New Thrombocytopenia Cure

Conquer Low Platelets

Alternative And Natural Therapies For Itp (idiopathic Thrombocytopenia Purpura). Live Free From Itp. Complete Program To Increase Platelets. This Is What You Will Learn With this Guide: The Two Herbs That can help bring up your platelets. The Two Vitamins needed to keep those platelets from dropping. What foods may cause your platelets to drop. How science has confirmed the benefits of these herbs in their use with low platelets. Why your doctor may not know about these natural alternatives and how you can assist him in helping you. Different tests that naturopathic doctors do to determine your real state of health that may reverse the course of your body drastically. Understand some of the reasons why people develop low platelets. Discover how your digestive tract may be the culprit to your low platelet level problems. How you can prevent the most drastic step a splenectomy. How you can restore your health so that you dont need any more dangerous drugs. Get your life back and stop ending up in the hospital all the time. Learn why your immune system is attacking your platelets and how to calm it down. Learn what over the counter medications to stay away from if you have low platelets Read more here...

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Duration of thrombocytopenia

Use of GMCSF was associated with significantly greater thrombocytopenia (Table 17.52). The median nadir platelet count after control cycles was 59 X 109 l versus 29.5 X 109 l with GMCSF cycles (p < 0.0001). GMCSF also prolonged platelet recovery time (> 75 X 109 l) (GMCSF, 16 days versus control, 14 days p 0.0001) and patients randomized to receive GMCSF had a significantly greater platelet transfusion requirements (p < 0.0001).

Discharge And Home Healthcare Guidelines

The cardiovascular system becomes depressed, leading to depression of the vasomotor center in the brain and to hypotension. Conversely, in some individuals, intoxication causes the release of catecholamines from adrenal glands, which leads to hypertension. Intoxication depresses leukocyte movement into areas of inflammation, depresses platelet function, and leads to fibrinogen and clotting factor deficiency, thrombocytopenia, and decreased platelet function.

HIV and Kidney Disease

Thrombotic microangiopathy in the setting of HIV infection is being increasingly recognized and has even been proposed as an AIDS-defining illness. It is seen more often in Caucasians as compared with African-Americans or Hispanics. Features include fever, diarrhea, hemolytic anemia, thrombocytopenia, renal failure, and neurological symptoms. Mortality rates are high even in the setting of aggressive treatment like plasma exchange and relapse is often seen in survivors. The pathogenesis of HIV-associated thrombotic microangiopathies is unknown.

Clinical manifestation

Bite minimally symptomatic fewer than 10 of bites result in severe skin necrosis signs of progression within 48-72 hours of the bite mild-to-severe pain beginning 2-8 hours after bite central papule and associated erythema occur 6-12 hours after bite purple vesicle sometimes ulcerates stellate necrotic area sometimes ensues. Constitutional signs and symptoms hemol-ysis hemoglobinuria thrombocytopenia disseminated intravascular coagulation fever headache malaise arthralgia nausea vomiting

PThalassemia Phenotype With Normal pGlobin Gene Sequences

A limited proportion of individuals with the p-thalasse-mia carrier phenotype show completely normal p-globin gene sequences as well as normal LCR sequences. Recently, mutations in the general transcription factor TFIIH coding for a specific helicase have also been shown to be associated with p-thalassemia carrier phenotype besides tricothiodystrophy. Furthermore, depending on the site of mutation, mutations in GATA-1 resulted either in dyserythropoietic anemia and thrombocytopenia or thrombocytopenia and p-thalasse-mia carrier phenotype. The results indicate that the p-thalassemia carrier phenotype may result from mutation in a transcription factor regulating the function of the p-globin gene.

