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Christoph Sucker

Publications and source records attributed to Christoph Sucker.

16 recordsLinked to original sources

Monitoring oral anticoagulation may require determination of single coagulation factor activities in patients with antiphospholipid syndrome.

We describe a 32-year-old man with secondary antiphospholipid syndrome (APS) who received oral anticoagulation with phenprocoumon after deep vein thrombosis. Conventional monitoring of oral anticoagulation by INR measurement was impaired by coagulation factor inhibition in vitro due to a strong lupus anticoagulant. The case illustrates that monitoring of oral anticoagulation may require determination of single coagulation factor activities in selected patients with APS.

Administration, Oral↗

Adult Langerhans cell histiocytosis.

Langerhans cell histiocytosis (LCH) is a proliferative histiocytic disorder of unknown cause originating from dendritic cells. The clinical presentation of LCH is highly variable. Although the features of this disease have been well described in children, they remain poorly defined in adults. Here, we review the current knowledge about adult LCH, focussing on clinical presentation, diagnosis, treatment, and prognosis.

Adult↗

Effects of cardiac surgery on hemostasis.

Cardiac surgery affects both coagulation and platelet function. Revision of surgery due to bleeding has to be performed in 2% to 6% of patients undergoing cardiac surgery and is generally associated with a marked deterioration in prognosis. Factors contributing to acquired hemostatic abnormalities in cardiac surgery include the use of anticoagulants as well as the activation and consumption of coagulation factors and platelets induced by the extracorporeal circulation. Prophylactic use of antifibrinolytic agents such as aprotinin and tranexamic acid has been demonstrated to reduce the blood loss by half. Adequacy of heparin-induced anticoagulation in the perioperative setting is commonly controlled by the activated clotting time. This method also indicates the correct reversal of the heparin effect by protamine. In recent years, thrombelastography has proved to be valuable for diagnosis of coagulopathy associated with cardiac surgery. In addition, the use of thrombelastography-based algorithms has been shown to reduce transfusion requirements. In contrast to point of care methods, laboratory assessment of hemostasis is more time-consuming and, thus, often not as rapidly available as required. At this time, the therapy for perioperative hemostatic abnormalities is based mainly on the administration of blood components (fresh frozen plasma and platelet concentrates). In the future, recombinant activated factor VIIa might prove to be a therapeutic option in patients with otherwise untractable bleeding, but the efficacy of recombinant activated factor VIIa has yet to be defined for this indication.

Blood Coagulation Disorders↗

Amyloidosis and bleeding: pathophysiology, diagnosis, and therapy.

Amyloid diseases can be associated with potentially life-threatening hemorrhage. Pathogenetic factors contributing to the abnormal bleeding tendency in this setting are heterogeneous and depend on the type of amyloidosis and pattern of organ involvement. In patients with light-chain (AL) amyloidosis, acquired hemostatic abnormalities, including coagulation factor deficiencies, hyperfibrinolysis, and platelet dysfunction, can be regarded as the most important pathogenetic factors. In patients with other types of amyloidosis, acquired hemostatic defects are rare, and amyloid deposition has also been reported to be the main cause of abnormal bleeding manifestations. Amyloid angiopathy with increased fragility of blood vessels and impaired vasoconstriction may promote bleeding in this setting. Rupture of solid organs caused by amyloid deposition also was reported. Whereas therapeutic options in bleeding caused by local amyloid deposition are restricted to supportive measures and, in severe cases, surgery, acquired hemostatic defects may be treated according to the causative mechanism. In this review, we focus on bleeding risks in patients with amyloid diseases. Current concepts with regard to pathophysiology, diagnosis, and treatment are summarized and discussed.

Amyloid↗

Citrate plasma levels in patients under regional anticoagulation in continuous venovenous hemofiltration.

BACKGROUND: Different methods of regional anticoagulation using citrate in continuous hemofiltration have been described. To date, only such surrogate parameters as pH, anion gap, total calcium concentration, or total calcium-ionized calcium ratio have been proposed to reflect increased plasma citrate levels and thus risk for side effects. However, none of these parameters has been correlated with plasma citrate levels in critically ill patients. METHODS: Sixteen patients were treated with continuous venovenous hemofiltration (CVVH) and citrate anticoagulation for a mean of 13 +/- 9 days. Citrate levels were measured every other day, and correlations were calculated with the mentioned parameters. RESULTS: Steady-state citrate levels on treatment day 3 were 16.39 +/- 15.77 mg/dL (range, 2.63 to 73.49 mg/dL [853 +/- 821 micromol/L; range, 137 to 3825 micromol/L]). The highest correlation was found between citrate plasma level and total calcium-ionized calcium ratio (R = 0.85; P < 0.001). pH (R = -0.15) and anion gap (R = 0.36) were not helpful in estimating citrate plasma levels in patients treated with citrate-CVVH. CONCLUSION: Calculating total calcium-ionized calcium ratio is a simple tool that correlates best with citrate plasma levels. We recommend close monitoring of this parameter in all patients administered high doses of citrate as part of regional anticoagulation protocols.

