We report the case of 64-year-old female patient with pulmonary embolism and bilateral femoropopliteal deep vein thrombosis caused by heparin-induced thrombocytopenia type II (HIT II) resistant to danaparoid sodium and subsequently administered lepirudin in whom a single late plasmapheresis performed on day 6 of the initiation of treatment of HIT reversed the course of the disease, preventing its highly potential fatal outcome. Primarily administered lepirudin was not only ineffective but even led to further aggravation of the patient's clinical state and platelet count drop in the first stage of the HIT treatment. The improvement of the patient's clinical state was not achieved before therapeutic plasma exchange (TPE) had removed the greatest part of pathogenetic circulating substrate. Only after TPE, lepirudin, introduced again, led to the platelet count recovery. In the subsequent course of the treatment, lepirudin was combined with an overlapping oral anticoagulant. Previously positive heparin aggregation test and fast particle gel heparin-platelet factor 4 immunoassay were normalized as well as the patient's clinical status. Early plasmapheresis, administered within 4 days of the onset of thrombocytopenia in HIT, as a beneficial therapeutic measure in certain individual cases, is indisputable. However, our results do not concur with previously reported findings of the so far most comprehensive study on plasmapheresis performed in the management of HIT with thrombosis, discrediting late plasmapheresis administered 4 days after the onset of the disease not only as ineffective, but even as an aggravating factor. Our results suggest the possible beneficial impact of late plasmapheresis as a method that may reverse a prothrombotic process and lead to a fast improvement in the patient's platelet count, especially in cases initially resistant to thrombin inhibitors.
METHODS:A total of 30 patients with typical histological and immunohistochemical SMZL patterns were examined. Splenectomy plus chemotherapy was applied in 20 patients, while splenectomy as a single treatment-option was performed in 10 patients. Prognostic factor and overall survival rate were analyzed.
RESULTS:Complete remission (CR) was achieved in 20 (66.7%), partial remission (PR) in seven (23.3%), and lethal outcome due to disease progression occurred in three (10.0%) patients. Median survival of patients with a splenectomy was 93.0 mo and for patients with splenectomy plus chemotherapy it was 107.5 mo (Log rank = 0.056, P > 0.05). Time from onset of first symptoms to the beginning of the treatment (mean 9.4 mo) was influenced by spleen dimensions, as measured by computerized tomography and ultra-sound (t = 2.558, P = 0.018). Strong positivity (+++) of CD20 antigen expression in splenic tissue had a positive influence on OS (Log rank = 5.244, P < 0.05). The analysis of factors interfering with survival (by the Kaplan-Meier method) revealed that gender, general symptoms, clinical stage, and spleen infiltration type (nodular vs diffuse) had no significant (P > 0.05) effects on the OS. The expression of other antigens (immunohistochemistry) also had no effect on survival-rate, as measured by a χ 2 test (P > 0.05).
CONCLUSION:Initial splenectomy combined with chemotherapy has been shown to be beneficial due to its advanced remission rate/duration; however, a larger controlled clinical study is required to confirm our findings.
We present the case of a 64 year-old female patient, with a clearly positive family history of venous thromboembolism (VTE), multiple VTE episodes (massive pulmonary embolism, ovarian venous plexus thrombosis, deep venous thrombosis with submassive pulmonary embolism and second deep venous thrombosis) and myocardial infarction. Laboratory tests revealed the resistance to the activated protein C, elevated FVIII and PAI-1. The patient was found to be a heterozygous carrier of FV Leiden, MTHFR C677T and PAI-1 4G/5G mutations. She was diagnosed with essential thrombocythemia at the age of 60. The thirty-three-year follow-up of our patient and detection of recurrent thrombotic episodes in the light of multiple coagulation defects with proved acquired risk factors, contributes to the risk stratification in the group of patients with very high risk. In case of our patient, we stress inadequacy of widely-accepted standard prevention measures. In our opinion, patients with very high risk require additional mechanic and specific medicament methods of VTE prevention.
The stated prognostic factors that include age, cytogenetics findings and granulocytic dysplasia analysis could contribute to adequate risk stratification of t-AML, though fuller results would require additional analyses.
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