What Are the Causes of Fever with Thrombocytopenia?

Secondary thrombocytopenia, also known as acquired thrombocytopenia, is secondary to thrombocytopenia caused by other diseases and involves a considerable number of diseases. Such as drug-induced immune thrombocytopenia, other immune thrombocytopenia such as Evans syndrome, chronic lymphocytic leukemia, various acute leukemias, lymphomas, systemic lupus erythematosus, rheumatoid arthritis, hyperthyroidism and so on.

Secondary thrombocytopenia

nickname: Acquired thrombocytopenia
Visiting department: Dermatology
Common locations: skin

Common causes: Platelet dysfunction
Common symptoms: Reduced platelet production, excessive platelet destruction, and abnormal platelet distribution

Symptoms and signs of secondary thrombocytopenia

1. There is an incubation period before the occurrence of bleeding symptoms of drug-induced immune thrombocytopenia. The short-term can occur within hours after taking the medicine, and the elderly can develop it within months. Usually 5-10 days. It is often accompanied by chills, fever, headache, nausea, and vomiting.

Second, other immune thrombocytopenia patients with manifestations of systemic skin purpura, epistaxis or menstrual bleeding, fatigue, pale, deep urine. Occasionally, signs of kidney damage such as hypertension, hematuria, and azotemia can be seen. Nervous system symptoms are rare.

Third, coagulopathy

1. Aplastic anemia and myelopathic diseases: Aplastic anemia caused by various reasons has the characteristics of reduced bone marrow megakaryocytes and decreased platelet production. Platelet reduction can be the earliest manifestation of aplastic anemia, It is possible that hemoglobin and granulocytes returned to normal after treatment, and platelets have not recovered. Myelopathic diseases such as thrombocytopenia during infiltration of cancer, most of the tumor cells damage the megakaryocytes and thin legs, so the platelet production is reduced. Examination of the bone marrow in the above two cases can confirm the diagnosis. The former has low bone marrow hyperplasia and reduced megakaryocytes; the latter can detect tumor cells.

2, physical and chemical factors inhibit the bone marrow: physical and chemical factors such as ionizing radiation, alkylating agents, anti-metabolites, cytotoxic agents, etc. In the treatment of malignant tumors, thrombocytopenia is a common complication, or directly poisons bone marrow cells, or an immune response occurs. Most of these factors cause diffuse damage to the bone marrow, and patients show reduced whole blood. However, megakaryocytes are sensitive to the effects of radiation in a small number of patients. Because of certain diseases, they can only show thrombocytopenia and megakaryocytes.

3. Factors that selectively inhibit megakaryocytes: chlorothiazide drugs and their synergists can cause platelet reduction, in addition to the mechanism by which platelet antibodies are produced, also by inhibiting platelet production. And the latter is more important. Generally believed to be a pharmacological effect. Patients show suppressed bone marrow, megakaryocytes are reduced, and mild asymptomatic patients can take up to 25% of the drug. Individual pregnant women taking this medicine can cause congenital thrombocytopenia in the newborn, and the mother may be asymptomatic.

4. Poor megakaryocyte production: The disease is rare, and megakaryocytes and platelets are significantly reduced, often accompanied by congenital malformations, such as kidney, heart, bone graft, etc. The prognosis is poor, and about 2/3 of children die from intracranial hemorrhage within 8 months. Rubella during pregnancy and oral D860 may be the cause of the disease.

5. Other: Estrogen can occasionally cause megakaryocyte-free thrombocytopenia. Ethanol can inhibit platelet production, which is the more common cause of chronic thrombocytopenia caused by long-term heavy drinking. There are few clinical manifestations of bleeding, and platelets can be recovered after stopping drinking.

IV. Ineffective platelet production The disease is common in some patients with megaloblastic anemia with vitamin B <sub> 12 </ sub> or folic acid deficiency, which manifests as thrombocytopenia, some patients have a tendency to bleeding, and some manifest as whole blood Decreased, bone marrow megakaryocytes are normal or even increased, so it is ineffective platelet production. With the treatment of infantile poverty, platelets can return to normal.

