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Biomedical subjects

M Cattaneo

Publications and source records attributed to M Cattaneo.

At least 109 records · Page 6Linked to original sources
PubMed1992

Intramuscular anti-D immunoglobulins for home treatment of chronic immune thrombocytopenic purpura.

To assess the efficacy of home treatment with intramuscular anti-D immunoglobulins (anti-D IgG) in patients with idiopathic or HIV-related chronic immune thrombocytopenic purpura (ITP), we conducted an open label, non-controlled, prospective study with a follow-up of 6 months in 51 consecutive patients with HIV-related (n = 24) or idiopathic ITP (n = 27). Anti-D IgG (13 micrograms/kg) were infused intravenously for three consecutive days (induction therapy). Patients whose platelet counts failed to increase above 50 x 10(9)/l were given a second course of the same therapy. If their platelet counts remained lower than 50 x 10(9)/l, they were considered non-responsive. Patients who responded to induction therapy were injected intramuscularly with 6 micrograms/kg/week anti-D IgG if platelets were between 50 and 100 x 10(9)/l or 13 micrograms/kg/week if they dropped to less than 50 x 10(9)/l. After induction therapy, responses occurred in 20/24 HIV-related chronic ITP patients (83%) and in 14/27 idiopathic chronic ITP patients (52%). During follow-up, platelets remained above 50 x 10(9)/l in 17/20 HIV-related chronic ITP patients (85%) and in 8/14 (57%) idiopathic chronic ITP patients. We conclude that anti-D IgG are a valid therapeutic option for treatment of idiopathic and HIV-related chronic ITP, since they are safe, cheap and can be given intramuscularly at home.

Adolescent↗
PubMed1992

Desmopressin: a nontransfusional treatment of hemophilia and von Willebrand disease.

Desmopressin (1-deamino-8-D-arginine vasopressin) is a synthetic analogue of the antidiuretic hormone L-arginine vasopressin. Because it can raise circulating levels of factor VIII and von Willebrand factor, desmopressin is used for nontransfusional treatment of mild and moderate hemophilia and von Willebrand disease. Desmopressin also shortens the prolonged skin bleeding time in patients suffering from von Willebrand disease and is given to prevent or stop excessive bleeding in such conditions.

Animals↗
PubMed1991

Ticlopidine selectively inhibits human platelet responses to adenosine diphosphate.

Platelet aggregation and fibrinogen binding were studied in 15 individuals before and 7 days after the oral administration of ticlopidine (250 mg b.i.d.). Ticlopidine significantly inhibited platelet aggregation induced by adenosine diphosphate (ADP), the endoperoxide analogue U46619, collagen or low concentrations of thrombin, but did not inhibit platelet aggregation induced by epinephrine or high concentrations of thrombin. Ticlopidine inhibited 125I-fibrinogen binding induced by ADP, U46619 or thrombin (1 U/ml). The ADP scavengers apyrase or CP/CPK, added in vitro to platelet suspensions obtained before ticlopidine, caused the same pattern of aggregation and 125I-fibrinogen binding inhibition as did ticlopidine. Ticlopidine did not inhibit further platelet aggregation and 125I-fibrinogen binding induced in the presence of ADP scavengers. After ticlopidine administration, thrombin or U46619, but not ADP, increased the binding rate of the anti-GPII b/III a monoclonal antibody 7E3 to platelets. Ticlopidine inhibited clot retraction induced by reptilase plus ADP, but not that induced by thrombin or by reptilase plus epinephrine, and prevented the inhibitory effect of ADP, but not that of epinephrine, on the PGE1-induced increase in platelet cyclic AMP. The number of high- and low-affinity binding sites for 3H-ADP on formalin-fixed platelets and their Kd were not modified by ticlopidine. These findings indicate that ticlopidine selectively inhibits platelet responses to ADP.

Adenosine Diphosphate↗
PubMed1991

In vitro effects of picotamide on human platelet aggregation, the release reaction and thromboxane B2 production.

We studied the in vitro effects of picotamide (N,N' bis 3 picolyl-4-methoxy-isophthalamide) on human platelet aggregation, the release reaction and the production of thromboxane B2 (TxB2) induced by several platelet agonists. The effects of picotamide were compared to those of acetylsalicylic acid (ASA). Picotamide (0.5 mmol/l) inhibited platelet aggregation, the release of ATP and TxB2 production induced by ADP, arachidonic acid (AA), collagen or the prostaglandin endoperoxide (PE) analogue U46619. ASA (0.5 mmol/l) did not affect platelet aggregation and the release of ATP induced by U46619. Picotamide and ASA inhibited the AA-induced platelet TxB2 production both under stirring and non-stirring conditions, whereas the pure thromboxane A2 receptor antagonist BM13177 (0.5 mmol/l) was inhibitory only under stirring conditions. Since under non-stirring conditions platelet aggregation does not occur, picotamide directly inhibits TxB2 production, whereas BM13177 inhibits the potentiation of TxB2 production due to TxA2/PE-dependent platelet aggregation. Malondialdehyde (MDA) production by unstirred platelets stimulated with AA was not significantly inhibited by picotamide. In conclusion, picotamide inhibits the TxA2/PE-dependent platelet responses to agonists by a double mechanism: (i), TxA2/PE antagonism; (ii) inhibition of thromboxane synthase.