Acute Kidney Injury↗

Thrombelastography for the monitoring of lipopolysaccharide induced activation of coagulation.

During Gram-negative sepsis, lipopolysaccharide (LPS) activates toll-like receptor (TLR) 4 and induces complex responses of immune system and haemostasis. In the present study we investigated whether thrombelastography is suitable to monitor the LPS-induced activation of coagulation. Whole blood samples from healthy volunteers were incubated with LPS for various incubation periods (0-5 hrs), thereafter rotation thrombelastography was performed. Incubation of whole blood (>or=3 h) with LPS markedly reduced clotting time; after 5 hrs the variable was reduced from 459+/-39 sec to 80+/-20 sec while the other thrombelastography variables (angle alpha, clot formation time, maximal clot formation) remained unaltered. EC(50) of the LPS effect on whole blood clotting time was 18 microg/ml. In isolated leukocytes, diluted in platelet poor plasma, far lower LPS-concentrations were effective: 10 ng/ml LPS reduced clotting time from 439+/-68 sec to 200+/-56 sec. Experiments with the protein synthesis inhibitor cycloheximide and active site-inhibited factor VIIa revealed that LPS exerts its effects via the synthesis of tissue factor. Addition of tissue factor to whole blood samples revealed that a concentration of 100 fmol/l can be detected using thrombelastography. In whole blood samples the tissue factor concentration induced by LPS amounted up to 12 pmol/l. In summary, thrombelastography proved to be a sensitive and reliable tool for the determination of LPS-induced tissue factor mediated activation of haemostasis in whole blood samples.

Blood Coagulation↗

Determination of von Willebrand factor activity: evaluation of the HaemosIL assay in comparison with established procedures.

Determination of von Willebrand factor activity is required for diagnosis and classification of von Willebrand disease. In addition, von Willebrand factor activity can be of prognostic relevance in several clinical entities including thromboembolic and cardiovascular disorders in which elevated activity correlates with a poor prognosis. The HaemosIL assay (Instrumentation Laboratory GmbH, Munich, Germany) provides a new fully automated procedure for determination of von Willebrand factor activity. This assay measures binding of the von Willebrand factor to GP Ibalpha of the platelet glycoprotein complex Ib-V-IX. In our study, we analyzed 300 samples including those of patients with hereditary von Willebrand disease. The results obtained with the HaemosIL assay were compared to von Willebrand factor activities determined by established procedures. Activities determined with HaemosIL correlated with those activities determined as ristocetin cofactor (r = 0.88, p < 0.0001), collagen-binding (r = 0.93, p < 0.0001), and GP Ib-binding (r = 0.91, p < 0.0001). The comparability of results obtained by HaemosIL and the GP Ib-binding ELISA were excellent ([HaemosIL] = 0.96 infinity activity [GP Ib-binding ELISA] + 10.7), whereas activities determined by ristocetin cofactor or collagen-binding revealed more variance. Like the other assays, the HaemosIL failed to indicate a loss of high-molecular-weight von Willebrand factor multimers. The HaemosIL assay can replace the GP Ib-binding ELISA for the determination of von Willebrand factor activity. Advantages of this assay include accuracy of results, full automation, and, thus, broad availability. Since the assay does not predict the absence of high-molecular-weight multimers, multimeric analysis remains the procedure of choice for the differentiation of functional defects.

Automation↗

Recombinant activated factor VII in the treatment of near-fatal bleeding during pediatric brain tumor surgery. Report of two cases and review of the literature.

Recombinant activated factor VII (rFVIIa) was successfully used in two pediatric cases to control microvascular bleeding during brain tumor surgery. The agent demonstrated a marked effect on the intraoperative blood coagulation after failure of conventional therapy with fresh-frozen plasma, platelet concentrates, and inhibition of the fibrinolytic system. Remarkably, rFVIIa was effective in the present cases in which assessment of hemostasis yielded normal results. The use of rFVIIa should be considered in otherwise untreatable microvascular bleeding in pediatric neurosurgery.

Adolescent↗

[Spontaneous coronary spasm as a rare cause of survived sudden cardiac death].

CASE REPORT: A 39-year-old man was admitted to our intensive care unit after successful resuscitation because of ventricular fibrillation with clinical and electrographic signs of acute myocardial infarction. Coronary angiography showed normal coronary arteries. MINC syndrome (myocardial infarction with angiographically normal coronary arteries) was due to a severe proximal spontaneous spasm of the left anterior descending artery (LAD). Intracoronary ultrasound imaging demonstrated an eccentric fibrous plaque in the proximal segment of LAD and a fibrofatty plaque distal to the spastic segment. At the time of electrophysiologic study, the patient was noninducible. After starting therapy with calcium antagonist, nitrate and molsidomine, the patient was stable and symptom-free. CONCLUSION: Coronary spasm without significant organic stenosis is an important cause of sudden cardiac arrest and MINC syndrome. Because of the good prognosis under adequate treatment, exact diagnosis is important in the prevention of sudden death.

Adult↗