1,721,018 research outputs found
Acute renal failure associated with cocaine and alcohol abuse
No full textA broad spectrum of renal diseases is reported in cocaine abuse subjects, nevertheless the pathogenesis of the acute temporary renal failure is unclear. Cocaine may induce rhabdomyolysis and/or renal vasoconstriction being a powerful sympathomimethic drug and in turn renal failure. A 20-year-old man developed a reversible acute renal failure following an episode of cocaine and alcohol abuse. He was admitted for oliguria, swelling, pain and reduced strength in the left lower limb. The increase of serum creatinine and muscular enzymes and the presence of urinary granular and jaline casts were suggestive of rhabdomyolysis and renal damage. The clinical picture completely recovered after 15 days from the onset. We believe that an intense arterial vasoconstriction was the more probable mechanism of rhabdomyolysis and acute renal failure in this patient both because renal function recovered 5 days after forced diuresis and because biochemical indices of renal activity were always normal during 4 months after hospital discharge. Moreover, the report that the contemporary ingestion of alcohol and cocaine has an additive and synergistic effect causing the hepatic production of cocaethylene, a metabolite able to increase the systemic toxic effects of cocaine, may support our hypothesis
DIAGNOSIS ON A CASE OF CONN DISEASE
No full textCONDITION OF PRIMARY IPERALDOSTERONISM SHOULD BE SUSPECTED IN ALL PATIENTS WITH HYPERTENSION.PATIENT WAS SUBJECTED TO PHLEBOGRAPHY OF THE RENAL VEIN WITH SELECTIVEI.V. CATHETERIZATION AND VENOUS SAMPLING FOR ALDOSTERON
Association between high values of D-dimer and Tissue-plasminogen activator activity and first gastrointestinal bleeding in cirrhotic patients
No full textAbstract Cirrhotic patients with decompensated state and high serum levels of fibrin(ogen) degradation products are at high risk of bleeding. The aim of this study was to further analyse the relationship between hyperfibrinolysis and bleeding in cirrhosis by measuring plasma values of D-dimer and tissue plasminogen activator (t-PA) activity. One-hundred-twelve cirrhotic patients with oesophageal varices and without previous upper-gastrointestinal bleeding entered the study and were followed-up for 3 years. Patients were considered to have hyperfibrinolysis if they concomitantly had high values of D-dimer and t-PA activity. During the follow-up 34 (30%) patients bled. They had more severe liver failure (p = 0.0001) and variceal size (p = 0.0031) and higher prevalence of ascites (p = 0.0003), varices with red signs and hyperfibrinolysis (p = 0.0001) than patients who did not bleed. Multivariate analysis disclosed hyperfibrinolysis as the only marker predictive of bleeding (Hazard Ratio = 42.5, p < 0.001). Our findings suggest that screening for hyperfibrinolysis may be useful to identify cirrhotic patients at risk of bleeding
[The behavior of the fibrinogen polymerization curve in hypercholesterolemic subjects].
No full textSeveral epidemiological and clinical studies performed in subjects with risk factors for atherosclerotic cardiovascular events, have shown changes in plasma levels and/or activities of coagulation factors that could suggest a prothrombotic state. We studied the behaviour of the fibrinogen polymerization curve (FPC), a spectrophotometric technique evaluating the kinetics of fibrinogen transformation into fibrin, in 68 subjects with and without hypercholesterolemia. Significant differences were found between FPCs of subjects with serum cholesterol > 240 mg/dl and < or = 240 mg/dl respectively. In fact, FPCs of the first group showed high reaction velocity rate, short latency time and higher optical density rate, final readings; besides, the behaviour of FPCs was not correlated to plasma fibrinogen concentrations. Therefore, FPC could be a useful test to identify a thrombophilic condition in hypercholesterolemic patients
Intracranial hemorrage due to brain metastases in an Italian HCV patient with hepatocellular carcinoma
No full textBrain metastases from hepatocarcinoma are exceptional and only a few cases have been reported in the literature, mainly from Far-Eastern countries. Clinical diagnosis in asymptomatic patients with preserved liver function is difficult and usually late. In some cases, cerebral metastasis is the initial manifestation of HCC and patients may develop intracerebral hemorrage and have a stroke-like presentation. We report on the first Italian case of cerebral metastases from multifocal hepatocellular carcinoma in an asymptomatic HbsAg negative patient with unknown HCV related chronic hepatitis and no evidence of liver cirrhosis. For many years he had a mild liver enzyme elevation and the presence of multiple misinterpreted hypoechogenic hepatic lesions. The hepatic tumor spread to the lungs and the brain and the patient developed two major episodes of intracranial hemorrage. He had two nodular lesions in the brain and alpha-fetoprotein levels were more than 10,000 ng/ml. He died from neurologic causes, without major signs of liver failure
