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    Home > Active Ingredient News > Antitumor Therapy > Trusso syndrome: 1 case

    Trusso syndrome: 1 case

    • Last Update: 2022-11-25
    • Source: Internet
    • Author: User
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    01

    Preface

    The relationship between tumors and blood clots was first observed by Trousseau in 1865, hence the name Trousseau syndrome
    .
    Trusso syndrome is a paraneoplastic syndrome caused by hypercoagulability of malignant tumors leading to intravenous thrombosis, the pathogenesis is complex and unclear, mainly manifested as malignant tumor-related myocardial infarction, cerebrovascular accident and other arteriovenous embolic diseases; Acute cerebral infarction is a manifestation of Trusso syndrome that is easily overlooked
    .

    02

    Case history

    The 68-year-old male patient was admitted to the Department of
    Neurology of Tai'an Municipal Hospital due to dizziness, unsteady walking, flexible limb movement, and no slurred speech on November 19, 2020.
    During hospitalization, the laboratory repeatedly examined that D dimer was progressively increased, and conventional anti-platelet aggregation, lipid-lowering and stabilizing plaque, improving cerebral circulation, protecting brain cells and other treatments, the condition was progressively aggravated, and dysphagia, limb weakness, and confusion gradually
    appeared.

    Combined with the history of lung cancer, the condition did not progress after adjusting the treatment plan and adding low molecular weight heparin calcium, and the D-dimer decreased to 1.
    21mg/L after 3 days, and the D-dimer was reduced to normal after 2 weeks, and the low molecular weight heparin calcium was discontinued, and rivaroxaban tablets were taken orally
    .
    The final diagnosis: Trusso syndrome
    .

    03

    Case study

    The patient is an elderly man, acute onset, progressive exacerbation, consistent with progressive stroke manifestations, although there is basilar artery stenosis, but the patient has no other arteriosclerosis basis except mild hypertension, and conventional antiplatelet and improve circulation and other treatment effects are poor, combined with the patient's previous history of pulmonary mucus adenocarcinoma, the D-dimer in the course of the disease is progressively increased, the condition has not progressed after adjusting the treatment plan plus low molecular weight heparin calcium and other treatments, and after stopping anticoagulants on its own, lower extremity venous thrombosis and pulmonary embolism appear, Stable with re-anticoagulation, so the diagnosis: Trusso syndrome is clear
    .

    Admitted to the hospital on November 19, 2020, laboratory tests: blood routine, electrolytes, liver function, renal function, lung tumor markers, blood routine, urine routine, fecal sediment analysis results were normal, D dimer 0.
    64mg/L
    .
    The 24th D dimer was 4.
    19mg/L, and the 27th D dimer was 5.
    23mg/L
    .

    On November 27, when the LIS audit report found that the patient's D dimer continued to rise since 11.
    19, I quickly checked the patient's case, and the clinical treatment has been in routine antiplatelet and improve circulation, which should not occur according to conventional cases
    .

    Re-examination in accordance with the specimen re-examination process; Specimen review: the specimen had good traits, and no abnormalities such as fibrous, clot, hemolysis, etc.
    were found; Instrument status: the instrument is in good condition, quality control status: the indoor quality control of the project is under control
    .

    In order to exclude the false positive of D dimer, the dilution method was used to dilute 2 times, 4 times, 8 times, 16 times dilution, the results were linear, basically determined that there was no interference agent, and fibrinogen degradation products were also increased, excluding the false increase
    of D dimer.
    The accuracy of
    the results was further determined.
    After sending the results, the clinician was contacted, and the doctor had noticed the progressive increase in the patient's D dimer, adjusted the treatment regimen, and added low molecular weight heparin calcium
    .

    04

    Knowledge expansion

    One.
    Patients with malignant tumors have spontaneous recurrent migratory arteriovenous thromboembolism
    complicated by different degrees of coagulation and fibrinolysis mechanisms during the pathogenesis.
    The formation of a thrombus activates the fibrinolytic system, and plasmin can cut long chains of fibrin, eventually forming multiple fragments
    .
    The simplest D-D structure is the D dimer
    .
    D dimer levels in plasma are positively correlated
    with the number of large intracranial vessels involved in infarct foci.

    Two.
    D-dimer is a specific fibrin degradation product
    produced by plasmin hydrolysis of cross-linked fibrin.
    Its production or increase reflects the activation of the coagulation system and fibrinolytic system, and can be used as an auxiliary diagnosis
    of thrombotic diseases.
    However, due to its many influencing factors, false positive results are prone to occur, and it is now mostly used for the negative elimination index
    of thrombosis.
    D-dimer and other fragments should theoretically be included, and when FDP and D-dimer results are inverted, false positives
    for D-dimer are often indicated.

