RESUMO
The association of hyperthyroidism and ulcerative colitis (UC) is presented in two cases: a 61-year-old man and a 54-year-old woman. In the first case the onset of hyperthyroidism was detected at the age of 25, and the onset of ulcerative colitis at the age of 36. The second case presented severe hyperthyroidism started at the age of 51. In the latter case ulcerative colitis had been detected ten year earlier. To our knowledge this report seems to be the first one considering this association from the endocrinological standpoint. The association of these two diseases might suggest that the disturbance of even one organ specific immune lesion implies a wider disorder. Thus one might assume that the association of multiple organ-specific immune diseases represents an unsuccessful attempt to equilibrate the repertoire of idiotypes and anti-idiotypes belonging to the immune network.
Assuntos
Doenças Autoimunes/diagnóstico , Colite Ulcerativa/diagnóstico , Hipertireoidismo/diagnóstico , Doenças Autoimunes/patologia , Colite Ulcerativa/patologia , Feminino , Doença de Graves/diagnóstico , Doença de Graves/patologia , Humanos , Hipertireoidismo/patologia , Masculino , Pessoa de Meia-IdadeRESUMO
Based on the new acquisitions of knowledge on the immune network and on the regulating mechanisms of the immune system, the paper presents an original and at the same time a more pathophysiological classification of immune diseases according to: 1. the functionality stage (input--or antigen presentation, central--integrative, and output--effector), and 2. the immune ligand involved (immunoglobulin or Ti complex). From these new concepts it results that the main feature of the immune system reactivity is the antigen recognition. The authors bring arguments in favour of the assertion that immunity--characterized by recognition--is equal with autoimmunity--characterized by autorecognition, i.e., recognition of the self antigens. From this statement it ensues that: 1. an immune disease is a disease of internal regulation of the immune network, i.e., of the relationships between idiotypes and anti-idiotypes, and 2. any immune disease is an autoimmune disease, meaning that the pathogenetic significance of the so-called "autoimmune diseases" and of the "hypersensitivity diseases" is the same.
Assuntos
Doenças do Sistema Imunitário/classificação , Doenças Autoimunes/classificação , Doenças Autoimunes/etiologia , Doenças Autoimunes/imunologia , Doenças Autoimunes/patologia , Autoimunidade , Humanos , Sistema Imunitário/imunologia , Doenças do Sistema Imunitário/etiologia , Doenças do Sistema Imunitário/imunologia , Doenças do Sistema Imunitário/patologia , ImunidadeAssuntos
Doenças das Glândulas Salivares/diagnóstico , Doenças Autoimunes/diagnóstico , Doenças Autoimunes/terapia , Doenças do Colágeno/diagnóstico , Doenças do Colágeno/terapia , Humanos , Doença de Mikulicz/diagnóstico , Doença de Mikulicz/terapia , Doenças das Glândulas Salivares/terapia , Síndrome de Sjogren/diagnóstico , Síndrome de Sjogren/terapiaRESUMO
Leukocyte migration inhibitory factor (LMIF) activity was tested before and after glucagon administration both in vivo and in vitro. In vivo glucagon 1 mg i.v. vs saline administration inhibited LMIF production by T lymphocytes in 85.21% patients (p less than 0.01). In vitro glucagon in physiologic (125 pg/ml) and pharmacologic (50 ng/ml) doses increased the migration area vs PPD 250 microL (migration index 0.5127 vs 0.3210; p less than 0.05). These results show a significant inhibitory effect of glucagon upon LMIF activity. We suggest that glucagon acts by enhancement of the intralymphocytic cAMP/cGMP ratio (cyclic adenosine monophosphate/cyclic guanosine monophosphate).