Segregation of BVDV into Two Genotypes

However, the recognition of hemorrhagic syndrome in the late 1980s and early 1990s brought the concept of severe acute BVD once more to the forefront. Case records of cattle admitted to the Cornell College of Veterinary Medicine for the years 1977-87 revealed that 10 of clinically acute BVD infections in adult cattle were associated with thrombocytopenia. During this period an outbreak in the state of New York resulted in 50 of 100 animals in a milking herd becoming ill and 20 of them subsequently dying. Clinical signs included high temperatures, bloody diarrhea, hemorrhages, and prolonged bleeding from venipuncture sites. This disease came to be considered as a distinct form of severe acute BVD termed hemorrhagic syndrome. Severe acute BVD cases were reported with increasing frequency in North America in the early 1990s. These outbreaks were particularly devastating in the Canadian provinces of Quebec and Ontario. The disease in some ways resembled MD, but...

Pathology and Histopathology

A severe thrombocytopenia develops once infected animals develop fever and virus is detectable in peripheral blood. Currently, there are two explanations for thrombo-cyte depletion (1) abnormal peripheral consumption of thrombocytes may be responsible for thrombocytopenia and (2) progressive degeneration of megakaryocytes, which is observed to begin at day 1 p.i., can result in cell death and shortage of thrombocyte production. It is not clear whether direct or indirect effects are responsible for the latter phenomenon. In analogy to the clinical picture, the severity of pathological lesions depends on time of infection, age of the animal, and virulence of the strain.

Special Investigations

Abnormal findings include anemia, thrombocytopenia, coagulopathy, hyponatremia, and raised urea and creatinine. Hypocalcemia may occur in some cases, subsequent to the chelation of ionized calcium by triglycerides liberated by bacterial lipases. Leukocytosis with a white cell count above 15,000 mm3 and a left shift is found in more than 90 of cases. Neutrophilia indicates overwhelming bacterial infection. It is noteworthy that leukocytosis may not be present in immunosuppressed patients (Baskin et al. 1990 Laucks 1994). Anemia maybe present as part of the septic profile. Coagulopathy may be indicated by a raised prothrombin time (PT) and partial thromboplastin time (PTT), and thrombocytopenia. Raised fi-brinogen levels and positive D-dimers may herald the onset of disseminated intravascular coagulation (DIC).

Clinical Description

Although some patients are asymptomatic with coincidental detection of a leukocytosis on routine medical evaluation, the chronic phase of disease typically has an insidious onset with symptoms related to hypermetabo-lism, including fatigue, anorexia, weight loss, and night sweats. Massive splenomegaly is common. With disease progression, patients typically develop worsening anemia and thrombocytopenia. Without treatment, the median survival of CML is 4-5 years from diagnosis.

Trials with Multiple Agents

It is common in oncology to treat patients with drug combinations. Often, the dose of one agent is fixed and the goal is to find the MTD of the other agent administered in combination. Sometimes, two or three doses of one of the agents are selected with the goal of finding the MTD of the second agent for each dose of the first agent. For example, Rowinsky et al. (1996) described a trial where five doses of topote-can and two doses of cisplatin were selected for the study. Since topotecan and cisplatin cause similar toxicities such as severe neutropenia and thrombocytopenia it was not possible to distinguish which drug caused toxicity. Ivanova and Wang (2004) suggested conducting a single trial that uses the assumption of toxicity monotonicity in both directions, that is, for each agent toxicity is nondecreasing with dose when the dose of the other agent is fixed. Their nonparametric design for the problem uses the bivariate isotonic estimate of the probability of toxicity and is...

Clinical Experience with Drotrecogin Alfa Activated

Drotrecogin alfa (activated) was first tested in humans in 1995. At the time of the writing of this review, over 300 normal, healthy subjects have participated in multiple studies demonstrating the safety and pharmacokinetic profile of the protein. Regulatory approval of drotrecogin alfa (activated) was based on data from a single, randomized, placebo-controlled, phase III study 47 with supporting data from a single, randomized, placebo-controlled, phase II study 46 . The phase II study, completed in 1998, investigated multiple infusion rates and infusion durations of 48 and 96 h. Measures of coagulopathy (D-dimer, platelet count, fibrinogen level) was the primary endpoint of the effect of drotrecogin alfa (activated). In most patients, the platelet count and fibrinogen levels were normal and no effect of drotrecogin alfa (activated) therapy was observed 46 . However, concentrations of D-dimer were elevated in almost all patients. The decrease in D-dimer was only evident with infusion...