    In the case of quality control, D-dimer > FDP results have the following common influencing factors:

    1.
    Quality control before inspection, check whether the specimen has small clots, lipid turbidity, jaundice, hemolysis, etc
    .

    2.
    The specimen may contain heterophile antibodies (HA) and rheumatoid factor (RF), which can falsely increase
    the results.

    3.
    Special groups, such as tumor patients, pregnant women, estrogen therapy patients, etc
    .

    After excluding the above factors, D-dimer≥FDP can refer to the D-dimer≥FDP treatment process

    05

    Case summary

    Clinically, if the imaging finds multi-region, multifocal acute cerebral infarction, which is not consistent with the distribution of macrovascular area and watershed area, and is accompanied by significantly elevated D-dimer on laboratory examinations, in addition to screening traditional cerebral infarction risk factors, such as hypertension, diabetes, coronary heart disease, hyperlipidemia, smoking, alcoholism, homocysteinemia, etc.
    , it should also pay attention to the screening of systemic risk factors, be vigilant against Trusso syndrome, detect it as soon as possible, intervene in time, prevent and treat complications and further deterioration of the condition, reduce the pain of patients, and improve the cure rate

    D dimer is the most important indicator
    of thrombosis and thrombolytic activity.
    In recent years, it has become an essential indicator
    for the diagnosis and clinical detection of many other diseases.
    In deep vein thrombosis and pulmonary embolism, venous thromboembolism cannot be diagnosed based on elevated D dimer alone, but negative D dimer can basically exclude VTE
    .

    Elevated disseminated intravascular coagulation (DIC)D dimer is of high value for early diagnosis of DIC, usually rising several days before DIC occurs and showing higher than normal
    .
    In acute ischemic stroke, D dimer levels generally increase mildly in the first week of onset, increase significantly in 2 to 4 weeks, and return to normal
    .
    In addition, D dimer is elevated again, indicating a relatively high
    risk of cerebral infarction.
    Severe mycoplasma pneumonia is often accompanied by an increase in D dimer levels, and patients with severe mycoplasma pneumonia have significantly higher D dimer levels than mild cases
    .
    It is challenging to identify the causes of elevated D dimers, and to contact clinicians in a timely manner to improve the diagnostic value
    of D dimers in the clinic.

    06

    Expert reviews

    PLA 960 Hospital Chief Physician Zhang Jintao

    In addition to arterial cerebral infarction, this case has venous thrombosis and pulmonary embolism, and anticoagulation is effective, which is typical of Trusso syndrome
    .
    Mucin-producing tumors in the clinic are more likely to cause Trusso syndrome, such as gastric cancer, lung cancer, pancreatic cancer and ovarian cancer, the blood of these tumor patients is hypercoagulable, due to the increase in procoagulant activity in the body, anticoagulant activity is reduced, it should be noted that the survival rate of patients with Trusso syndrome for more than 1 year is only 12%, and the primary tumor is actively treated to improve the survival rate
    of patients.
    For patients with new-onset cerebral infarction, especially patients with few risk factors, significantly elevated D dimer, and multivascular area infarction, it is necessary to screen for tumors
    .

    This case fully reflects the importance of laboratory examination in clinical diagnosis, and provides ideas for communication between laboratory departments and clinical departments to improve the accuracy and efficiency of clinical diagnosis
    .

    References

    [1] LIU Haihua, LV Xiaohui, LIU Chenglong, et al.
    Pancreatic cancer with multifocal cerebral infarction:A case of Trusso syndrome[J].
    Chinese Journal of Neurology,2019,99(18):1432.
    )

    [2] CHENG Qiantao, CAO Xiangyang.
    A case of gastric cancer complicated with Trusso syndrome with cerebral infarction as the first symptom[J].
    Chinese Journal of Neurology,2014,47(3):213.
    )

    [3] CHENG Xuejiao, YI Ran, DONG Qi, et al.
    Research progress of Trousseau syndrome[J].
    Chinese Journal of Clinical Neuroscience,2019,27(01):90-97+112.
    )

    [4] LIU Haihua, LV Xiaohui, LIU Chenglong, et al.
    Pancreatic cancer with multifocal cerebral infarction:A case of Trusso syndrome[J].
    Chinese Journal of Neurology,2019,99(18):1432.
    )

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