A case of fever, eosinophilia, and pneumonia.

There is a broad differential for patients presenting with fever, eosinophilia, and pneumonia. We present a case of a 48-year-old man who presented with recurrent fever, pleuritic chest pain, and cough. His medical history was significant for a recent trip to Arizona. A chest X ray showed a right lower lobe infiltrate and CT examination of the chest showed extensive mediastinal lymphadenopathy. Tissue culture from a biopsy specimen of the mediastinal lymph nodes revealed growth of Coccidioides immitis and a diagnosis of coccidioidomycosis was made. He was treated with a total of a 9-month course of itraconazole and has remained disease free for >2 years. This case shows how a careful history and evaluation will direct the clinician to the correct diagnosis.

Adult-onset Still's disease: can recent advances in our understanding of its pathogenesis lead to targeted therapy?

Adult-onset Still's disease is a rare systemic inflammatory disease of unknown etiology, characterized by daily high, spiking fevers, evanescent rash, and arthritis. There is no single diagnostic test for adult-onset Still's disease; rather, the diagnosis is based on clinical criteria and necessitates the exclusion of infectious, neoplastic, and other 'autoimmune' diseases. Proinflammatory cytokines such as interleukin (IL)-1, IL-6, and IL-18, interferon-gamma, tumor necrosis factor, and macrophage colony-stimulating factor are elevated in patients with adult-onset Still's disease and are thought to have a major role in the pathogenesis of the disease. Treatment consists of nonsteroidal anti-inflammatory drugs, corticosteroids, immunosuppressants (methotrexate, gold, azathioprine, leflunomide, cyclosporin, and cyclophosphamide), intravenous immunoglobulin, and cytokine (tumor necrosis factor, IL-1 and IL-6) inhibitors. Recent advances in basic immunology have enhanced our ability to hinder the pathogenic mechanisms associated with adult-onset Still's disease and have led to a paradigm shift where targeted treatments have an increasingly important role.

Fetal sensitization to cow's milk protein and wheat: cow's milk protein and wheat-specific TNF-alpha production by umbilical cord blood cells and subsequent decline of TNF-alpha production by peripheral blood mononuclear cells following dietary intervention.

We present a case of fetal sensitization to cow's milk protein (CMP) and wheat, resulting in non-IgE mediated food allergy (NFA). Fetal sensitization was indicated by onset of NFA symptoms shortly after birth and CMP/wheat-specific tumor necrosis factor-alpha (TNF-alpha) production by cord blood mononuclear cells. Following dietary intervention, we observed a decline of TNF-alpha production by peripheral blood mononuclear cells with stimuli of these dietary proteins (DPs) but recurrence of reactivity was observed following viral gastroenteritis, while interleukin-10 production with these DPs persisted during his first 5 yr of life. This finding may indicate active suppressive mechanisms for maintaining oral tolerance.

Adjunctive treatment of disseminated Mycobacterium avium complex infection with interferon alpha-2b in a patient with complete interferon-gamma receptor R1 deficiency.

We report adjunct treatment of (interferon) IFN-alpha2b (Intron-A) in a patient with complete interferon-gamma receptor R1 (IFNGR1) deficiency suffering from disseminated infection with Mycobacterium avium complex (MAC) resistant to multiple anti-mycobacterial agents. A low dose of IFN-alpha2b (3 x 10(6) units/m(2) three times weekly subcutaneously) successfully attenuated progressive hepatosplenomegaly and abdominal/retroperitoneal/pelvic lymphadenopathy, although the patient continued to be mycobacteremic. This is the first report of a complete IFNGR1 deficiency treated with adjuvant IFN-alpha2b for disseminated MAC infection.