T cell peripheral subsets in lichen sclerosus et atrophicus.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
M Cattaneo
Publications and source records attributed to M Cattaneo.
Peripheral blood lymphocyte subpopulations in patients with viral warts.
Peripheral blood T-cell subpopulations were evaluated in 32 patients affected by viral warts and in 32 unaffected individuals belonging to a control group. A significant decrease was found in total lymphocytes as well as OKT3 and OKT4 subsets among affected patients. A significant negative correlation was also found between OKT3 and OKT4 numbers as well as OKT4/OKT8 ratio and duration and extent of lesions. A significant positive correlation was found between the duration and the extent of lesions and the percentage of OKT8 subsets, but not the total number of OKT8. These data confirm that a cell-mediated immune deficiency is present in patients with viral warts. We then discuss whether the decrease of cellular immunity in these patients is a primary event or, rather, the result of persistent verrucosis.
Adolescent↗
Controlled trial of desmopressin in liver cirrhosis and other conditions associated with a prolonged bleeding time.
The synthetic vasopressin derivative desmopressin (DDAVP) shortens a prolonged bleeding time (BT) in patients with uremia, congenital platelet dysfunction, and von Willebrand disease. To establish the limits of the clinical usefulness of DDAVP, a controlled randomized study was carried out in 53 patients and ten volunteers with different conditions that have in common a prolonged BT. DDAVP significantly shortened the BT in 21 cirrhotics (P less than .01), in eight patients with unclassified prolonged BT (P less than .05) and in ten volunteers taking the antiplatelet drugs aspirin (P less than .05) and ticlopidine. The BT changes were not statistically significant in 15 patients with severe thrombocytopenia nor in nine with congenital platelet dysfunction, even though a few patients with storage pool deficiency responded with a marked BT shortening. Our findings indicate that DDAVP might be given when biopsies or other surgical procedures must be carried out in patients with prolonged BT. However, the compound is often ineffective in patients with thrombocytopenia or congenital platelet dysfunction.
Adolescent↗
Mites and chronic urticaria.
Explore the source record for details and available documents.
Chronic Disease↗
[Skin pathology caused by drugs].
175 patients suffering from acute drug-induced skin pathologies were examined with particular reference to age of onset, clinical type and causative agent. The most common pathology was urticaria, followed by eczematous and exanthematic eruptions. The drugs most frequently responsible for such reactions were the analgesic-antipyretic-anti-inflammatory group, topical products and antibiotics. These data are discussed in detail.
Adolescent↗
Human platelet aggregation and release reaction induced by platelet activating factor (PAF-acether)--effects of acetylsalicylic acid and external ionized calcium.
The effects of the cyclo-oxygenase inhibition on PAF-acether-induced human platelet aggregation and secretion are controversial. We studied the above parameters on citrated platelet-rich plasma of 12 normal subjects before and after the in vivo administration of acetylsalicylic acid (ASA). Individual sensitivities to PAF-acether were highly variable. ASA completely inhibited the platelet secretion induced by low concentrations of PAF-acether, but caused only partial inhibition when platelets were exposed to high concentrations of PAF-acether. The concentration of PAF-acether which overcame the cyclo-oxygenase inhibition varied substantially, depending on the individual sensitivity of the platelets to it. The addition of CaCl2 2 mM to the samples did not affect the extent of the platelet secretion, but increased irreversible aggregation in samples taken both before and after the ASA administration. These data suggest that low concentrations of PAF-acether stimulate the human platelet secretion by activating the cyclo-oxygenase pathway, whereas higher concentrations also trigger other mechanism(s) that suffice to induce human platelet secretion and full aggregation.
Aspirin↗
Effect of ticlopidine on platelet aggregation, adherence to damaged vessels, thrombus formation and platelet survival.
