Penile pharmacotesting (PPT) with alprostadil (PGE1) represents the most common diagnostic approach to male erectile dysfunction (ED). A positive response - i.e. normal erectile rigidity of sustained duration - is presumed to exclude venous or arterial pathology with enough accuracy. To test this assumption we compared PPT vs. flowmetric results obtained by colour-duplex Doppler ultrasound (CDDU) in patients (pts) undergoing diagnostic evaluation for ED under conditions of maximal cavernous relaxation. A total of 195 non-consecutive impotent pts were diagnosed after dynamic CDDU as non-vasculogenic (NOR), or having arteriogenic (AR), veno-occlusive (VO) or mixed (MX) ED. Maximal erection obtained after PPT was scored as: type-1 (full tumescence - no sustained rigidity, angle on the abdominal plane >90 degrees), type-2 (sustained partial erection, valid for intromission, angle=90 degrees) and type-3 (sustained full erection, angle <90 degrees). Comparing PPT with flowmetric results, we found that a type-3 response had 20% false negative diagnosis of NOR (17% of AR- and 3% of VO- and MX-ED, respectively), while a type-2 response had 63% false negative diagnosis (20% of AR, 37% of VO- and 6% MX-ED, respectively). Type-1 response was associated with the presence of VO dysfunction in 99% of cases. These data suggest that a positive response to PPT (type-2 and type-3) assessed by the visual rating of erection is associated with both arterial (up to 20%) and/or VO (up to 43%) ED, as detected by CDDU. We conclude that PPT alone is a misleading diagnostic test to exclude vascular ED and that dynamic CDDU should be offered to pts investigated for male ED.
Employing purified extracellular matrix (ECM) proteins, i.e. type I, III, IV and V collagens (CI, CIII, CIV, CV), laminin (LM) and fibronectin (FN), as antigen sources we detected autoantibodies to conformational and/or denatured ECM antigens among 34 of 50 sera obtained from Hashimoto's thyroiditis (HT) patients and 6 of 51 control sera obtained from non-autoimmune thyroid disease patients and healthy donors (HT sera vs. control sera p=4x10-9 ) . Reactivity to conformational antigens, mostly due to autoantibodies of the IgG isotype, was observed in 30/50 HT sera and in 6/51 control sera (p=3.5x10-7 ) and was not always concomitant with that to linear antigens, found in 23/50 HT and in 6/51 control sera (p=1.6x10· 4 ) . Ultrastructural analysis of skin biopsies obtained from 18 HT patients without symptomatic cutaneous diseases revealed defects of the stratified squamous epithelium basement membrane in 11/18, alterations of the stroma in 13/18 and both basement membrane and stromal defects in 9/18. Interestingly, 13/13 (p=0.012) and 9/11 (p=0.012) patients with stromal and basement membrane defects respectively, exhibited serum antibodies to at least one ECM antigen involved in the organization of the altered tissue compartment. Lastly, 10/18 skin biopsies presented immunoglobulin (Ig) and/or complement (C3) deposits along the cutaneous basement membrane zone (BMZ) or in the papillary dermis and 9/10 sera from the same patients simultaneously showed antibodies to at least one ECM antigen involved in the organization of these two skin compartments. Besides, 8/11 HT patients with basement membrane defects exhibited Ig or C3 deposits along the BMZ. Our findings suggest that autoantibodies to ECM molecules might contribute to the development of asymptomatic extra-thyroid skin diseases in HT patients.Autoimmune thyroid disease encompasses a spectrum of conditions ranging from normal functional status to Grave's disease, characterized by frank hyperthyroidism, or Hashimoto's thyroiditis (HT), most often associated with hypothyroidism. HT is a common, chronic autoimmune disease characterized by lymphoid cellular infiltration and parenchymal cell destruction, ultimately
Growth hormone (GH), and prolactin (PRL) responses to the administration of growth hormone-releasing hormone (GHRH) (1 μg/kg) were evaluated in a group of 18 drug-free, acute, young male schizophrenics and in a group of age-matched normal controls. Cortisol responses were also evaluated. No difference in mean plasma GH, PRL and cortisol plasma basal values or in GH and PRL responses to GHRH between schizophrenics and controls was observed. Our failure to demonstrate a difference in GH response to GHRH between schizophrenics and controls would seem to indicate that GH secretory pituitary reserve is intact in young acute male schizophrenics. Cortisol values did discriminate between schizophrenics and controls (p< 0.05). In our sample, both schizophrenics and normal controls showed a slight but significant (p < 0.03) and transitory increase in plasma PRL response to GHRH.
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