Primary Nursing Diagnosis

Since DIC always occurs in association with another condition, medical treatment focuses on correcting the underlying disorder. In addition, the physician seeks to return the patient to normal hemostasis. Active bleeding is managed by blood component therapy. To ascertain the success of cell and factor replacement, constant surveillance of laboratory values is critical to determine which blood components should be administered. In general, packed red blood cells are used to improve oxygen delivery by increasing the hemoglobin content of the blood. Fresh-frozen plasma replaces many of the clotting factors, whereas cryoprecipitate is the best source of fibrinogen and factors V VIII, and XIII. Platelet transfusion is used when the platelet count falls below 100,000 mm3.

Immunophenotypic Analysis of Platelets

Resting platelets constitutively express many surface glycoproteins that are easily identified by flow cytometry. Upon platelet activation, many surface receptors are modulated in both copy number and conformation, while others, absent from the resting platelet surface, are newly expressed. This unit describes several strategies to evaluate platelet function by evaluating surface receptor expression on resting and activated platelets using flow cytometry. Three methods are described here in detail determination of resting platelet surface receptor expression (see Basic Protocol 1 and Alternate Protocol) determination of platelet activation using P-selectin (CD62P) expression (see Basic Protocol 2), which reflects platelet a-granule release (McEver, 2001), or PAC1 binding, which detects the activated conformation of glycoprotein (GP) IIb-IIIa (integrin aIIbp3 Shattil et al., 1985) and determination of procoagulant platelets and platelet-derived microparticles using annexin V binding or...

Symptomatic Management

Whereas in the past, splenectomy was frequently performed for the management of severe thrombocytopenia and or for relief of mechanical compression by the greatly enlarged spleen, by removing the main reservoir for Gaucher cells, splenectomy may induce or aggravate liver and bone involvement. Today, splenectomy is rarely indicated.

Ethical And Societal Considerations

Gaucher disease is caused by an enzymatic defect with consequent accumulation of glucocerebroside. Type I, the nonneuronopathic form, is rather common, with a predilection among Ashkenazi Jews. There is tremendous variability in age of onset, severity, and phenotypical expression in this type. Symptomatic presentation may include hepatosplenomegaly, anemia, thrombocytopenia, and skeletal or lung involvement. Life expectancy is unimpaired. The neuronopathic forms are pan-ethnic with a continuum of neurological and visceral signs and symptoms, and with decreased life expectancy. Diagnosis is performed by assay of p-glucocerebrosidase activity, and molecular analysis of mutations may broadly define genotype-phenotype correlations. ERT has proven to be safe and effective in ameliorating disease symptoms and signs however, it involves life-long intravenous therapy, is costly, and is incapable of crossing the blood-brain barrier. Thus, other forms of treatment, including bone marrow...

Development of Ceredase

The clinical trial that led to the approval of Ceredase was conducted on 12 patients, 4 adults and 8 children who were classified with Type I Gaucher Disease. Patients were given 60 IU of Ceredase kg of body weight by intravenous infusion once every 2 weeks for between 9 and 12 months. Part way through the trial, the dose of two severely affected children was increased to 60 IU kg every week. All patients in the trial showed a clinical response with a reduction in spleen volume and an increase in hemoglobin. Other clinical improvements observed in several patients included a reduction in liver size, reduction in plasma glucocerebroside and serum levels of tartrate-resistant acid phosphatase (a lyso-somal enzyme that is elevated in some lysosomal storage diseases), and an increase in platelet count. Some evidence of an improvement in the bone disease was observed in three of the patients 57 .