V. Thrombopoietin deficiency This disease is due to thrombocytopenia due to congenital thrombopoietin deficiency. The disease is mostly hereditary, with hemorrhage from infancy, decreased platelet counts, normal megakaryocyte numbers, and no special changes in morphology and structure.

Six, periodic thrombocytopenia This disease is a bleeding disorder caused by periodic thrombocytopenia of unknown cause. The disease is more common, and thrombocytopenia and thrombocytosis or normal appear alternately at regular intervals, the interval is usually 20-30 days. The disease is more common in women, and its onset is often consistent with menstruation. Platelets are reduced during menstruation and bleeding is increased. Megakaryocytes generally do not decrease, mainly skin and mucous membrane bleeding, and there is no specific treatment.

Seven, thrombocytopenia caused by spleen disease Under normal circumstances, 1/3 of the platelets in the body are stagnated in the spleen. When there is splenomegaly, such as portal hypertension, Gaucher disease, lymphoma, sarcoidosis, Folty syndrome, etc. , Platelet count can be reduced, but the total amount of platelets in the body does not decrease. Injection: After epinephrine, the platelet count can increase significantly within a certain period of time. Sometimes, there may be factors that increase platelet destruction.

Eight, infectious thrombocytopenia This disease is a thrombocytopenic bleeding disease caused by a virus, bacteria or other infection.

1. Viral infections: Viral infections that can cause thrombocytopenia include measles, rubella, herpes simplex, chickenpox, cytomegalovirus infection, viral hepatitis, influenza, mumps, infectious mononucleosis, epidemic hemorrhagic fever, cats Claw fever, dengue fever, etc. The virus can invade megakaryocytes and reduce platelet production. The virus can also adsorb to platelets, resulting in increased platelet destruction; certain patients with severe measles and patients with epidemic hemorrhagic fever consume platelets due to diffuse intravascular coagulation.

2. Bacterial infections: Many bacterial infections can cause thrombocytopenia, including Gram-positive and negative bacterial sepsis, meningococcus, bacteremia, typhoid fever, tuberculosis, bacterial endocarditis, scarlet fever, brucellosis. Bacterial toxins inhibit platelet production or increase platelet destruction, and can also increase platelet consumption due to toxins affecting the function of blood vessel walls. In short, in patients with pure thrombocytopenia, if there is a clear sign of infection, the disease should be considered. After the primary infection is controlled, the platelet recovers.

Causes of secondary thrombocytopenia

In this type of disease, platelet numbers are normal, but blood clots do not form normally and bleeding time is prolonged. Platelet dysfunction may be caused by endogenous platelet defects or by exogenous factors that alter its normal platelet function. Defects in platelets may be hereditary or acquired. Tests of the coagulation stage to stop coagulation (such as PTT and PT) are normal in most cases, but not all. Due to the widespread use of aspirin that affects platelet function, acquired platelet dysfunction is common, and many other drugs can cause platelet dysfunction. Many clinical diseases (such as myeloproliferative diseases, myelodysplastic diseases, uremia, macroglobulinemia, multiple myeloma, cirrhosis, and systemic lupus erythematosus) can also affect platelet function. Aspirin can slightly extend the bleeding time of normal subjects, but it can make the bleeding time significantly for patients with original platelet dysfunction or severe hemagglutination disorder (such as the treatment dose of heparin or severe hemophilia) extend. During extracorporeal circulation, blood flow through the pump oxygenator can cause platelet dysfunction and prolong bleeding time. Regardless of the patient's platelet count, platelet concentrate should be given whenever there is significant bleeding and prolonged bleeding after cardiac surgery. Platelet dysfunction appears to be mainly due to activation of fibrinolysis on the surface of platelets, leading to the loss of platelet membrane glycoprotein Ib binding sites to VWF. The literature reports that during surgery extracorporeal circulation, administration of aprotinin, a protease inhibitor that neutralizes plasmin activity, can prevent prolonged bleeding time and reduce the amount of blood transfusion. Patients with uremia may have prolonged bleeding of unknown cause due to chronic renal failure. During effective dialysis, bleeding time can be temporarily reduced after the introduction of cryoprecipitate or desmopressin. Infusion of red blood cells or injection of erythropoietin can increase the number of red blood cells and shorten the bleeding time.

