Search

Onychomycosis is a chronic and intractable disease whose prevalence increases during aging. In elderly patients, if onychomycosis is left untreated and progresses to a severe stage it may cause functional decline of the lower limbs due to foot pain. This could lead to a decline in activities of daily living and secondary impairment such as cognitive decline. Thus, the treatment of onychomycosis in elderly patients is important. We have previously shown that fosravuconazole is relatively safe and effective for onychomycosis in elderly patients. In the present study, we continued the follow‐up study and investigated the efficacy of re‐administration of fosravuconazole in patients with recurrent onychomycosis. One hundred and twenty‐five patients aged ≥65 years who had been initially diagnosed with onychomycosis at our hospital's dermatology department, and who had responded well to fosravuconazole at 48 weeks after the initial treatment, were followed up until 144 weeks after the start of the initial treatment. Patients who experienced a recurrence within 24 weeks after the start of the follow‐up were assigned to the short‐term recurrence group, and those who experienced a recurrence after 24 weeks were assigned to the long‐term recurrence group. All patients in both groups were re‐treated with fosravuconazole to evaluate its efficacy. The short‐term and long‐term recurrence groups consisted of 17 (14.3%) and 10 (8.4%) patients, respectively. There were no significant differences in mean age and sex ratio between the two groups. There were no serious adverse effects in either group, and the toenail opacity ratio was significantly reduced after 12 weeks of re‐treatment in both groups. The short‐term and long‐term recurrence groups were significantly more likely to have wedge‐shaped onychomycosis and total dystrophic onychomycosis, respectively. The results suggest that re‐administration of fosravuconazole is safe and as effective as the first administration for elderly patients with recurrent onychomycosis. This study was registered at UMIN‐CTR (UMIN000053516). [ABSTRACT FROM AUTHOR]

Thiazolidinediones (TZDs) improve glycemic control and insulin sensitivity in patients with type 2 diabetes mellitus (T2DM). There is growing evidence from in vivo and in vitro studies that TZDs improve pancreatic [beta]-cell function. The aim of this study was to determine whether TZD-induced improvement in glycemic control is associated with improved [beta]-cell function. We studied 11 normal glucose-tolerant and 53 T2DM subjects [age 53 [+ or -] 2 yr; BMI 29.4 [+ or -] 0.8 kg/[m.sup.2]; fasting plasma glucose (FPG) 10.3 [+ or -] 0.4 raM; Hb [A.sub.1c] 8.2 [+ or -] 0.3%]. Diabetic patients were randomized to receive placebo or TZD for 4 mo. Subjects received 1) 2-h OGTT with determination of plasma glucose, insulin, and C-peptide concentrations and 2) two-step euglycemic insulin (40 and 160 mU*[m.sup.-2]*[min.sup.-1]) clamp with [3-[sup.3]H]glucose. T2DM patients were then randomized to receive 4 mo of treatment with pioglitazone (45 mg/day), rosiglitazone (8 mg/day), or placebo. Pioglitazone and rosiglitazone similarly improved FPG, mean plasma glucose during OGTT, Hb [A.sub.1c], and insulin-mediated total body glucose disposal ([R.sub.d]) and decreased mean plasma FFA during OGTT (all P < 0.01, ANOVA). The insulin secretion/insulin resistance (disposition) index [[DELTA]ISR([DELTA]UC)/Aglucose(AUC)/IR] was significantly improved in all TZD-treated groups: +1.8 [+ or -] 0.7 (PIO + drug-naive diabetics), +0.7 [+ or -] 0.3 (PIO + sulfonylurea-treated diabetics), and 0.7 [+ or -] 0.2 (ROSI + sulfonylurea-withdrawn diabetics) vs. -0.2 [+ or -] 0.3 in the two placebo groups (P < 0.01, all TZDs vs. placebo, ANOVA). Improved insulin secretion correlated positively with increased body weight, fat mass, and [R.sub.d] and inversely with decreased plasma glucose and FFA during the OGTT. In T2DM patients, TZD treatment leads to improved [beta]-cell function, which correlates strongly with improved glycemic control. type 2 diabetes; insulin secretion; insulin secretion/insulin resistance index

We examined the relationship between peripheral/hepatic insulin sensitivity and abdominal superficial/deep subcutaneous fat (SSF/DSF) and intra-abdominal visceral fat (VF) in patients with type 2 diabetes mellitus (T2DM). Sixty-two T2DM patients (36 males and 26 females, age = 55 [+ or -] 3 yr, body mass index = 30 [+ or -] 1 kg/[m.sup.2]) underwent a two-step euglycemic insulin clamp (40 and 160 mU * [m.sup.-2] * [min.sup.-1]) with [3-[sup.3]H]glucose. SSF, DSF, and VF areas were quantitated with magnetic resonance imaging at the [L.sub.4-5] level. Basal endogenous glucose production (EGP), hepatic insulin resistance index (basal EGP X FPI), and total glucose disposal (TGD) during the first and second insulin clamp steps were similar in male and female subjects. VF (159 [+ or -] 9 vs. 143 [+ or -] 9 [cm.sup.2]) and DSF (199 [+ or -] 14 vs. 200 [+ or -] 15 [cm.sup.2]) were not different in male and female subjects. SSF (104 [+ or -] 8 vs. 223 [+ or -] 15 [cm.sup.2]) was greater (P < 0.0001) in female vs. male subjects despite similar body mass index (31 [+ or -] 1 vs. 30 [+ or -] 1 kg/[m.sup.2]) and total body fat mass (31 [+ or -] 2 vs. 33 [+ or -] 2 kg). In male T2DM, TGD during the first insulin clamp step (1st TGD) correlated inversely with VF (r = -0.45, P < 0.01), DSF (r = -0.46, P < 0.01), and SSF (r = -0.39, P < 0.05). In males, VF (r = 0.37, P < 0.05), DSF (r = 0.49, P < 0.01), and SSF (r = 0.33, P < 0.05) were correlated positively with hepatic insulin resistance. In females, the first TGD (r = -0.45, P < 0.05) and hepatic insulin resistance (r = 0.49, P < 0.05) correlated with VF but not with DSF, SSF, or total subcutaneous fat area. We conclude that visceral adiposity is associated with both peripheral and hepatic insulin resistance, independent of gender, in T2DM. In male but not female T2DM, deep subcutaneous adipose tissue also is associated with peripheral and hepatic insulin resistance. visceral fat; deep and superficial subcutaneous fat