonged prothrombin time and acute renal failure. Other causes of acute hepatitis, such as a virus or drugs were excluded, and improved liver and renal function followed hemodynamic stabilization. We conclude that ischemic hepatitis should be considered whenever acute hepatitis follows a recent episode of systemic hypotension, especially in the context of concomitant CHF.