In July, 2007, an 84-year-old Japanese man, with a bodymass index of 23 kg/m2, presented in a cold sweat and shivering. Clinical examination was unremarkable. His blood glucose was low (3·1 mmol/L). He was not taking any medications. Platelet count (285×109 per L) and HbA1c (5·0%) were normal. His symptoms resolved and he was discharged. At follow-up 1 month later, his platelet count had fallen to 56×109 per L and his HbA1c had risen (fi gure). Despite treatment with several antidiabetic agents, including acarbose, pioglitazone, and metformin, HbA1c increased to 9·0% 9 months after the fi rst visit, and he was still experiencing frequent hypoglycaemic attacks. Antibodies against insulin were not detected, but antibodies against the insulin receptor were present. Our patient’s serum inhibited binding of iodine-125-labelled insulin to the insulin receptor of IM-9 cells by 69·1% at a 1 to 4 dilution. Fasting plasma insulin was very high (137·9 mU/L), indicating severe insulin resistance. Type B insulin resistance syndrome was diagnosed. In the mean time, thrombocytopenia also worsened, with the platelet count falling to 10×109 per L. Antibodies against platelets (PA IgG) were detected (302 fg/platelet). Leucocytes, erythrocytes, infl ammatory markers, and complement factors were all within normal limits. Bonemarrow aspirate showed no evidence of megakaryocyte hypoplasia. There were no fi ndings suggesting collagen diseases. CT showed no evidence of pancreatic tumour, liver cirrhosis, or splenomegaly. On the basis of these fi ndings, immune thrombocytopenic purpura (ITP) was diagnosed. Helicobacter pylori infection was detected by the carbon-14 urea breath test and eradication therapy (amoxicillin, lansoprazole, and clarithromycin) was given for 7 days. Following H pylori eradication (confi rmed by breath test) platelet count increased and HbA1c decreased. 6 months after H pylori eradication PA IgG decreased (80 fg/platelet), insulin receptor antibodies were not detectable, HbA1c normalised, and hypoglycaemic episodes no longer occurred. Notably, fasting plasma insulin decreased to 10·1 mU/L, confi rming striking improve ment of insulin resistance. When last seen in February, 2009, our patient was not taking glucoselowering drugs; anti-IR antibodies were still undetectable, and HbA1c was normal (4·8%). Our patient had not had any new hypoglycaemic symptoms. Type B insulin resistance syndrome is a rare cause of diabetes with severe insulin resistance and is caused by polyclonal immunoglobulin G antibodies directed against the insulin receptor. These antibodies block insulin binding to the receptor, resulting in hyperglycaemia. Paradoxically, hypoglycaemia, particularly while fasting, is occasionally associated with this disorder. Type B insulin resistance syndrome is frequently associated with other auto immune diseases. Our patient’s clinical course strongly suggests that type B insulin resistance syndrome and ITP developed simultaneously and that both improved with H pylori eradication, which is the recommended treatment for ITP. In this case, H pylori eradication also ameliorated type B insulin resistance syndrome. There is increasing evidence that H pylori infection is directly involved in modulating host immune responses. Furthermore, H pylori eradication reportedly ameliorates some immunological disorders, including anti phospholipid antibody syndrome and rheumatoid arthritis. Our case suggests an H pylori infection-related pathological mechanism underlying type B insulin resistance syndrome. There is no established eff ective therapy for type B insulin resistance syndrome. Indeed, it was very diffi cult to manage our patient’s diabetes, which was also associated with occasional hypoglycaemia; treatment was no longer necessary after H pylori eradication. In cases of type B insulin resistance syndrome, testing for H pylori infection may be worthwhile, with a view to treating the infection if present.