An overview on immune system and migraine.

The pathogenesis of migraine is still unclear, but much evidence led us hypothesize that it can be associated with immune system modification, so that a role for cytokines has been suggested. Cytokines are important mediators of the immune and inflammatory pathways and their receptors are widely express in central nervous system (CNS) by all cell types, including neurons, indicating that they can act on neuronal receptors. Cytokines are now considered to be the pain mediators in neurovascular inflammation. Furthermore cytokines may be a cause of the migraine pain: in fact an high levels of chemokines could stimulate the activation of trigeminal nerves, the release of vasoactive peptides or other biochemical mediators, such as nitric oxide, and then to cause inflammation. In this scenario, many studies on humans have focused the attention on peripheral and central levels of cytokines, but data obtained are highly controversial. Since at the moment there is not a conclusive evidence of the role played by cytokines in migraine, the authors present and comment the latest reports regarding cytokine modification and the role of the immune system in migraine.

Clinical and epidemiological observations regarding the 1998 Kauai murine typhus outbreak.

Five cases of murine typhus occurring on southwestern Kauai in 1998 are described, following an investigation by the Department of Health. Two cases also had concurrent leptospirosis. Recent habitat changes of peridomestic animals and their fleas may have increased the risk for developing murine typhus. Increased suspicion of typhus by island physicians and more aggressive rodent control activities are recommended.

Septic embolization arising from infected pseudoaneurysms following percutaneous transluminal coronary angioplasty: a report of 2 cases and review of the literature.

Septic embolization arising from infected pseudoaneurysms following percutaneous transluminal coronary angioplasty (PTCA) constitutes a distinct clinical and histopathologic entity. Pseudoaneurysms are a potential complication of both cardiac catheterization and PTCA. Repeated or prolonged catheterization increases the risk of bacterial seeding of these sites, resulting in septic embolization. Characteristic clinical features include fever within 2 to 5 days, unilateral embolic disease, and Staphylococcus aureus septicemia. Culture and examination of biopsy specimens of the embolic lesions typically demonstrate gram-positive microorganisms. We describe 2 patients presenting with ipsilateral palpable purpura, petechiae, and livedo reticularis caused by septic emboli from infected pseudoaneurysms. The recommended treatment includes administration of appropriate systemic antibiotics and surgical resection of the infected pseudoaneurysm. Both cholesterol and septic emboli should be considered in the differential diagnosis of ipsilateral embolic disease induced by invasive vascular procedures.

Systemic Malassezia furfur infection in an adult receiving total parenteral nutrition.

Malassezia furfur sepsis developed in a woman with hyperemesis gravidarum while she was receiving total parenteral nutrition supplemented with lipids. Fever, chills, dyspnea, pleuritic chest pain, and multiple bilateral pulmonary nodular infiltrates were the primary clinical manifestations. Lysis-centrifugation fungal blood cultures supplemented with olive oil grew M furfur. Treatment included removal of the central venous catheter line, discontinuation of the lipid emulsion, and antifungal chemotherapy. Malassezia furfur sepsis complicating total parenteral nutrition may be more common in adults than once suspected. A high index of suspicion is required to diagnose this infection, and the addition of olive oil to the fungal culture medium will provide the necessary growth factors to isolate this fungus.

Computed tomographic appearance of pulmonary alveolar proteinosis in adults.

Two cases of adult pulmonary alveolar proteinosis are presented with emphasis on the computed tomographic findings in both cases. Each patient demonstrated a pattern of diffusely increased lung density on both standard radiographic and computed tomographic examinations of the lung. There was no evidence of adenopathy, pleural effusion, or cardiomegaly in either patient. The diagnosis of pulmonary alveolar proteinosis was established in both patients by open lung biopsy. The optical microscopy and electron microscopy examinations of the biopsy material in each instance demonstrated marked filling of the alveoli with periodic-acid-Schiff-positive material and intraalveolar lamellar bodies. The diagnosis of sarcoid was entertained prior to the open lung biopsy in one patient, a young adult black male. Although the computed tomographic appearance was similar in each case and of no value in the diagnosis of pulmonary alveolar proteinosis, it was helpful in assessing the extent of the disease within the lung.