Continuing maintenance therapy

The main toxicity during this phase of treatment is myelosuppression. The incidence and severity of this is related to the dose of 6-MP administered and to genetic variations in xenobiotic pathways of thiop-urine metabolism, principally in the polymorphisms of the enzyme thiopurine methyltransferase (TPMT).85,86 The cumulative dose of thiopurine received during the continuation period is predictive of survival.87,88 Children who never become neutropenic during continuation therapy have a poorer outcome than those who have episodes of neutropenia.89-92 Thus, the maximum tolerated dose needs to be given. As the dose tolerated varies from time to time in every child, delivering optimal therapy while preventing severe neutropenia and thrombocytopenia requires the routine monitoring of full blood counts and regular dose adjustment. If the dose is escalated too quickly, it will lead to prolonged periods of neutropenia. As therapy needs to be temporarily stopped during this time, this will...

Flow Cytometric Analysis of Reticulated Platelets

The precise identification of platelets in unseparated whole blood is an another critical aspect of the procedure. This can be achieved by the counterstaining of abundantly expressed platelet-specific glycoproteins such as GPIIb IIIa (CD41 CD61) or GPIb (CD42b) with phycoerythrin-labeled monoclonal antibodies. Such dual-color staining of unseparated whole blood samples avoids selective cell losses that may occur during the enrichment of platelets by centrifugation, and also serves as a basis for reliable platelet identification both in thrombocytopenia and in samples with abnormal platelet light-scatter characteristics.

Treatment Immunity and Prevention

There is no specific treatment for CTFV infection. Symptomatic treatment includes relief of fever and pain with paracetamol. Salicylates should be avoided because of thrombocytopenia and occurrence of bleeding disorders. An experimental vaccine (formalin-inactivated, purified CTFV) developed in the 1960s (stopped in 1970s) has been used for people at high risk of exposure to infection, and produced long-lasting immunity. After three doses, neutralizing antibodies persist for 5 years. Acaricides or repellents such as permethrin, DEET (N,N-diethyl-meta-toluamide), and picaridin may be used to control ticks in rodent niches and as repelling agents to ticks.

Assessment of the mother

Platelets are consumed due to the endothelial activation. A falling count, particularly to less than 100 x 109 l may indicate a need to consider delivery. Counts above 50 are likely to support haemostasis. An increasing haematocrit or haemoglobin indicates hypovolaemia, which is characteristic of severe disease. If labour is anticipated then clotting abnormalities should be checked as pre-eclampsia can cause disseminated intravascular coagulation. This is important if regional anaesthesia is used, which is preferable to general anaesthesia. Renal tubular function can be assessed by measuring uric acid, which is a marker of disease severity, although normal levels can occur in severe disease. Acute fatty liver can result in spuriously high levels of uric acid (along with high white cell count, and low glucose). Urea and creatinine are associated with late renal involvement and generally not useful as indicators of disease severity. Liver transaminases should be measured to indicate...

Intrapartum care of preeclampsia

Many units have now developed a severe pre-eclampsia protocol. Cases which require protocol determined management are often defined as those with severe hypertension (greater than 170 110 mmHg) or hypertension with an additional complication such as headache, visual disturbance, epigastric pain, clonus (more than three beats) or a platelet count less than 100 or AST more than 50 IU units per litre.

Description Medical Coagulation Disorders

I diopathic thrombocytopenia purpura (ITP) is an acquired hemorrhagic disorder that is characterized by an increased destruction of platelets because of antiplatelet antibodies. The antibodies attach to the platelets, reduce their life span, and lead to a platelet count below 100,000 mm3 but occasionally as low as 5000 mm3. ITP can be divided into two categories acute and chronic. Acute ITP is generally a self-limiting childhood disorder, whereas chronic ITP predominantly affects adults and is characterized by thrombocytopenia of more than 6 months. The most life-threatening complication of ITP is intracerebral hemorrhage, which is most likely to occur if the platelet count falls below 1000 mm3. Hemorrhage into the kidneys, abdominal cavity, or retroperitoneal space is also possible. Prognosis for acute ITP is excellent, with nearly 80 of patients recovering without treatment. The mortality rate from hemorrhage is 1 in children and 5 in adults. Older age and a previous history of...