Ticlopidine (100 mg/kg/day or 400 mg/kg/day) was administered to rats and rabbits for 48 hr before and during the experiments. Aggregation studies of twice-washed platelets resuspended in Tyrode solution containing apyrase and 0.35% albumin showed that inhibition by ticlopidine of aggregation induced by ADP, collagen, sodium arachidonate or thrombin persisted after resuspension, as did inhibition of the release of 14C-serotonin from prelabeled platelets. Thus the inhibitory effect of ticlopidine or its metabolite is not readily reversed. In both species, ticlopidine prolonged platelet survival when it had been shortened by the insertion of an indwelling aortic catheter, although only the higher dose was effective in rabbits. In this species, this dose also prolonged platelet survival in sham-operated animals. Ticlopidine did not have a significant effect on the clearance of rabbit platelets when their survival had been shortened by pretreatment with neuraminidase. Ticlopidine did not affect the number of 51Cr-labeled platelets that accumulated on the injured vessel wall in rats with indwelling aortic catheters or the amount of thrombus that formed around the catheters in the aortas of the rabbits. It also did not affect the accumulation of platelets in vivo on rabbit aortas de-endothelialized with a balloon catheter. Thus, although ticlopidine inhibited platelet aggregation and release and prolonged shortened platelet survival, it did not inhibit platelet adherence to the damaged wall or thrombosis caused by chronic arterial injury. It is evident that effects on platelet survival and thrombosis do not correlate. The reason for the prolongation of platelet survival is unknown.
Animals↗
[Periarticular calcifications. A little-known sign of psoriatic arthritis].
The hands of 40 patients with psoriasis were examined by conventional and direct magnification radiograms. In 5 cases the hands showed typical psoriatic arthropathy. In 5 other cases only small calcifications in the soft tissues at distal interphalangeal joints were visible: according to clinical and laboratory data, these lesions could be in connection with psoriatic arthritis.
Adolescent↗
Bile lipid composition and haemostatic variables in a case of high density lipoprotein deficiency (Tangier disease).
A 62-year-old man with clinical and biochemical findings consistent with homozygous Tangier disease is presented. Widespread atherosclerosis was present. Bile lipid analysis showed a low molar percentage of cholesterol with a low saturation index. The data suggest that high density lipoprotein cholesterol may act as a preferential precursor of biliary cholesterol. Coagulation and platelet studies indicated that the patient's platelets were hyper-responsive to aggregating agents and produced an increased amount of thromboxane B2. A platelet storage pool deficiency was also found.
Aged↗
Cirrhosis associated with multiple transfusions in thalassaemia.
The study of surgical liver biopsy specimens obtained during splenectomy in 86 children with thalassaemia indicated that such patients may develop liver disease that evolves into cirrhosis. Histological characteristics suggest that it is post-necrotic cirrhosis. Onset of cirrhosis in some patients may occur as early as 7-8 years old, and at age about 15-16 years most children with thalassaemia show features of cirrhosis. In addition to fibrosis, hepatitis, or even aggressive hepatitis may develop as has also been observed in patients without thalassaemia who have undergone multiple transfusions. This study presents the current probable evolution of liver disease in patients with thalassaemia and may thus serve as a reference from which to evaluate any future progress in the treatment and care of patients with Cooley's disease.
Adolescent↗
DDAVP enhances platelet adherence and platelet aggregate growth on human artery subendothelium.
The effect of intravenous 1-deamino (8-D-arginine)vasopressin (DDAVP) administration on platelet interaction with human artery subendothelium was investigated with flowing blood from five normal individuals and 12 patients with von Willebrand's disease (vWD). Three of the patients were diagnosed as vWD subtype I, four as subtype IIa, and five as subtype IIb. DDAVP administration to normals enhanced platelet adherence, in parallel with increasing plasma levels of factor VIII-related antigen ( FVIIIR :Ag) and ristocetin cofactor activity ( FVIIIR :RCF). Platelet aggregate formation was transiently increased within 90 minutes. Platelet adherence in patient blood before DDAVP infusion was subnormal. In patients with subtype I, administration of DDAVP normalized the bleeding time, enhanced the platelet adherence, and transiently improved the platelet aggregate formation. The platelet adherence was more corrected than would have been expected on the basis of the FVIIIR :Ag and FVIIIR :RCF levels. In patients with subtype IIa, infusion of DDAVP increased the FVIIIR :Ag levels approximately threefold, without affecting the FVIIIR :RCF levels, and in only two of four patients was a transiently enhanced platelet adherence with a corresponding shortening of the bleeding time observed. In patients with subtype IIb, administration of DDAVP increased the FVIIIR :Ag levels about threefold and the FVIIIR :RCF levels five to tenfold, but decreased the platelet adherence significantly. The bleeding time values were not normalized. A close association between the bleeding time values and corresponding platelet adherence values before and after DDAVP infusion was observed. Normalization of the bleeding time was paralleled with normalization of platelet adherence. We conclude that DDAVP improves the primary hemostasis by causing enhanced FVIII-vWF-mediated platelet adherence. DDAVP has little or no effect on the bleeding time in patients with subtype IIa and subtype IIb, because the platelet adherence is not normalized.
