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Biomedical subjects

V Biarese

Publications and source records attributed to V Biarese.

At least 37 records · Page 2Linked to original sources
PubMed1984

[Behçet's disease. II. Etiopathogenetic and therapeutic aspects. Personal observations].

The aetiopathogenesis of Behcet's disease is still not known. In the light of current knowledge, the most likely hypothesis seems to be that of an autoimmune reaction set off by viral, bacterial or other antigens. The reaction may manifest itself in the vascular system, and cause vasculitic conditions in genetically susceptible subjects. The existence of a constitutional susceptibility factor would seem to be confirmed by the high and significant incidence of determinant histocompatibility antigens: HLA-B5 in Japan and in Mediterranean countries, HLA-A2 and HLA-A28 in Great Britain and the United States. Corticosteroids are most commonly used to treat the disease; immunosuppressants are also recommended--possibly in association with corticosteroids. Three personally observed cases of Behcet's disease are reported. The first was an example of the disease in its complete form (oral and genital aphthae, ocular lesions); the second case incomplete (no genital aphthae); and the third characterised by severe neurological involvement (neuro-Behcet).

Adult↗
PubMed1984

[Behçet's disease. I. Clinical and histopathological aspects].

Behçet disease is characterised by a triple symptom picture (genital and oral aphthae, ocular lesions) named after the Turkish dermatologist, Hulusi Behçet. It is found all over the world, but is particularly frequent in Japan and the Mediterranean basin. Adult males are primarily affected. The classic symptomatological triad may be accompanied by other manifestations involving the skin (hypersensitivity to microtrauma is a peculiar feature), joints, nervous system, gastroenteric system, cardiovascular system (phlebitis, phlebothrombosis), lungs and kidneys. There is a chronic course marked by periods of exacerbation and remission, which may last for years. Diagnosis is clinical only, since neither the laboratory data nor the histopathological signs of vasculitis are truly pathognomonic. The prognosis quoad valetudinem is uncertain with regard to the eye lesions, which may result in blindness. The prognosis quoad vitam is usually good, though it is poor if the nervous system is involved, or in the event of lung and large vessel lesions, since death may occur from haemoptysis or the rupture of aneurysms.

Behcet Syndrome↗
PubMed1984

[Hutchinson-Horton giant cell arteritis and rhizomelic polymyalgia. III. Current pathogenetic and nosographic aspects].

There is much evidence to suggest that temporal arteritis and rhizomelic polymyalgia are both immunological diseases. The classic results of experimental pathology are discussed, together with the relations between rhizomelic polymyalgia and both virus hepatitis B and the HLA system. From the clinical standpoint, it is now agreed that differences in individual response may lead to either a synovial or an arteritic response in both forms. Their association in what Hamrin has called "polymyalgia arteritica" is also common.

Antigen-Antibody Complex↗
PubMed1984

[Hutchinson-Horton giant cell arteritis and rhizomelic polymyalgia. II. Rhizomelic polymyalgia. Arteritic polymyalgia].

Rhizomelic polymyalgia is an inflammatory form. Its site of choice is the shoulder girdle and it is almost solely observed in elderly subjects. An account is given of its epidemiological, clinical and anatomopathological aspects. Its aetiology is also discussed with particular reference to its possible immunological or vascular origin. The rheumatic symptoms of rhizomelic polymyalgia are similar to those observed in temporal arteritis. Since artery lesions are found in most cases, the name "polymyalgia arteritica" has been suggested as an alternative clinical description by Hamrin .

Adrenal Cortex Hormones↗
PubMed1984

[Hutchinson-Horton giant cell arteritis and rhizomelic polymyalgia. I. Hutchinson-Horton arteritis].

Temporal arteritis (also known as Horton's or giant cell arteritis) is a panarteritis of the large and medium-calibre cranial vessels. An account is given of its epidemiological, clinical and anatomopathological aspects and its involvement of the locomotor apparatus (Horton's rheumatism). Reference is also made to the close relationship between temporal arteritis and pulseless disease. Some workers are of the opinion that they share the same aetiology, and that their clinical expression in different areas is dictated by age and constitutional factors.

5'-Nucleotidase↗
PubMed1980

[The lymphoid-like cells in blastic transformation of chronic myeloid leukemia].

The natural history of chornic myeloid leukaemia (CML) usually ends with a blastic transformation (BT). In 30% of cases, BT displays the cytomorphological, cytochemical, immunological and biochemical features and the response to therapy observed in acute lymphoblastic leukaemia (ALL). The presence of lymphoid-like cells in a blood disease classically interpreted as a disorder of the myeloid strain led to the suggestion that CML is a disease of a stem cell capable of displaying both myeloid and lymphoid characters. It is thought that this is due to the fact that the Ph1 alteration strikes a premyeloid and prelympoid stem cell that presents myeloid features in the chronic stage of CML and in myeloblastic BT, whereas it displays lymphoid characteristics in the lymphblastic BT of CML and Ph1+ ALL. This fact lends support to the unicystic haematopoietic theory of Ferrata. Reference is made to a case in which the BT of CML was marked by the predominant presence of cells with a lymphoblastic appearance.

Cell Transformation, Neoplastic↗
PubMed1977

[Immunopathology of the hepatic damage caused by alcohol. Recent acquisitions].

Recent findings in the pathogenesis of alcoholic liver disease suggest that immunological factors play a leading part in addition to the damaging action of alcohol. Immunological phenomena affected by Mallory's bodies take on considerable importance with respect to humoral immunity. As regards cell immunity, the leucocyte migration inhibition test shows that the lymphocytes of liver-diseased alcoholics can produce the migration inhibiting factor. Deposit of collagen in the liver appears to be induced by lymphocytes sensitized by Mallory's bodies. Recent experimental studies based on the use of collagen synthesis inhibitors (colchicine and penicillamine) may have therapeutic implications.

Antibody Formation↗