Pharmacologic Highlights

Increases antibody titer and antigen-antibody reaction provides passive immunity against infection and induces rapid but short-term increases in platelet count Many children are managed as outpatients with frequent outpatient visits for therapeutics and platelet counts. If the platelet count is less than 15,000 mm3, the condition may be considered serious enough to warrant hospitalization. Institute safety precautions to prevent injury and the resultant bleeding and to assist with ambulation. Protect areas of hematoma, petechiae, and ecchymoses from further injury. Avoid intramuscular injections, but if they are essential, apply pressure for at least 10 minutes after the intramuscular injection and for 20 minutes after venipuncture. Avoid nasotracheal suctioning, if possible, to prevent bleeding. If a child is being managed as an outpatient, discuss the home environment with the parents or caregivers. Encourage the parents to set up one or two rooms at home (such as the child's...

Developmental History of the Enzyme 1051 Preclinical Development

The theoretical lack of systemic activation after rFVIIa treatment has been supported by preclinical data. Studies in the standard rabbit stasis model, developed as a thrombosis model in which injury was induced to the vessel wall, have demonstrated that rFVIIa (100 to 1000 g kg b.w.) or prothrombin complex concentrate (factor VIII inhibitor bypass activity FEIBA 50 to 100 U kg Immuno, Deerfield, IL) caused clot formation at the site of injury after 30 min of stasis (restricted blood flow). This reflects the normal pharmacological response to tissue injury. rFVIIa caused no change in platelet count or fibrinogen concentration even 3 h after administration. Furthermore, no changes were noted in anti-thrombin levels, nor was there any evidence of generation of soluble fibrin monomers, as judged by an ethanol gelation test. In contrast, FEIBA caused a significant dose-dependent decrease in platelets and fibrinogen, suggesting a general activation of the coagulation system. Administration...

Venous thromboembolism

A case for reducing the dose to intermediate or prophylactic level, but this requires an individual assessment and consideration of continuing risk factors 54 . If UFH is used this can be by either intravenous infusion, followed by 6 months subcutaneous therapeutic LMWH, or adjusted-dose subcutaneous UFH, or adjusted-dose subcutaneous UFH or therapeutic LMWH for both initial and long-term treatment. There is a case for IV UFH in massive life-threatening PE with haemodynamic compromise (where thrombolytic therapy should also be considered). With UFH a mid-interval activated partial thromboplastin time (APTT) of 1.5-2.5 times control should be achieved. However, APTT testing is often poorly performed and an apparent heparin resistance in late pregnancy can lead to unnecessarily high doses. If a woman is treated exclusively with LMWH and has not previously been exposed to UFH there is no need to monitor the platelet count otherwise this should be monitored after initiating treatment and...

Other Considerations for Small Populations

Compared with normal analysis, there is an increased importance to ensure that no false-positive events be present when analyzing rare events. In our study of NKT cells in patients with autoimmune thrombocytopenia, for example, less than 50 positive events could be counted in the samples we had available (9). Clearly then, nonspecific events can skew the data and so results that already have a CV of 20 would become less reliable. As the number of total events acquired increases, so may the number of unspecific events. Again, if a few false-positives were present in a population of 1000 positive events, this may not affect the results very much. But what if only 25 positive events were recorded using the specific antibody and 10 events appeared in the gate when the same high number of total events were acquired and those 10 events were either unlabeled or labeled with a well-chosen isotype control (that is, with the same protein fluorochrome ratio and protein concentration and...