Adenosine Diphosphate↗
PubMed1991

Risk of thromboembolic complications in patients with inflammatory bowel disease. Study of hemostasis measurements.

A large number of hemostasis measurements complications were performed in 20 patients with inflammatory bowel disease; whose changes have been associated with an increased risk of thromboembolic. Of the 20 patients, 9 (45%) had one or more changes suggestive of activation of the hemostatic system. Such changes were more frequently observed in patients with active disease. Two patients had changes in the fibrinolytic system (high plasminogen activator inhibitor-1 levels) and 2 in the natural anticoagulants (low antithrombin III activity). Nine patients had increased plasma fibrinogen levels and 6 patients had slightly increased levels of anticardiolipin antibodies. Most of the changes observed were not related to the type, location or activity of the disease. These data show that various biochemical abnormalities may be found in patients with inflammatory bowel disease, which may account for their increased risk of thrombosis, and suggest that multiple mechanisms may interact in determining such complications.

Adult↗
PubMed1990

Subcutaneous desmopressin (DDAVP) shortens the prolonged bleeding time in patients with liver cirrhosis.

The intravenous infusion of 1-deamino-8-D-arginine vasopressin (DDAVP) shortens the prolonged bleeding time in patients with congenital or acquired bleeding disorders, including patients with uremia or liver cirrhosis. We carried out a double-blind, placebo-controlled crossover study in ten patients with liver cirrhosis to evaluate whether or not their prolonged bleeding times could be shortened by subcutaneous injections of DDAVP (0.3 microgram/kg), a more practical route of administration than intravenous infusions. One hour after DDAVP injection the bleeding time was significantly shortened (p less than 0.05). After 4 h, however, the bleeding time shortening was no longer statistically significant. There was no bleeding time change after placebo. Plasma levels of von Willebrand factor antigen (vWF:Ag) did not significantly increase after DDAVP or placebo. The study shows that subcutaneous DDAVP is an alternative method for short-term shortening of the bleeding time in liver cirrhosis.

Adolescent↗
PubMed1990

Released adenosine diphosphate stabilizes thrombin-induced human platelet aggregates.

Normal human platelets aggregated by thrombin undergo the release reaction and are not readily deaggregated by the combination of inhibitors hirudin, chymotrypsin, and prostaglandin E1 (PGE1). In contrast, thrombin-induced aggregates of platelets from patients with delta-storage pool deficiency (delta-SPD), which lack releasable nucleotides, are readily deaggregated by the same combination of inhibitors. The ease with which delta-SPD platelets are deaggregated is caused by the lack of stabilizing effects of released ADP, since: (1) exogenous adenosine diphosphate (ADP) (10 mumol/L), but not serotonin (2 mumol/L), abolishes the ability of these inhibitors to deaggregate delta-SPD platelets; (2) thrombin-induced aggregates of platelets from a patient (V.R.) (whose platelets have a severe, selective impairment of sensitivity to ADP, but normal amounts of releasable nucleotides) can be readily deaggregated, and addition of ADP does not stabilize the platelet aggregates; (3) apyrase or creatine phosphate (CP)/creatine phosphokinase (CPK), added before thrombin, make control platelets more easily deaggregated by hirudin, chymotrypsin, and PGE1, and do not change the deaggregation response of delta-SPD platelets and of V.R.'s platelets. Thrombin-induced aggregation and release of beta-thromboglobulin in control, delta-SPD, and in V.R.'s platelets was similar and not inhibited by apyrase or CP/CPK. The stabilizing effect of ADP on platelet aggregates is specific, since epinephrine in the presence of apyrase to remove traces of released ADP does not stabilize the aggregates of control, delta-SPD, or of V.R.'s platelets. Because epinephrine increases fibrinogen binding to thrombin-stimulated platelets to a greater extent than ADP, but does not stabilize the aggregates, it is unlikely that the additional fibrinogen binding sites induced by ADP have a major role in inhibiting deaggregation by the combination of inhibitors.

Adenosine Diphosphate↗
PubMed1990

Spontaneous platelet aggregation during pregnancy in a patient with von Willebrand disease type IIB can be blocked by monoclonal antibodies to both platelet glycoproteins Ib and IIb/IIIa.