Arginine Vasopressin↗
Chronic liver disease in children with leukemia in long-term remission.
Liver disease during chemotherapy and after its completion was studied in 103 leukemic children in long-term remission. Seventy developed chronic liver disease during therapy; 22 out of 56 with adequate follow-up showed persisting abnormality or deterioration of liver function after stopping therapy. In 38 studied prospectively, biopsies were obtained at treatment withdrawal. Five showed chronic lobular, 17 chronic persistent, 9 chronic active hepatitis whereas 7 had minimal changes. These children had transiently detectable serum hepatitis-B virus (HBV) markers during (44.4%), at completion of (7.8%) and subsequent to (48.3%) chemotherapy. Serum HBV markers correlated significantly with both severity of histologic changes (P less than 0.05) and persistent biochemical abnormalities for over 6 months after treatment suspension (P less than 0.001). No direct relationship was found between drug administration and liver damage. The data from the study suggest that in leukemic children viral infections contribute to chronic liver damage, which can jeopardize the long-term prognosis of acute leukemia.
Acute Disease↗
Primary polypeptide hormones and mucin-producing malignant carcinoid of the larynx.
A case of primary malignant laryngeal carcinoid with dual endocrine and mucous differentiation is reported. Histologically the tumor showed a characteristic organoid pattern and exhibited Alcian-blue, periodic acid-Schiff, and Grimelius silver positivity. By the immunoperoxidase technique calcitonin, ACTH, and alpha-hCG subunit were demonstrated in the tumor cells. Electron microscopy revealed two different types of endocrinelike cells: mucous cells and occasional cells containing both endocrinelike granules and mucin droplets. Diagnostic morphologic criteria of this rare tumor entity are discussed and reference to biologic behavior and possible histogenesis is made.
Adrenocorticotropic Hormone↗
Effect of aspirin and sodium salicylate on thrombosis, fibrinolysis, prothrombin time, and platelet survival In rabbits with indwelling aortic catheters.
We have studied the effect of different doses of aspirin on platelet function, PGI2 formation, platelet survival, thrombosis, fibrinolysis, and prothrombin time in rabbits with indwelling aortic catheters. The thrombi formed around indwelling aortic catheters were found to have a large fibrin component, and their formation was inhibited by heparin administration. Thus, in these experiments we examined the effect of aspirin (a weak inhibitor of thrombin-mediated platelet aggregation) under conditions in which thrombin was a major factor in the initiation and growth of the thrombi. Only very high doses of aspirin tended to inhibit thrombus formation over the 5-day period of observation, and a statistically significant inhibition of thrombus formation was produced by equivalent concentrations of sodium salicylate. The failure of high doses of aspirin to achieve a significant inhibition of thrombosis under the conditions of these experiments (whereas an equivalent dose of sodium salicylate was inhibitory) could be due to aspirin inhibition of PGI2 formation. Shortened platelet survival was not affected by aspirin treatment or the dose sodium salicylate that inhibited thrombus formation. The tendency to inhibit thrombus formation appeared to be unrelated to an effect on platelets but was associated with prolongation of the one-stage prothrombin time and increased whole blood fibrinolytic activity; doses of aspirin that inhibited platelet aggregation in response to sodium arachidonate or collagen, and PGI2 formation by the vessel wall, did not have a significant effect on the amount of thrombus present at 5 days. However, the high doses of aspirin that inhibited PGI2 formation were associated with a tendency to increased thrombus formation during the first 3 hr after insertion of the catheter. The results of these experiments show that when thrombin is an important factor in the formation of thrombi, aspirin is a weak inhibitor of thrombosis unless doses are used that provide sufficient salicylate to interfere with blood coagulation and promote whole blood fibrinolytic activity. These results also show that thrombus formation can be inhibited without an apparent change in platelet survival.
Animals↗
Biochemical analysis of a public H-2 specificity revealed by an anomalous reaction of an alloantiserum with a chemically induced C57BL/10 fibrosarcoma.
