Sarcoidosis is a multisystemic disorder histologically characterized by a noncaseating granulomatous inflammatory process. The etiology remains unclear, but tumor necrosis factor ␣ seems to play a crucial role. Herein we describe a patient with severe sarcoidosis involving the lung and liver. Various treatment regimens with azathioprine, methotrexate, cyclophosphamide, and pentoxifylline failed to control the disease. Therefore, salvage therapy with infliximab was commenced. Arthritis and pulmonary and liver involvement improved. We were then able to taper the corticosteroid treatment to a lower-dose regimen with no need for additional immunosuppressive treatment. To our knowledge, this is the first reported case of successful treatment of multiorgan sarcoidosis that was previously resistant to conventional therapy.

The significance of antibodies against alpha-fodrin compared to antibodies against Ro (SSA) as markers of Sjögren's syndrome has been controversially discussed. We therefore compared the association of alpha-fodrin and Ro antibodies with dry eyes and dry mouth in the general population. In 168 "normal" participants, the prevalence of IgA antibodies against alpha-fodrin was 5% and of IgG antibodies against alpha-fodrin was 3%. IgA antibodies against alpha-fodrin were present in 3 of 4 and IgG antibodies against alpha-fodrin in 2 of 4 participants with the combination of dry eyes and dry mouth (P = 0.0002 and 0.005). Only one participant had antibodies against Ro and had dry eyes but normal saliva production. Antibodies against alpha-fodrin are associated with sicca syndrome and may be valuable diagnostic markers in patients with Sjögren's syndrome lacking Ro antibodies.

Objective: To study the prevalence of vitamin B 6 deficiency in common variable immunodeficiency and the impact of vitamin B 6 supplementation on immune function in the disorder. Design: Open, non-blinded. Setting: Medical School Hannover, Hannover, Germany. Subjects: Plasma vitamin B 6 concentrations were measured in all the 54 common variable immunodeficiency (CVID) patients visiting our outpatients' clinics in 2005. Interventions: The 17 patients with a decreased vitamin B 6 concentration were recommended to take 50 mg of vitamin B 6 /day for 3 months. Then, vitamin B 6 concentrations, absolute number of lymphocyte populations and immunoglobulin concentrations were controlled. Results: Vitamin B 6 concentrations were reduced in 17/54 patients. All 11/17 patients following our advice to substitute vitamin B 6 had normal vitamin B 6 plasma concentrations 3 months later. In parallel, the number of CD4 þ T cells significantly increased. In contrast, concentrations of serum immunoglobulins were not improved. Conclusions: Vitamin B 6 deficiency is common in CVID. The vitamin deficiency is not the cause of CVID and vitamin supplementation does not relieve humoral immunodeficiency. Nevertheless, vitamin B 6 should be measured in CVID to avoid possible long-term complications of its deficiency.

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