Scleroderma-like syndrome triggered by gadolinium.
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Gadolinium↗
Biomedical subjects
Rainer Nowack
Publications and source records attributed to Rainer Nowack.
Hypophosphatemia and hungry bone syndrome in a dialysis patient with secondary hyperparathyroidism treated with cinacalcet--proposal for an improved monitoring.
Rapid correction of severe and prolonged hyperparathyroidism (HPT) by surgical parathyroidectomy (PTX) occasionally causes a so-called "hungry bone syndrome". According to the reports available in the literature, this syndrome occurs after PTX in patients on dialysis with severe and long-lasting secondary or tertiary HPT with high bone turnover, e.g. markedly raised serum alkaline phosphatase. The syndrome is characterized by prolonged hypocalcemia with hypocalcemic symptoms, as well as a usually mild decrease of serum phosphate after PTX. The syndrome is also known from correction of primary HPT, or persistent HPT after renal transplantation, and after medical treatment of thyrotoxicosis. The hungry bone syndrome refers to the recalcification or remineralization that occurs in bone after correction of HPT. The calcimimetic drug cinacalcet is a new option for the treatment of secondary hyperparathyroidism in patients with renal failure. We present a cinacalcet-treated dialysis patient with severe secondary HPT and raised alkaline phosphatase who developed hypocalcemia and such pronounced hypophosphatemia and severe diffuse bone pain ("hungry bone syndrome") during treatment that the drug had to be discontinued. About two months later, a second exposure to a low dose of cinacalcet (30 mg/d) again led to hypophosphatemia (serum phosphate decreased from 2.5 to 0.7 mmol/1). We recommend that the laboratory monitoring of cinacalcet-treated patients should include phosphate levels and not only intact PTH and calcium, as currently suggested.
Calcium↗
Herbal teas interfere with cyclosporin levels in renal transplant patients.
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Beverages↗
Treatment of refractory Wegener's granulomatosis with antithymocyte globulin (ATG): an open study in 15 patients.
BACKGROUND: A subset of patients with Wegener's granulomatosis does not respond sufficiently to cyclophosphamide and glucocorticosteroids or suffers of intolerable side effects. Anecdotal data suggest that antithymocyte globulin (ATG) may be a treatment option for these patients. We now describe 15 patients treated with ATG for refractory Wegener's granulomatosis. METHODS: Fifteen patients with histologically proven active refractory Wegener's granulomatosis (seven unresponsive to cyclophosphamide, eight intolerant) were treated with ATG by a protocol (SOLUTION protocol) designed by the European Vasculitis Study (EUVAS) Group. RESULTS: Before ATG administration, patients had received a mean of 5.2 (range 2 to 7) different therapeutic approaches including glucocorticosteroids and cyclophosphamide in all and experimental therapies in six, without control of disease activity [2.8 (range 1 to 7) relapses during a disease duration of 63.2 (range 18 to 180) months]. Thirteen of 15 patients showed a favorable response to ATG with partial (N= 9) or complete (N= 4) remission. During a follow-up of 21.8 (range 6 to 68) months, seven patients relapsed after a mean of 8.4 (range 2 to 24) months (five minor and two major relapses). Six patients are free of relapse for 22.3 (range 7 to 64) months. Two patients died, 1 and 3 days following the first dose of ATG, due to pulmonary hemorrhage and infection (one each). Although further immunosuppressive treatment was required in all surviving patients, a less intensive regimen could be applied in 12. Beside fever and chills associated with the first gift of ATG, ATG was well tolerated, with infections being observed in five cases and serum sickness in two. CONCLUSION: Anti-T-cell-directed treatment with ATG may be a therapeutic option for severe refractory Wegener's granulomatosis if simultaneous infections and fluid overload have been ruled out. In patients with alveolar hemorrhage, ATG should only be used under special caution.
Adult↗
15-Deoxyspergualin in patients with refractory ANCA-associated systemic vasculitis: a six-month open-label trial to evaluate safety and efficacy.
The combination of cyclophosphamide (CYC) and oral corticosteroids is effective in the majority of patients with antineutrophil cytoplasmic antibody-associated vasculitis (AASV), but it carries substantial risk of drug-related morbidity and mortality. New regimens are desired, especially in refractory cases. The immunosuppressant 15-deoxyspergualin (DSG) is effective in experimental autoimmune disease and transplantation as well as in acute kidney transplant rejection in humans. To assess the efficacy and safety of DSG, an open label multicenter trial was conducted in patients with AASV who were either unresponsive or had contraindications for standard immunosuppressants. Included were 19 cases of Wegener granulomatosis and one case of microscopic polyangiitis. Nine of them had received CYC shortly before study entry without apparent therapeutic success. DSG (0.5 mg/kg per d) was given for 2 to 3 wk until the WBC count dropped to 3000/ micro l followed by a rest until at least a WBC of 4000/ micro l was reached again. This was repeated up to six cycles. During the study, no other immunosuppressants besides steroids were allowed. Disease improvement during treatment with DSG was achieved in 70% of cases (six cases of complete remission; eight cases of partial remission). Leucopenia occurred in each patient in a regular pattern during the cycles and was transient without exception. No mortality or septicemia was observed. Mild to moderate infections mainly in the respiratory tract were observed but resolved under adequate treatment without sequel. It is concluded that treatment with DSG is successful in patients with refractory Wegener granulomatosis under careful monitoring of WBC count.
Adult↗
Upregulation of CD14 and CD18 on monocytes In vitro by antineutrophil cytoplasmic autoantibodies.
The expression of CD14, CD18, and major histocompatibility complex II on unprimed monocytes from healthy donors after incubation with IgG from patients with antineutrophil cytoplasmic autoantibody (ANCA)-positive active Wegener's granulomatosis (n = 6) and microscopic polyangiitis (n = 6) in comparison with IgG from healthy controls (n = 6) was studied. Monocytes were incubated with IgG (100 microg/ml) at 37 degrees C, and expression of antigens was measured by fluorescence-activated cell sorter after 18 h. Cytoplasmic ANCA (C-ANCA) IgG and perinuclear ANCA (P-ANCA) IgG in comparison with control IgG increased the expression of CD14 (49.2% [SD: 37, P: < 0. 001], and 55.8% [SD: 41, P: < 0.05]) and CD18 (11.4% [SD: 18, P: < 0. 01] and 8% [SD: 26, P: < 0.05]) but did not change the major histocompatibility complex II expression. Upregulation of CD14 started after 6 h and reached a peak after 10 to 14 h of incubation and was not inhibited by polymyxin B. F(ab)(2) fragments of C- and P-ANCA IgG also increased expression of CD14 and CD18 as compared with control IgG F(ab)(2), but for CD14 less than with complete IgG. ANCA IgG depleted of antiproteinase 3 and antimyeloperoxidase antibodies by immunoadsorption failed to upregulate CD14. Monoclonal murine antibodies against proteinase 3 and myeloperoxidase yielded a strong upregulation of CD14 when compared with an isotype control or human control IgG. The data show that CD14 and CD18 are upregulated on monocytes by C- and P-ANCA IgG in vitro, as well as by monoclonal antibodies against proteinase 3 and myeloperoxidase and that this effect is not dependent on Fc gamma receptor crosslinking. Upregulation of CD14 and CD18 on monocytes by ANCA suggests a pathogenetic role of ANCA monocyte interactions in systemic vasculitis.
Antibodies↗