D-25 is a H-2 alloantiserum produced in (B10.D2 X C3H.NB) (H-2d X H-2p)F1 mice after immunization with B10.RIII(H-2r) cells, and which is known to recognize the H-2.25 public antigen on H-2k haplotypes. The "anomalous" reaction of D-25 with a partially purified deoxycholate-solubilized glycoprotein of B10-1 (H-2b) fibrosarcoma was studied with various biochemical techniques. The 125I-labelled precipitates were analysed both in one- and two-dimensional SDS-PAGE and by a partial proteolysis peptide mapping (Cleveland's mapping). The results indicate first that the D-25-related antigen was a genuine H-2 antigen normally associated with the B2-microglobulin, second that this antigen was borne by the Kb but not Db gene products, and finally that D-25 was able to precipitate the same antigen on normal H-2b spleen cells. We conclude that this serum recognized a normal H-2 specificity shared by H-2b and H-2r haplotypes and tentatively identified as the public antigen H-2.54 which for the first time could be assigned to the K but not to the D region of the H-2b haplotype.
Animals↗
The inhibitory effects of exogenous arachidonic acid on rabbit platelet aggregation and the release reaction.
Although arachidonic acid causes rabbit platelet aggregation and the release of granule contents in suspensions of washed platelets when used in concentrations of approximately 50-300 microM, higher concentrations (500 microM) cause neither aggregation nor release. Suspensions of platelets from rabbits wee exposed to arachidonic acid (250 microM) for 15 min, allowed to recover in the presence of PGE1 for 30 min, washed, and resuspended; in some experiments, the platelets were treated with aspirin before being exposed to arachidonic acid. Aggregation of platelets pretreated with arachidonic acid was inhibited in response to ADP; this effect was greater with the non-aspirin-treated platelets and persisted for at least 4 hr after resuspension. The association of 125I-fibrinogen with the platelets as a result of ADP stimulation was also inhibited. Aggregation and release of granule contents in response to collagen and low concentrations of thrombin was inhibited, but the inhibition could be overcome by higher concentrations. Thrombin induced further release of granule contents from platelets exposed to arachidonic acid without pretreatment with aspirin. Platelets that had been exposed to arachidonic acid, either with or without pretreatment with aspirin, did not aggregate or undergo further release upon stimulation with arachidonic acid after they were washed and resuspended. Inhibition of the lipoxygenase pathway with eicosatetraynoic acid (ETYA) or nordihydroguaiaretic acid (NDGA) did not affect the inhibition caused by arachidonic acid, so it is unlikely that a product of this pathway is responsible for the inhibition. Mixing experiments indicated that the pretreated platelets did not form a thromboxane-A2-like activity, and that they were unresponsive to aggregation and release induced by products formed from arachidonic acid. Experiments with 3H-arachidonic acid showed that after 45 min of incubation with platelets, only 1.1% of the 3H-arachidonic acid remained as free arachidonic acid in the platelets. Although cyclic-AMP was slightly increased 1 min after the addition of arachidonic acid, the cyclic-AMP concentration was the same as that of control platelets after the platelets were washed and resuspended, indicating that increased cyclic-AMP is not likely to be responsible for the persistent inhibitory effect. Thus, the inhibitory effect of pretreatment with arachidonic acid is a general effect on responses to a variety of aggregating agents that act through different mechanisms, and the inhibition is not related to thromboxane-A2 formation. The possibility of membrane perturbation resulting in the unavailability of receptors may explain the persistent inhibitory effect, but the responsible reactions have not been identified.
Adenosine Diphosphate↗
Biochemical characterization of the anomalous reaction of anti-H-2b alloantiserum with a chemically induced sarcoma of H-2k origin.
Explore the source record for details and available documents.
Animals↗
Increased fibrinopeptide A after prothrombin complex concentrates.
Prothrombin complex concentrates (PCC) are known to carry a risk of thromboembolism. We have chosen to reassess the problem of detecting in vivo signs of activation of the clotting mechanism by assaying fibrinopeptide A (FpA) after PCC administration in hemophilic patients during bleeding episodes. FpA was significantly increased above baseline levels 15 to 60 min after the infusion of 19 doses of 5 different types of commercial PCC in 14 hemophilia B patients treated for bleeding episodes or dental extractions. A more marked increase followed 16 infusions of the activated PCC FEIBA and Auto IX in 4 hemophilia A patients with F. VIII inhibitors. There was no significant FpA change after F. VIII concentrates administered to a control group of 7 patients with hemophilia A. These findings suggest that circulation of thrombin occurs frequently after PCC administration, even though clinical manifestations of thromboembolism appear to be relatively rare.
Blood Coagulation Factors↗