| 1. |
- Andersson, Staffan, et al.
(författare)
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Assessment of autonomic nerve function in myotonic dystrophy
- 1990
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Ingår i: Journal of the Autonomic Nervous System. - : Elsevier BV. - 0165-1838 .- 1872-7476. ; 29:3, s. 187-192
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Tidskriftsartikel (refereegranskat)abstract
- The function of the autonomic nervous system was studied in 23 patients with myotonic dystrophy, from a defined population in northern Sweden with an extremely high prevalence of this disease. Heart rate variability tests showed only minor signs of parasympathetic dysfunction. Blood pressure and plasma noradrenaline measurements in recumbent and upright positions showed no signs of sympathetic neuropathy. Increased plasma levels of noradrenaline was an unexpected finding. Our study does not support the hypothesis that cardiac arrhythmias, orthostatic hypotension, gastrointestinal motility disturbances and urinary bladder dysfunction in myotonic dystrophy are caused by autonomic neuropathy, and we believe that these symptoms should rather be ascribed to a defective function of the target organs
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| 2. |
- Nilsson, B, et al.
(författare)
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Reconstitution of the alternative pathway of complement by plasma infusions given to a patient with an SLE-like syndrome associated with a hereditary C3 dysfunction.
- 1994
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Ingår i: Annals of the Rheumatic Diseases. - 0003-4967 .- 1468-2060. ; 53:10, s. 691-694
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To reconstitute a dysfunctional form of complement factor C3 in a patient with a systemic lupus erythematosus (SLE)-like syndrome.METHODS: The propositus was treated with plasma infusions during five sessions over a period of eight months.RESULTS: The alternative pathway was reconstituted to normal levels for approximately two to three days after each infusion. C3 fragments were incorporated into previously detected deposits of IgG and IgM at the dermal-epidermal junction and the immune complex levels gradually decreased during the whole treatment period.CONCLUSION: The reconstitution appears to result in the solubilisation of tissue immune complexes and a subsequent transportation to the fixed macrophage system.
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| 3. |
- Nilsson, U R, et al.
(författare)
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Hereditary dysfunction of the third component of complement associated with a systemic lupus erythematosus-like syndrome and meningococcal meningitis.
- 1992
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Ingår i: Arthritis and Rheumatism. - 0004-3591 .- 1529-0131. ; 35:5, s. 580-586
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: We describe a dysfunction of C3 in a patient with a systemic lupus erythematosus (SLE)-like syndrome. Alternative pathway complement function was absent, but classical pathway complement function was partially intact.METHODS: We used functional, preparative, and immunochemical techniques in the study.RESULTS: The patient's C3 proved normally susceptible to trypsin proteolysis and partially resistant to classical pathway, but completely resistant to alternative pathway, convertase-dependent cleavage.CONCLUSION: The dysfunction, thus, was caused by a failure of C3 to interact with the C3 convertases, rather than by a lack of a proteinase-sensitive cleavage site in the deficient protein.
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