Background Tobacco smoking is a major risk factor for atherosclerotic and cardiovascular disease. Studies have found evidence that smoking cessation is associated with weight gain, which is itself a leading cause of cardiovascular disease. Aim The present study sought to determine how smoking cessation and associated weight gain affect adiponectin levels and insulin resistance. Methods Fifty-two male habitual smokers were treated for 2 months with transdermal nicotine patches, and the 28 subjects who successfully quit smoking were analyzed. Subjects were divided into two sub-groups according to their weight change: weight maintainers and weight gainers. Serum adiponectin levels and the homeostasis model assessment ratio (HOMA-R) were evaluated at the beginning of the study, and at 1 week and 9 weeks after cessation of patch use. Results In weight gainers (n=18), serum adiponection levels tended to increase at 1 week after the end of treatment (mean difference 0.4±1.0 μg/mL, p=0.08). Moreover, after 9 weeks, adiponectin levels were significantly decreased in weight gainers (mean difference between 1 week and 9 weeks 0.8±0.9 μg/mL, p=0.002). In weight maintainers, adiponectin levels increased slightly after smoking cessation, but changes were not significant. In weight gainers, HOMA-R index was significantly increased (mean difference between baseline and 9 weeks 0.4±0.7, p=0.01), while in weight maintainers, HOMA-R index showed no differences throughout the study. Conclusion Our findings suggest that the adverse effects of weight gain attenuate some of the beneficial effects of smoking cessation.

The patient was a 68-year-old woman who had experienced recurrent febrile episodes since 66 years of age. Despite various examinations and treatments, the etiology remained unclear. Further examinations following another referral failed to uncover the cause. Therefore, despite her age, it was presumed that she had familial Mediterranean fever. An analysis of the familial Mediterranean fever (MEFV) gene detected heterozygous L110P, E148Q, and R202Q mutations. No further febrile episodes occurred after colchicine treatment was initiated. Familial Mediterranean fever presenting in patients in their sixties is extremely rare.

We herein report a case of a 75-year-old woman who presented with a low-grade fever, repeated cold-induced urticaria, and painful leg edemas with neutrocytosis. Because her mother also had cold-induced urticaria and her skin lesions histologically showed neutrophilic dermatitis, we suspected that she had familial cold autoinflammatory syndrome, a subtype of cryopyrin-associated periodic syndromes. Sequencing of the NLRP3 and MEFV genes revealed that she carried both the p.A439V missense mutation and p.E148Q homozygous mutation, which is commonly detected in familial Mediterranean fever patients. The administration of colchicine reduced the frequency and severity of her skin rash and leg edema.

Few clinical studies have so far focused on gastrointestinal motility in patients with eosinophilic gastroenteritis. A 29-year-old man was evaluated for epigastralgia of unknown origin. A histopathological examination of biopsy specimens from the duodenum revealed numerous eosinophilic infiltrations. Eosinophilic enteritis was therefore diagnosed. The patient received oral prednisolone and his symptoms improved. Both at the onset and at relapse of the disease, the maximal 13 CO2 excretion time (Tmax) of 13 C-acetate breath test was noted to have increased levels of excretion. Recovery of this parameter was observed in parallel with clinical improvements after treatments. This is the first report of a case of eosinophilic enteritis in which the 13 Cacetate breath test was effective for assessing the disease activity and evaluating the effectiveness of treatment.