Complications of secondary thrombocytopenia

Severe patients may have vomiting blood, blood in the stool, very few patients may have intracranial hemorrhage, manifestations of intracranial hypertension, and even coma.

Clinical manifestations of secondary thrombocytopenia

Reduced platelet production, which is common in blood diseases such as aplastic anemia and acute leukemia, and after the application of certain chemotherapy drugs, often accompanied by anemia and leukopenia;

Excessive platelet destruction, most of which are unknown, and some of them are secondary to autoimmune diseases and certain drugs;

The distribution of platelets is abnormal, which is common in splenomegaly.

Diagnosis of secondary thrombocytopenia

I. Significance of Bleeding Time (BT) Measurement Prolonged bleeding time is found in abnormal vascular structures or functions: such as scurvy, telangiectasia, and von Willebrand disease. Platelet count abnormalities: such as thrombocytopenic purpura and thrombocytosis caused by various reasons. Platelet dysfunction: such as platelet disease, platelet weakness. Others: such as hypofibrinogenemia, primary and secondary fibrinolysis, and anticoagulant substances in the blood circulation.

Significance of Aspirin Tolerance Test This test is an important method for diagnosing vascular pseudohemophilia. The bleeding time of mild patients in this disease can still be normal, but the bleeding time can be prolonged after taking aspirin.

3. Capillary fragility test Significance: More than 10 new bleeding points are positive, indicating increased capillary fragility, which can be seen in the following situations: abnormal capillary wall: such as hereditary hemorrhagic capillary dilatation, allergic purpura, scurvy, Infectious vascular purpura. Thrombocytopenia: such as primary or secondary thrombocytopenic purpura. Platelet dysfunction diseases: such as platelet asthenia, platelet disease, drugs and certain diseases cause platelet acquired functional defects.

IV. Significance of von Willebrand Factor (VWF) determination The reduction of von Willebrand factor is seen in: von Willebrand disease and carriers of Hemophilia. Increased vascular pseudohemophilic factors are found in: endothelial injury, such as ischemic cardio-cerebral vascular disease, peripheral vascular disease; hypercoagulable state diseases, such as nephrotic syndrome, pregnancy hypertension, uremia, etc .; other such as After major surgery, diabetes, hyperlipidemia, DIC, etc. V. Significance of 6-keto-prostaglandin F1a (PG F1a) determination 6-keto-prostaglandin reduction is seen after congenital platelet arachidonic acid metabolism deficiency disease or oral non-steroidal anti-inflammatory drugs such as aspirin; hypercoagulable state and Thrombotic diseases, such as coronary heart disease, cerebral arteriosclerosis, cerebral thrombosis, diabetes, glomerular disease, peripheral vascular thrombosis, etc.

Treatment of secondary thrombocytopenia

1. Since the thrombocytopenia of this disease is secondary, it is critical to treat the primary disease, and the platelet count often improves with the improvement of the primary disease.

2. The etiology of this disease is complex and can be caused by poisoning, drug allergies, infections, autoimmunity, dyslipidemia, genetic factors, etc. There is no special treatment for western medicine. Early application of traditional Chinese medicine is necessary.

Differential diagnosis of secondary thrombocytopenia

The disease needs to be distinguished from primary thrombocytopenia

Preventive care for secondary thrombocytopenia

1. Actively participate in sports activities. Enhance physical fitness. Improve disease resistance.

2. Pay attention to prevent respiratory infections. measles. chicken pox. Rubella and hepatitis. Otherwise it is easy to induce or aggravate the condition.

3. Acute phase or when the amount of bleeding is large. Go to bed. Restrict activities. Eliminate their fear and tension.

4. Avoid trauma and collision. So as not to cause bleeding.

5. When the platelet count is lower than 20 × 109 / L. Close observation of changes in the condition. Prevent various traumas and intracranial bleeding.

6. The diet should be light. Rich in nutrition. Easy to digest. Hematemesis. Those with blood in the stool should enter a semifluid diet. Avoid hard food and crude fiber food. Avoid spicy food. Usually eat more peanuts with clothing. Jujube and other food.