Spontaneous platelet aggregation appeared in a patient with von Willebrand disease type IIB during the 37th week of pregnancy. This phenomenon was not associated with symptoms of thrombosis and the patient delivered by caesarean section with no complications. Her platelet-poor plasma (PPP) aggregated normal platelet-rich plasma (PRP) and washed platelets. Aggregation was inhibited by monoclonal antibodies with known specificity for the platelet receptors of von Willebrand factor (vWF), i.e. the glycoprotein Ib (GPIb) and the GPIIb/IIIa complex. A monoclonal antibody, which selectively inhibits the binding of vWF to the GPIIb/IIIa complex, did not block aggregation, suggesting that spontaneous aggregation is not dependent on the binding to GPIIb/IIIa of vWF from patient plasma. Aggregation induced by patient plasma could also be blocked either by two monoclonal antibodies raised against vWF or by a fragment derived from trypsin digestion of normal vWF which blocks the ristocetin-induced binding of normal vWF to platelets. These findings indicate that the spontaneous platelet aggregation in this patient results from the binding of her vWF to GPIb but is independent from the binding of her vWF to GPIIb/IIIa.

Adult↗
PubMed1990

[Evaluation of the anti-comedo effect of azelaic acid using the technique of horny layer biopsy and scanning electron microscopy].

Hyperkeratosis of the follicular channel is the most common finding in acne skin. The hyperkeratosis may represent an altercated keratinization process or the consequence of the abnormal sebum production and excretion. Several review demonstrated the anti-comedo activity of azelaic acid in acneic skin. This action may be due either to an anti-hormonal effect or to a change in keratin production. The aim of this work is to investigate the anti-comedo activity of 20% azelaic acid cream topically applied in a group of teen-agers affected by acne. A horny layer biopsy with cyanoacrylate glue was performed before and after four months of treatment with azelaic acid cream in ten acne patients. About 1 cm square horny layer biopsy was metallized and observed at the scanning electron microscopy to count the number of comedos. With this method we detected a reduction of about 26% of the comedos after four months of azelaic acid treatment. The result we obtained is in accordance with previous works about the anti-comedo activity of azelaic acid.

Acne Vulgaris↗
PubMed1989

DDAVP shortens the prolonged bleeding times of patients with severe von Willebrand disease treated with cryoprecipitate. Evidence for a mechanism of action independent of released von Willebrand factor.

After infusion of cryoprecipitate, the very prolonged bleeding time of patients with severe von Willebrand disease (vWD) is shortened but not always normalized in spite of normalization of plasma von Willebrand factor (vWF) levels. Therefore treatments that further improve primary hemostasis in severe vWD patients are needed. Since DDAVP shortens the bleeding time in a variety of bleeding disorders, we investigated in a double-blind, placebo-controlled crossover study the effects of the intravenous (IV) infusion of DDAVP (0.3 microgram/kg) on the bleeding times of 10 patients with severe vWD treated with cryoprecipitate. Their very prolonged bleeding times (greater than 30 minutes), partially corrected by the infusion of cryoprecipitate (14 +/- 2 minutes, mean +/- SEM), were further shortened by the administration of DDAVP (9 +/- 2 minutes, P less than .01) but not of saline (15 +/- 3 minutes, ns). Plasma vWF levels, raised from unmeasurable to normal values by cryoprecipitate, were not changed after DDAVP or saline. The defective deposition of platelets from eight patients onto human umbilical artery subendothelium was increased but not normalized by cryoprecipitate and was not significantly affected by DDAVP or saline. Therefore the infusion of DDAVP after cryoprecipitate may be of clinical benefit for management of bleeding episodes in severe vWD patients. Since severe vWD patients do not have releasable tissue stores of vWF, DDAVP must shorten their prolonged bleeding times independently of released vWF.

Bleeding Time↗
PubMed1989

Early presence of activated ('exhausted') platelets in malignant tumors (breast adenocarcinoma and malignant melanoma).

To evaluate whether or not the finding of platelet activation in patients with tumors is related to the stage of malignancy, a study of biochemical markers indicative of the presence of circulating activated ('exhausted') platelets was carried out in 95 untreated patients with breast adenocarcinoma or malignant melanoma, localized or spread to regional lymph nodes with no detectable distant metastasis. These tumors were chosen as examples of tumors which can be accurately staged for localization or spread, and as examples of mucin-secreting tumors (breast adenocarcinoma) or neuroectodermic tumors (malignant melanoma). Results were compared with those for 26 patients with benign breast disease, 23 blood donors and 50 hospital workers. The most frequent abnormalities were low levels of intraplatelet ADP and 5-hydroxytryptamine and high ATP/ADP ratios. Although these abnormalities occurred with both types of tumor, they were more frequent and marked for melanomas and breast carcinomas spread to regional lymph nodes. Our data indicate that the presence of exhausted platelets is an early finding in patients with malignant tumors.

Adenocarcinoma↗