Context:Although evidences for association of androgenetic alopecia (AGA) with metabolic syndrome (MetS) are accruing, inconclusiveness with respect to the gender specificity and differential association of MetS with increasing severity of AGA continues to persist. Furthermore, data specific to Indian settings are relatively sparse.Aims:The present study aimed at assessing the frequency of MetS in individuals with early AGA in Indian settings.Settings and Design:A case-control study was conducted at a trichology clinic in Bengaluru between April 2012 and September 2012 with a total of 85 cases of AGA and 85 age-matched controls.Materials and Methods:The Norwood-Hamilton classification was used to assess the grade of AGA. MetS was defined according to the National Cholesterol Education Program Adult Treatment Panel III criteria. Blood pressure, blood glucose, lipid parameters, and body mass index along with anthropometric measurements were assessed in all study participants.Statistical Analysis Used:Chi-square test was used to compare proportions between groups. Means were compared between groups using Student's t-test.Results:MetS was seen in a higher proportion of patients with AGA (43.5%) as compared to the control group (2.4%) and the differences were statistically significant (P < 0.001). As compared to controls, patients with AGA had higher triglycerides (P < 0.001), systolic blood pressure (P < 0.001), diastolic blood pressure (P < 0.001) along with significantly lower high-density lipoprotein cholesterol levels (P < 0.001). Severity of AGA was not associated with MetS.Conclusions:AGA is associated with MetS in male Indian patients aged <30 years. Studies with large sample sizes may be required to conclusively define any putative associations between AGA grades and MetS.

The effects of alterations in platelet activity on arrhythmias, haemodynamics and extent of necrosis during coronary ligation for 30 min were assessed in rabbits. Reduction of platelet counts to less than 1% of control by intravenous injection of platelet antiserum (1 ml kg-1 i.v.) reduced the volume of necrosed tissue from 23 +/- 2% to 15 +/- 1%, P less than 0.01 (expressed as % of total LV) and attenuated the hypotensive effect of ischaemia. Pretreatment with the platelet activating factor (PAF) antagonist BN 52021 also attenuated the hypotension and necrosis caused by coronary ligation 23 +/- 2% vs 14 +/- 1%, P less than 0.01. Pretreatment with the thromboxane antagonist CGS 13080 attenuated the hypotensive response to ischaemia but had only a very small effect on the area of necrosis. Administration of PAF at 10 min following coronary ligation markedly increased the volume of necrosed tissue 36 +/- 2%, P less than 0.01 and caused VF and haemodynamic collapse in 10 out of 12 animals. Pretreatment with platelet antiserum or the PAF antagonist BN 52021 reversed this effect of PAF. Pretreatment with CGS 13080 attenuated the marked hypotensive effect of PAF but failed to reverse its necrotic or arrhythmogenic effects. These findings indicate that platelet activation contributes to the necrosis and hypotension following coronary ligation and that platelet-activating factor may contribute to this. The ameliorating effects of platelet antiserum or BN 52021 support the concept that inhibition of platelet activity may have a useful role in the treatment of acute myocardial infarction.

The effects of two novel platelet activating factor (PAF) antagonists BN50726 and BN50739 on arrhythmias, haemodynamics and extent of necrosis during myocardial ischaemia and reperfusion were investigated in anaesthetized rabbits subjected to coronary artery ligation. BN50739 reduced heart rate prior to coronary artery occlusion (P < 0.005) but had no other significant haemodynamic effects at this time. BN50739 and BN50726 did not significantly alter heart rate or blood pressure during 30 min of ischaemia or 30 min of reperfusion, compared to control hearts. BN50739 and BN50726 had no effect on the incidence of arrhythmias during ischaemia. BN50726 significantly reduced the incidence of reperfusion ventricular fibrillation compared to controls (0% v 40%, P < 0.05), and improved survival (80% v 39%, P < 0.05). Similar trends were observed with BN50739. BN50726 reduced the extent of necrosis compared to control hearts (18 ± 2% v 30 ± 3%, P <0.01). A similar trend was observed with BN50739. These results demonstrate that PAF antagonism with BN50726 attenuates reperfusion‐induced arrhythmias and preserves myocardium in the early phase of ischaemia, independently of haemodynamic effects.

1 The effects of cicletanine on arrhythmias, haemodynamics and extent of necrosis during myocardial ischaemia were investigated in rabbits subjected to coronary ligation. 2 Cicletanine increased cardiac output prior to coronary occlusion (P<0.01) but had no other significant haemodynamic effects at this time and did not significantly alter heart rate, blood pressure or cardiac output during 30 min of ischaemia or 30 min of reperfusion. 3 Ventricular fibrillation and mortality were greater in control (65% and 60% respectively) than treated animals (15.4% and 15.4%, P<0.01). 4 The extent of myocardial necrosis expressed as a percentage of the area at risk was also reduced by cicletanine from 61 ± 8% in controls to 37 ± 6% (P<0.05). 5 These findings indicate that cicletanine attenuates arrhythmias and preserves myocardium in the early phase of ischaemia and this effect appears to be independent of an established antihypertensive action.

No abstract