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Q fever is a zoonotic disease caused by Coxiella burnetii--an obligate, gram negative, intracellular bacteria. The term Q (Query) was first used because at the time the disease was named its etiology was unknown. Q fever is divided into acute and chronic infections characterized by different evolution, serological profiles and treatment. Pericarditis, as a manifestation of Q fever is rare and difficult to diagnose. This is due to the following: firstly, the clinical presentation of acute Q fever is pleomorphic, nonspecific and self limited, and secondly, the diagnosis relies on the physician's interest and the presence of a reliable diagnostic laboratory. The objective of that review is to increase the physician's awareness of the clinical presentation of Q fever, to discuss the importance of the diagnosis and laboratory tests and to guide the physician as to when to provide treatment and the relevant patient population to be treated.

Congestive heart failure causes substantial morbidity and mortality. Symptoms and physical findings can help in diagnosis, but have limited sensitivity and specificity. Objective measurement of ventricular function is essential in virtually all patients in whom heart failure is suspected; reversible causes of heart failure must be sought. Out-patient management includes education and counseling, emphasis on and assessment of compliance with diet, and pharmacological treatment. Angiotensin-converting enzyme inhibitors are the mainstay of treatment but are underused, and maximal doses are not given, apparently because of concern about side-effects. Diuretics should be administered only as needed to manage fluid overload. Calcium channel blockers are relatively contraindicated in patients with impaired ventricular function. Patient follow-up should be guided by results of the medical history and physical examination. Routine serial testing of ventricular function and exercise performance is discouraged.

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired disorder of blood cells which originate from an abnormal hematopoietic stem cell. The condition is characterized by nocturnal hemoglobinuria, chronic hemolytic anemia, and thrombosis. We describe a 60-year-old woman with PNH admitted with abdominal pain and jaundice, who had dark urine on arising after a night's sleep. The diagnosis was established by the typical clinical story and a positive Ham test. She was successfully treated with Halotestin and folic acid. Although PNH is rare, it should be considered in the differential diagnosis of hemolytic anemia. Early diagnosis and treatment are important.

A 19-year-old man presented with chest pain, dyspnea and dry cough. Chest X-ray and computerized tomography showed a large, anterior, mediastinal mass. 2-dimensional echocardiography demonstrated a large amount of pericardial fluid. Serum alpha-fetoprotein was increased. Fine-needle, aspiration cytology during anterior mediastinotomy revealed malignant cells. Anterior thoracotomy demonstrated a large, anterior, mediastinal mass extending into the pericardial sac. The tumor was incompletely resected and 700 ml of pericardial fluid were removed. Histological examination showed a malignant, mixed, germ cell tumor. Cytologic examination of pericardial fluid revealed malignant tumor cells. Postoperatively, combined chemotherapy was administered and 3 years later the patient is free of symptoms.

3 patients with recurrent, symptomatic hypoglycemia associated with increased insulin and C-peptide blood levels are described. 2 men aged 37 and 21-years had mental and social problems and although they had access to sulfonylurea drugs, both denied intake. 1 was scheduled for pancreatectomy, but as a result of the vigilance of the surgeon, the operation was canceled. By demonstrating sulfonylurea in their urine, a definitive diagnosis of factitious hypoglycemia was established, and further invasive procedures were avoided. The third was a woman aged 40-years had malignant insulinoma with liver metastases, proven by cytology. The common and differentiating clinical and laboratory characteristics of hypoglycemia due to insulinoma and factitious hypoglycemia secondary to sulfonylurea intake are discussed, and the importance of urine analysis demonstrating the presence of sulfonylurea is emphasized.

In ischemic hepatitis, which is not rare, there is a marked but transient increase in serum aminotransferase activity to at least 20 times the upper limit of normal, without any other cause for hepatic necrosis. It is generally preceded by an acute cardiac complication, usually pulmonary edema or a tachyarrhythmia, causing decrease in cardiac output, or may follow acute respiratory failure. The typical histological lesion is centrilobular hepatic necrosis. We present 2 cases of ischemic hepatitis due to hypotension following rapid atrial fibrillation, sepsis and acute respiratory failure, highlighting the different etiologies, laboratories results, and the relative benign course, described in the literature. The patients were a woman aged 80 and a man aged 76. Awareness of the place of this disorder in the differential diagnosis of acute hepatitis may save needless, dangerous investigations.

On the fifth day of a course of antibiotic therapy for acute Klebsiella pyelonephritis, a 21-year-old pregnant woman developed adult respiratory distress syndrome. She improved rapidly on fluid restriction and intravenous furosemide and did not require mechanical ventilation. 17 weeks later, after 40 weeks of pregnancy, she spontaneously delivered a healthy male infant weighing 3280 g.