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Biomedical subjects

G F Altomare

Publications and source records attributed to G F Altomare.

At least 37 records · Page 2Linked to original sources
PubMed1989

[Growth factors in the pathogenesis of progressive systemic sclerosis].

Scleroderma is a connective tissue disorder characterized by vascular lesions, fibrosis and inflammation. The pathogenesis of this disease is not clear. A vascular lesion, possibly caused by deposition of immune complexes or by release of cytotoxic factors, seems to be at the origin of the disease. As a consequence, platelet adhesion and activation might occur in sclerodermic patients. The observation that platelet might release, upon aggregation, a potent mitogenic factor, named Platelet Derived Growth Factor (PDGF) has focused interest on platelets as the potential mediators of the fibrotic process, characteristic of systemic scleroderma. We found an increased mitogenic activity in plasma derived serum (PDS) of a group of patients with progressive systemic sclerosis (PSS), as compared to control subjects. The activity was inhibited by incubation with anti-PDGF IgG's, suggesting that abnormal PDGF levels might indeed be present in plasma of PSS patients.

Adult↗
PubMed1988

Ketanserin in the treatment of progressive systemic sclerosis.

Now progressive systemic sclerosis (PSS) is considered a disease of small vessels with which many immunologic alterations are associated. The presence in the blood of large amounts of serotonin can be considered a very important aggravating factor able to cause the sclerodermic alterations. The authors have treated 10 PSS patients with ketanserin, a selective antagonist of the S2 serotonin receptors, which are found in small vessels and platelets. Their results show that ketanserin represents an efficacious and very well tolerated therapy for treatment of the initial vascular symptoms of PSS.

Adult↗
PubMed1987

Arachidonic acid and LTB4 enhance aggregation of psoriatic peripheral blood mononuclear leukocytes in vitro.

The aim of the reported series of experiments was to examine the possible role played by arachidonic acid (Aa) derivatives in monocyte aggregation in psoriasis. Twenty patients with active plaque-type psoriasis covering not less than 20% of body surface area and 20 age-matched controls were investigated. Peripheral blood monocytes were harvested according to the technique recently set up by Colotta et al. These preparations usually contained more than 95% monocytes, as assessed by morphology and esterase staining. Aggregation tracings were plotted using a common platelet aggregation recorder system and expressed in arbitrary units. Aa sodium salt, acetylsalicylic acid (ASA), indomethacin, nordihydroguaiaretic acid (NDGA), and leukotriene B4 (LTB4) were used during testing. Aa induced an enhanced aggregation of mononuclear leukocytes (MNL) in psoriatic patients versus normal controls in a concentration-dependent way. Furthermore, neither ASA nor indomethacin inhibited Aa aggregation, while both markedly increased the aggregation response in psoriasis. LTB4 induced an enhancement aggregation in psoriasis, whereas NDGA strongly inhibited it. Although the pathophysiological significance of MNL aggregation described here remains obscure, assembly of the cells at the site of psoriatic skin might be a crucial event.

Adult↗
PubMed1987

Occupational dermatitis in bakers: a clue for atopic contact dermatitis.

6 patients are described who developed contact dermatitis after cereal contact on atopic skin for periods of 2 to 20 years. 2 patients were wheat flour patch-test-positive. They had punch biopsies taken for standard histological and immunohistochemical investigation by labeling with monoclonal antibodies, anti-DR and anti-IgE. Sections showed features of contact dermatitis. There were many dendritic cells located perivascularly in the papilla and in the epidermidis, intensely positive for monoclonal anti-IgE antibody. In control atopic subjects, there were a few perivascular IgE positive cells, probably mastocytes. This study shows that there may be a relationship between some allergens and atopic eczema in patients exposed to them in the course of their work. In some cases, there was a true allergic contact dermatitis, seen through the clinical and histological characteristics, and the results of immunohistochemical study.

Adult↗
PubMed1986

Complement cleavage products in the phototoxic reaction of porphyria cutanea tarda.

We have measured C3, C4, CH50 and complement cleavage products C3a and C5a in in sera and plasma from PCT patients and normal controls 10 min and 1, 4 and 24 h after UVA irradiation. We found elevated C3a concentrations in PCT patients immediately after UVA irradiation and 24 h later. The same was true for CH50, whereas C3, C4 and C5a did not change significantly. No such changes occurred in normal controls. Our data suggest that activation of the complement cleavage product C3a by porphyrin and UV light triggers a series of events that cause tissue damage.

Adult↗