Protein-losing gastroenteropathy (PLG) can occur as a manifestation of various diseases including autoimmune disorders, and optimal therapy of these underlying diseases may be the only effective remedy for PLG. In the present report, we describe a case of a 54-year-old woman with PLG associated with an autoimmune disease, presumably CREST syndrome. She failed to respond to steroid treatment. Subsequently, cyclosporine was initiated, which resulted in a rapid recovery. The patient was successfully treated with low-dose cyclosporine for five years. There has not been, to our knowledge, any report of PLG successfully treated with cyclosporine. Cyclosporine therapy may be effective not only in inducing but also in maintaining complete remission in patients with autoimmune-associated PLG, especially refractory or intolerable to steroids and/or immunosuppressive therapies. (Internal Medicine 43: 397-399, 2004)

Summary. Factor VIII (FVIII) inhibitors appear in 3-20% of haemophilia A patients after injection of FVIII concentrates. However, autoantibodies to FVIII are also reported in nonhaemophiliacs. In these patients FVIII inhibitor disappears spontaneously or diminishes in response to immunosuppressive therapy. However, a few patients show resistance to immunosuppressive therapy. We describe a non-haemophilic elderly patient with acquired FVIII inhibitor who failed to respond to prednisolone. He was treated with doublefiltration plasmapheresis (DFPP) which resulted in a very rapid reduction in inhibitor levels and resolution of symptoms.

A 36-year-old womanwith ulcerative colitis presented with fever, chest and back pain, and fatigue sensation of the arm. Her upper limb pulses were absent. Angiography showed multiple aneurysms of the aorta and its branches, consistent with Takayasu's arteritis. She showed HLA-B35but no B52, which is the typical haplotype among the coexistence cases of both diseases. Prednisolone was effective. The possible pathogenic association of the disorders is discussed. (Internal Medicine 42: 897-898, 2003)

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We examined the effect of climbazole on the induction of rat hepatic microsomal cytochrome P450 (P450), and compared the induction potency with other N-substituted azole drugs such as clorimazole. We found that climbazole is found to be a potent inducer of rat hepatic microsomal P450 as clorimazole. Induced level of P450 by climbazole was almost similar in extent to clorimazole when compared with other imidazole drugs in a dose-and time-dependent manner. Parallel to the increase in P450, climbazole increased aminopyrine and erythromycin N-demethylase, ethoxycoumarin O-deethylase, and androstenedione 16 and 15 /6 hydroxylase activities; however, clorimazole did not induce aminopyrine N-demethylase activity irrespective of its marked increase in P450 content. Immunoblot analyses revealed that climbazole induced CYP2B1, 3A2 and 4A1. The present findings indicate that climbazole is a new potent inducer of hepatic microsomal P450 and drug-metabolizing enzymes like clorimazole, but it may have some differential mechanism(s) for these enzymes' induction in rat liver.