Prednisone and Azathioprine Medication
Prednisone and Azathioprine Medication
Corticosteroids and 3, 4-diaminopyridine are used in treatment of LEMS with limited success. The muscle weakness of Lambert-Eaton will improve as the cancer treatment progresses in some cases. If cancer is present, treatment should focus on cancer therapy. Treatment is directed at decreasing the autoimmune response or improving the transmission of the disrupted electrical impulses.
Therapy is best coordinated with the primary care physician and appropriate consultants. Fever, muscle weakness may increase with hot weather, or illness use of hot tubs or hot showers. Immunosuppressive drugs such as prednisone and azathioprine can be used to reduce the autoimmune response and lessen symptoms in individuals with the syndrome but without cancer. Steroids and immunosuppressive agents have not been tested in randomized controlled trials other possible treatments such as plasma replace.
After the immunosuppressive drugs prednisolone and azathioprine were started, his clinical symptoms improved. The Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder of peripheral cholinergic transmission in which autoantibodies decrease the presynaptic release of acetylcholine at the neuromuscular junction and autonomic system. Here, we present our experience with cases of LEMS who are noncarcinomatous. We studied the efficacy of plasmapheresis, analyzing the clinical score, electrophysiological finding, and the titer of anti-P/Q-type voltage-gated calcium channel (P/Q-VGCC) antibody. However, clinical improvement was transient; intravenous immunoglobulin (IVIg) therapy was followed by additional PE. She had a clinical and electromyologic improvement, and her P/Q-VGCC antibody titers decreased. The first case, a 72-year-old female presenting with leg weakness, was treated by plasma exchange (PE). The P/Q-VGCC antibody titres decreased immediately after these aphereses, but recovered to the pretreatment levels 1 week after them. The second case, a 73-year-old male presenting with leg weakness, was treated by PE and double-filtration plasmapheresis. Recent results suggest that the antibodies to P/Q-type calcium channels are the principal pathogenic factors in LEMS. It is speculated that no sufficient efficacious improvement could be obtained by apheresis alone because of a high rate of P/Q-VGCC antibody production. His antibody titers decreased gradually after immunosuppressive therapy. Considering our experiences and other literature, we discuss the indication of apheresis treatment of LEMS Her clinical status and CMAP amplitude correlated closely with the anti-P/Q-VGCC antibody titers.
Corticosteroids and 3, 4-diaminopyridine are used in treatment of LEMS with limited success. The muscle weakness of Lambert-Eaton will improve as the cancer treatment progresses in some cases. If cancer is present, treatment should focus on cancer therapy. Treatment is directed at decreasing the autoimmune response or improving the transmission of the disrupted electrical impulses.
Therapy is best coordinated with the primary care physician and appropriate consultants. Fever, muscle weakness may increase with hot weather, or illness use of hot tubs or hot showers. Immunosuppressive drugs such as prednisone and azathioprine can be used to reduce the autoimmune response and lessen symptoms in individuals with the syndrome but without cancer. Steroids and immunosuppressive agents have not been tested in randomized controlled trials other possible treatments such as plasma replace.
After the immunosuppressive drugs prednisolone and azathioprine were started, his clinical symptoms improved. The Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder of peripheral cholinergic transmission in which autoantibodies decrease the presynaptic release of acetylcholine at the neuromuscular junction and autonomic system. Here, we present our experience with cases of LEMS who are noncarcinomatous. We studied the efficacy of plasmapheresis, analyzing the clinical score, electrophysiological finding, and the titer of anti-P/Q-type voltage-gated calcium channel (P/Q-VGCC) antibody. However, clinical improvement was transient; intravenous immunoglobulin (IVIg) therapy was followed by additional PE. She had a clinical and electromyologic improvement, and her P/Q-VGCC antibody titers decreased. The first case, a 72-year-old female presenting with leg weakness, was treated by plasma exchange (PE). The P/Q-VGCC antibody titres decreased immediately after these aphereses, but recovered to the pretreatment levels 1 week after them. The second case, a 73-year-old male presenting with leg weakness, was treated by PE and double-filtration plasmapheresis. Recent results suggest that the antibodies to P/Q-type calcium channels are the principal pathogenic factors in LEMS. It is speculated that no sufficient efficacious improvement could be obtained by apheresis alone because of a high rate of P/Q-VGCC antibody production. His antibody titers decreased gradually after immunosuppressive therapy. Considering our experiences and other literature, we discuss the indication of apheresis treatment of LEMS Her clinical status and CMAP amplitude correlated closely with the anti-P/Q-VGCC antibody titers.
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