Use of Diuretics in the Treatment of Hypertension in Pregnancy

Hypertension in pregnancy can be broadly divided into preexisting hypertension (chronic hypertension), hypertension of pregnancy (usually appearing within the first trimester, but can develop at any time) and preeclampsia eclampsia (occurring in the third trimester). Preeclampsia is characterized by hypertension, proteinuria, edema, and hyperuricemia, with or without associated liver dysfunction and coagulopathy (HELLP syndrome hemolysis, elevated liver enzymes, and low platelets). Eclampsia is diagnosed when hypertension is severe and convulsions occur. An early indication of developing hypertension in pregnancy is failure to observe the normal fall in BP during the

Involvement of Factor H in Human Disease

Hemolytic uremic syndrome (HUS) is a leading cause of pediatric kidney failures and is generally a sequela of bacterial infections. It is characterized by thrombocytopenia, microangiopathic hemolytic anemia and acute renal failure. The rare atypical HUS (aHUS) is not linked to infection, but is sporadic or familial. Full recovery from typical HUS is the norm, but the long-term diagnosis for sufferers of aHUS - 5-10 of cases of HUS - is unfavorable. Single and double amino-acid changes that occur predominantly in the C-terminal segment of CFH (CCPs 19 and 20) have been identified in 10-15 of patients with aHUS (Buddles et al. 2000 Heinen et al. 2006 Richards et al. 2001 Warwicker et al. 1998) (http www. ). In many cases the variant form of CFH is present in plasma at approximately normal levels (Kavanagh et al. 2007). Mutations in membrane cofactor protein and factor I have also been linked to aHUS. This topic has been the subject of a recent review (Kavanagh et al. 2007),...

Atypical Hemolytic Uremic Syndrome

Hemolytic uremic syndrome (HUS) causes the majority of kidney failures in children and is typically associated with bacterial infections. It is characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute renal fail-ure.30,31 A related disorder of the microvasculature is thrombotic thrombocytopenic purpura (TTP). TTP occurs mainly in adults, and is normally accompanied by neurological deficits but TTP and HUS are regarded by many clinicians as a different manifestation of the same pathophysiological process.

Hematologic Syndromes

The association of bleeding diathesis and intravascular coagulopathy abnormalities in patients with prostate cancer has been reported. Bleeding problems in the prostate cancer patient may result from the effects of the tumor on hemostatic mechanisms or from the treatment of the tumor by cytotoxic and other agents. Among the tumor-related bleeding problems are disseminated intravascular coagulation, primary fibrinolysis, thrombocytopenia, acquired platelet dysfunction, and circulating inhibitors or anticoagulants. Disseminated intravascular coagulation is associated with hypercoagulability state in most solid tumors, whereas in prostate cancer tumors the most common presentation is acute promyelocytic leukemia bleeding. Treatment-related bleeding disorders include the common problem of thrombocytopenia secondary to myelosup-pressive chemotherapy as well as the interesting micro-angiopathic hemolytic anemia syndrome associated with mitomycin C and other agents (de la Fouchardiere et al....

Chemotherapy treatment

IR patients, who achieved complete clinical remission after induction of remission therapy, proceeded to phase 2 of the treatment schedule. During this phase of treatment, IR patients were randomized to receive or not prophylactic GCSF. The phase 2 block was count dependent and chemotherapy was withheld or delayed if either the neutrophil count (ANC) and or the platelet count were < 0.2 X 109 l and 50 X 109 l respectively. GCSF commenced (10 ig kg day subcutaneously) 24 hours after completion of the cytarabine cycle and continued till the ANC and platelet counts were 0.2 X 109 l and 50 X 109 l respectively.

Hivaids Introduction

Infants with perinatal acquired AIDS are normal at birth but may develop symptoms within the first 18 months of life. Clinical manifestations in children include fever decreased CD4 count anemia decreased WBC count (less than 3,000 cells mm3) neutropenia (absolute neutrophil count of less than 1,500 cells mm3) thrombocytopenia myelosuppression vitamin K deficiency hepatitis pancreatitis stomatitis and esophagitis meningitis retinitis (common with low CD4 counts) otitis media and sinusitis (chronic or recurrent) lymphadenopathy hepatosplenomegaly recurrent bacterial infections (especially, Streptococcus pneumoniae and Haemophilus influenzae) Mycobacterium infections (MAC) or tuberculosis cytomegalovirus (CMV) failure to thrive (in infants) chronic diarrhea neurologic involvement, (developmental delays and microcephaly in infants, or loss of motor skills in the older child) and pulmonary infections (Pneumocystis carinii PCP , lymphocytic interstitial pneumonitis LIP , and pulmonary...

