Paracoccidioidomycosis (PCM) is an endemic disease in the southeast region of Brazil, which includes the state of Espírito Santo (ES). This historic case series analyses 546 patients treated in this state from 1978 to 2012. Patients aged from 7 to 83 years, 509 males and 37 females, yielding a ratio of 13.7:1. Most of the patients (81.4%) originated from rural areas in ES, 71.0% being farmers. A higher concentration of cases was observed in municipalities located along the western range of the state. Sixty patients (11.0%) had an acute/subacute form of the disease, 485 (88.9%) had a chronic form, and one had a subclinical form. The most affected organs included the lungs, oropharyngeal mucosa, lymph nodes, skin, and larynx. The diagnosis was confirmed by histopathology in 252 (46.2%) cases, direct examination in 168 (30.7%), both exams in 111 (20.3%) and serology in 15 (2.8%). Tuberculosis, acquired immune deficiency syndrome, leishmaniasis, and intestinal parasites were the most frequently associated infectious diseases. From 328 patients followed up, total regression of the lesions was observed in 17.4%, partial regression in 77.4%, and no regression in 17 (5.2%) cases. Regarding the number of cases in this series, ES emerges as an important endemic area for PCM in Brazil.

Background/aim:Estrogen deficiency induces myocardial contractile dysfunction and increases cardiovascular disease risk. However, the mechanism underlying this response is unclear. Our aim was to investigate whether AT₁ receptor blockade would prevent ovariectomy-induced myocardial contractile dysfunction. Methods: Female rats (8 weeks old, 280 g) that underwent bilateral ovariectomy were randomly assigned to receive daily treatment with losartan (OVX + LOS, 15 mg/kg, s.c., in 0.9 % NaCl), placebo (OVX), estrogen replacement (OVX + E2, 1 mg/ kg, once a week, i.m.) and SHAM for 58 days. Results: Losartan and estrogen treatment 1) prevented ovariectomy-induced weight gain and slight hypertrophy, 2) restored the positive inotropic responses to Ca²⁺ and isoproterenol in the isolated papillary muscle in the OVX group, 3) prevented the reduction in SERCA2a levels and the increase in phospholamban (PLB) expression in the OVX group, 4) abolished the increase in superoxide anion that was increased in the OVX group, and 5) normalized the increase in p22^phox expression after ovariectomy. Estrogen treatment but not losartan restored the increase in serum angiotensin converting enzyme activity in the OVX group. Conclusion: This study demonstrated that myocardial contractile dysfunction induced by ovariectomy and expression of key Ca²⁺-handling proteins were prevented by losartan treatment and that AT₁ receptor activation is involved in this response.

Carvedilol has beneficial effects on cardiac function in patients with heart failure but its effect on ovariectomy-induced myocardial contractile dysfunction remains unclear. Estrogen deficiency induces myocardial contractile dysfunction and increases cardiovascular disease risk in postmenopausal women. Our aim was to investigate whether carvedilol, a beta receptor blocker, would prevent ovariectomy-induced myocardial contractile dysfunction. Female rats (8 weeks old) that underwent bilateral ovariectomy were randomly assigned to receive daily treatment with carvedilol (OVX+CAR, 20 mg/kg), placebo (OVX) and SHAM for 58 days. Left ventricle papillary muscle was mounted for isometric tension recordings. The inotropic response to Ca2+ (0.62 to 3.75 mM) and isoproterenol (Iso 10−8 to 10−2 M) were assessed. Expression of calcium handling proteins was measured by western blot analysis. Carvedilol treatment in the OVX animals: prevented weight gain and slight hypertrophy, restored the reduced positive inotropic responses to Ca2+ and isoproterenol, prevented the reduction in SERCA2a expression, abolished the increase in superoxide anion production, normalized the increase in p22phox expression, and decreased serum angiotensin converting enzyme (ACE) activity. This study demonstrated that myocardial contractile dysfunction and SERCA2a down regulation were prevented by carvedilol treatment. Superoxide anion production and NADPH oxidase seem to be involved in this response.

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