Inhibition of tissue-factor-mediated thrombin generation by simvastatin
No full textA previous study has shown that simvastatin reduces in vivo clotting activation and monocyte tissue factor (TF) expression. This effect, however, was only in part attributable to the reduction of serum cholesterol, suggesting that more than one mechanism may be involved. Furthermore, it was not investigated if the inhibition of clotting activation was dependent upon the reduced expression of monocyte TF. In order to assess if simvastatin directly affects clotting activation, we developed an in vitro method in which clotting system is activated by monocytes stimulated with LPS. Monocytes were prepared from blood taken from healthy volunteers or patients with hypercholesterolemia and incubated with heparinized plasma plus either simvastatin (0.01-10 mu M) or medium as control. Samples were then stimulated with LPS (4 mu g/ml) and after 6 h the rate of thrombin generation, assessed by prothrombin fragment (F) 1 + 2, was measured. In separate experiments, we measured the expression of TF by monocytes which were incubated with simvastatin and then stimulated with LPS. The study showed that compared to control, LPS-stimulated monocytes induced abundant formation of F1 + 2, which was inhibited by simvastatin in a dose-dependent manner. Simvastatin also inhibited dose dependently the monocyte expression of TF. This study suggests that simvastatin inhibits the rate of thrombin generation by directly interfering with the monocyte expression of TF. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved
Hydrogen peroxide as trigger of platelet aggregation.
No full textIn order to verify if H2O2 affects platelet function, platelet-rich plasma and human washed platelets were incubated with subthreshold concentrations (STC) of collagen or arachidonic acid or ADP and/or with 75-150-mu-M H2O2. While H2O2 alone did not affect platelet aggregation, it amplified platelet aggregation response in samples stimulated with STC of arachidonic acid and collagen but not in samples stimulated with STC of ADP. When platelets were preventively treated with aspirin, a cyclooxygenase inhibitor, the platelet activation by H2O2 was not observed. Thromboxane A2 (TxA2) was not produced by human washed platelets stimulated with STC of arachidonic acid, collagen or by H2O2 alone. On the contrary, when STC of agonists were tested on platelets supplemented with H2O2 an evident TxA2 production was seen. This effect was prevented by aspirin pretreatment or by the addition of catalase, an enzyme which destroys H2O2. This study suggests that H2O2 triggers the activation of platelets exposed to STC of collagen and arachidonic acid, via the cyclooxygenase pathway
Association between low-grade disseminated intravascular coagulation and endotoxemia in patients with liver cirrhosis.
No full textBACKGROUND & AIMS: Hyperfibrinolysis may complicate the clinical course of liver cirrhosis. The aim of this study was to evaluate if, in cirrhosis, hyperfibrinolysis is primary or secondary to intravascular clotting activation and if endotoxemia is associated with activation of clotting and/or the fibrinolytic system.
METHODS: Clotting, fibrinolytic indexes, and endotoxemia were studied in 41 cirrhotic patients and 20 healthy subjects.
RESULTS: Twenty-seven cirrhotic patients (66%) had high plasma levels of prothrombin fragment F1 + 2, a marker of thrombin generation. Nineteen patients had elevated values of D-dimer, a marker of fibrinolysis in vivo. All patients
with high values of D-dimer also had high values of prothrombin fragment F1 + 2. Endotoxemia was elevated in patients with severe liver failure and significantly
correlated to prothrombin fragment F1 + 2. Thirty patients were treated for 7 days either with standard therapy (n = 15) or with standard therapy plus nonabsorbable antibiotics (n = 15). Although standard therapy did not significantly change laboratory indexes, a significant reduction of endotoxemia, prothrombin fragment F1 + 2, and D-dimer was found in those patients who received the combined treatment.
CONCLUSIONS: This study shows that, in cirrhotic patients, hyperfibrinolysis is not a primary phenomenon but occurs as a consequence of clotting activation and that endotoxemia might play a pathophysiological role
- …