Use of Clinical Endpoints in a Novel Disease Target

In the absence of either clinically convincing data relating a surrogate endpoint to clinical outcome or, alternatively, intrinsically meaningful surrogates, it is extremely difficult to design pivotal studies of rare disorders using surrogate endpoints. This is unfortunate, as these are the rare heterogeneous long-standing disorders for which surrogates are most useful and needed, particularly when disease prevention and not reversal is the only achievable endpoint. In some disorders, there are intrinsically meaningful surrogates that can allow their use. For Gaucher's disease, the authorities noted that treated patients showed changes in anemia and thrombocytopenia that were intrinsically meaningful and supported the interpretation of the associated decreases in spleen size. Even though hemoglobin or platelet count endpoints may be laboratory values, the clinical benefit of a higher hemoglobin level or platelet count is established and accepted in other disorders.

Common Nursing Diagnoses See Ineffective Tissue Perfusion

Defining Characteristics (Specify in iron deficiency anemia irritability, anxiety, blood loss in the stool, hypochronic RBCs, normal or near normal RBC count, decreased serum ferritin and iron in sickle cell anemia pallor, weakness, anorexia, easy fatigability, jaundice and developmental delays in aplastic anemia pallor, fatigue, weakness, loss of appetite, normochromic, normocytic RBCs in reduced numbers, leukopenia, thrombocytopenia risk of spontaneous bleeding or bleeding after mild to severe trauma .)

Itp Introduction

Idiopathic thrombocytopenic purpura (ITP) is an acquired hemorrhagic blood disorder. It is characterized by excessive destruction of platelets (thrombocytopenia) and purpura (a discoloration caused by petechiae beneath the skin). Etiology is unknown but it is believed to be an autoimmune response to disease-related antigens. ITP is classified into two forms 1) acute form, which arises usually after an upper respiratory infection, measles, mumps, or chickenpox and 2) chronic form, which is unresponsive to treatment (with persistent thrombocytopenia) beyond 6 months of diagnosis. Classic signs and symptoms of ITP may include easy bruising with petechiae, and or ecchymosis over bony prominences bleeding from mucous membranes (i.e., epistaxis, bleeding gums) hematuria hematemesis hemarthrosis hematomas over the lower extremities. ITP is seen most frequently between the ages of 2 and 10 years in children. It is rarely seen in infants less than 6 months of age. Treatment is primarily...

Leukemia And Lymphoma Introduction

Pathologic effects of leukemia include the replacement of normal bone marrow elements by leukemic cells which results in clinical manifestations of anemia, neutropenia, and thrombocytopenia. Symptoms related to anemia may result in fatigue, weakness, pallor, and lethargy. Neutropenia predisposes the child to febrile episodes and infection. Symptoms related to thrombocytopenia may result in cutaneous bruises or purpura, petechiae, epistaxis, melena, and gingival bleeding. Other common symptoms related to leukemic infiltration include hepatosplenomegaly and lymphadenopathy bone and joint pain anorexia abdominal pain weight loss. Other symptoms, that are very rare, may include hematuria, gastrointestinal bleeding, or central nervous system (CNS) bleeding. Prognosis is based on age and initial WBC at diagnosis, sex, histologic type of the disease, number of chromosomes, the DNA-index, morphology and cell-surface immunologic markers.

Clinical Picture and Pathogenesis

And increase in serum creatinine, and then polyuria), and thrombocytopenia, but the extent of hemorrhages (hematuria, petechiae, internal hemorrhages), requirement for dialysis treatment, hypotension, and case-fatality rates are much higher in HFRS caused by Amur, Dobrava, or Hantaan viruses than in NE caused by Puumala or Saaremaa viruses. About a third of NE patients experience temporary visual disturbances (myopia), which is a very characteristic if not pathognomonic sign of the disease. Notably, the clinical consequences of all of the hantaviral pathogens in humans vary from none to fatal. Severe NE is associated with a certain haplotype, HLA-B8, DR3, DQ2 alleles, severe HPS with HLA-B35, and mild NE with HLA-B27. Yet, although Puumala virus infection is generally associated with mild HFRS, NE may have significant long-term consequences. A 5-year followup study demonstrated that 20 of NE patients had a somewhat increased systolic blood pressure and proteinuria. This is important,...

