Although mechanism and incidence rate remain unclear, there seems little doubt that PPIs may cause hypomagnesemia. We should obtain blood Mg levels prior to initiation of PPIs when patients are expected to be on treatment for long period of time and in those with other potential causes of hypomagnesemia. Use of H2-blockers may be an appropriate alternative.

Background: Few studies evaluated the clinical outcomes of Community Acquired Pneumonia (CAP), Hospital-Acquired Pneumonia (HAP) and Health Care-Associated Pneumonia (HCAP) in relation to the adherence of antibiotic treatment to the guidelines of the Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) in hospitalized elderly people (65 years or older). Methods: Data were obtained from REPOSI, a prospective registry held in 87 Italian internal medicine and geriatric wards. Patients with a diagnosis of pneumonia (ICD-9 480-487) or prescribed with an antibiotic for pneumonia as indication were selected. The empirical antibiotic regimen was defined to be adherent to guidelines if concordant with the treatment regimens recommended by IDSA/ATS for CAP, HAP, and HCAP. Outcomes were assessed by logistic regression models. Results: A diagnosis of pneumonia was made in 317 patients. Only 38.8% of them received an empirical antibiotic regimen that was adherent to guidelines. However, no significant association was found between adherence to guidelines and outcomes. Having HAP, older age, and higher CIRS severity index were the main factors associated with in-hospital mortality. Conclusions: The adherence to antibiotic treatment guidelines was poor, particularly for HAP and HCAP, suggesting the need for more adherence to the optimal management of antibiotics in the elderly with pneumonia

The pathology of postoperative granulomatous peritonitis is poorly understood, but a hypersensitivity reaction may be a likely mechanism. A patient's history is important, because surgeons should be aware of this rare cause of ascites.

A 73-year-old man complained of epigastric discomfort, dysphagia, and weight loss of 8 kg over the prior 2 months; he denied hematemesis, hematochezia, melena, diarrhea, fever, or any other symptoms. The patient had severe leg weakness with intermittent bladder and bowel incontinence caused by a spinal cord compressing D6 fracture, hypertension, a repaired abdominal aortic aneurysm, and recurrent venous thromboembolism, for which a filter was inserted in the inferior cava vein. There was neither personal and family history of allergy, nor any gastrointestinal disorders, including cancer and peptic ulcer disease.The physical examination was unrevealing: the vital signs were normal and stable, and laboratory studies were normal except for a hemoglobin 9.8 g/dl, hematocrit 38.8%, total protein 6.9 g/dl, and albumin 3.0 g/dl. A computed tomography of the abdomen showed thickened gastric walls, an air fluid level in the lower esophagus, and abundant intraperitoneal fluid around the liver and the spleen, and in the pelvis. Endoscopy of the upper gastrointestinal tract revealed an almost complete obstruction of the gastric lumen by giant folds of the mucosa with rugae closely resembling cerebral convolutions with a finely nodular (cobblestone) appearance (Fig.

A 63-year-old man presented to the emergency department (ED) with left-sided abdomen pain. The patient reported a 5-day history of pain under the right shoulder blade and in the lumbar region, associated with constipation, but not with vomiting, diarrhea or any change in urination. The patient was taking prescribed medications: sennonides and rifaximin that had solved the constipation, but had not completely relieved the abdominal pain. His past medical history was significant for an appendectomy many years prior. He denied having any prior medical problems or allergies. On physical examination, he was oriented, alert, comfortable and in no acute distress. The vital signs were: heart rate of 90 beats/min., blood pressure 130/80 mmHg, respiratory rate 16 breaths/min, and temperature 35.8°C. The cardiovascular and respiratory examinations were unremarkable. The abdomen was soft, but the patient had tenderness in the epigastric region and in the right hypochondrium with guarding, and a mildly positive Murphy's sign. No rebound tenderness, tenderness at McBurney's point, palpable masses or abnormal pulsations was noted. Digital rectal examination was normal. On auscultation, normal bowel sounds were heard. The genitourinary examination was normal. Laboratory analysis revealed a lipase level of 225 U/L (range 6-50 U/L), amylase level of 93 U/L (range 13-53 U/L) and blood glucose level of 146 mg/dL (range 70-110 mg/dL). The serum blood urea nitrogen, creatinine, liver function tests, albumin, electrolytes, lactate dehydrogenase level and complete blood count (CBC) were normal. Coagulation studies, including prothrombin time, activated partial thromboplastin time and serum fibrinogen, were unremarkable. A chest and abdomen radiographs and an abdominal ultrasonography were performed, but all of them were unrevealing. An electrocardiogram demonstrated rapid atrial fibrillation without any acute injury pattern. A thoracoabdominal computed tomography (CT scan) showed a superior vena caval (SVC) filling defect with a subtotal occlusion that extended into the right atrium, like the suprahepatic IVC, with a dishomogeneous aspect. A partial filling defect was also noted at the level of the portal vein, extended up to the left portal vein and the superior mesenteric vein. The interpretations suggested a significant vascular thrombosis. The CT images also revealed gastric walls' thickening. Anticoagulant therapy was started, and the patient was admitted to an internal medicine ward. Laboratory analysis was ordered to re-evaluate the CBC and the chemistry panel, to monitor the coagulation profile and the urine analysis, to perform a screening for pro-thrombotic states (with homocysteine blood level test, the protein C and protein S test and the test for anti-cardiolipin antibodies) and to control tumor markers (with PSA test and CA 19-9 and CEA tumor markers tests) on the possibility that the thrombosis was a paraneoplastic syndrome. The lipase level was 72 U/L, the gamma-glutamyltranspeptidase (GGT) level was 126 U/L (range 10-4...