Therapeutic Applications

Ancrod has been used in Europe and Canada since 1968 for various conditions, including heparin-induced thrombocytopenia and deep-vein thrombosis. It was first described for use in stroke patients in 1983. The U.S. Stroke Treatment with Ancrod Trial (STAT) assessed the efficacy and safety of ancrod in the treatment of acute stroke. The study randomized 500 patients to ancrod or placebo treatment initiated within 3 h of symptom onset. Treatment was given as a continuous 72-h infusion, followed by 1-h infusions at 96 h and 120 h. The results of the trial have shown that patients benefit in neurological outcome (placebo 34 vs. ancrod 42 ) with only a modest increase in bleeding risk 82,89-92 . The European Stroke Treatment with Ancrod Trial (ESTAT) increased the time of initiating treatment to 6 h after symptom onset, but this trial was terminated as no efficacy was found on interim analysis 93 .

Treatment strategy

All patients received multi-agent combination chemotherapy regimen comprising vincristine 2mg m2 cycle , doxorubicin (70 mg m2 cycle over 2 days) and cyclophosphamide (1800mg m2 cycle) with mesna (VAdriaC) during cycles 1,3,5,9,11,13 and 15 alternating with ifosfamide (9 gm m2 cycle) with mesna and etoposide (500 mg m2 cycle) (IE) during cycles 2,4,6,7, 8,10,12,14,16,17 and 18. The dose of doxo-rubicin and cyclophosphamide during cycles 9, 11, 13 and 15 were reduced to 50mg m2 and 1200 mg m2. Each cycle commenced 3 weeks after the preceding cycle and was blood count dependent (i.e. neutrophil count > 1 X 109 l and platelet count > 75 X 109 l). 25 reductions in the doses of IE were made for patients who had > 7 day delay in commencement of chemotherapy cycle due to prolonged neutropenia. Radiotherapy was used for local tumor control and commenced at week 12 after 5 cycles of chemotherapy.

Molecular Diversity Of

Type 2B VWD is characterized by increased affinity of the mutant VWF for platelet and reduction in high molecular weight multimers (Fig. 2). The remaining VWF multimers are not hemostatically effective and cause bleeding and thrombocytopenia in the patients that can be exacerbated during physical exercise, stress, and pregnancy. This defect is identified in the laboratory by enhanced ristocetin-induced platelet aggregation. Type 2B is inherited as an autosomal dominant and accounts for less than 20 of all type 2 VWD. Aside from a single amino acid insertion, the genetic defect is generally found to be a point mutation in the A1 domain of VWF gene that contains the glycoprotein Ib (GpIb) binding domain and results in a gain of function. The most frequent mutations are Arg1306Trp, Arg1308Trp, Val1316Met, and Arg1314Gln accounting for 90 of the subtype.

Cardiovascular and coagulation system

Changes take place in the cardiovascular and coagulation systems which have practical and clinical implications and these are summarized in Table 10.1. Although both heart rate and cardiac output fall in the early puerperium there may be an early rise in stroke volume and together with the rise in blood pressure due to increased peripheral resistance it is a time of high risk for mothers with cardiac disease. Such mothers require extra supervision at this time (see Chapter 26). Although it is assumed that by 6 weeks the woman's body has changed physiologically back to the non-pregnant state, it can be seen from Table 10.1 that cardiac output may remain elevated for up to 24 weeks post-natally. During the immediate post-natal period, fibrinolytic activity is increased for 1-4 days before it returns to normal by 1 week. Platelet counts are normal Coagulation Fibrinogen Clotting factors Platelet count Fibrinolysis

Substrate Reduction Therapy

A pivotal trial of SRT was carried out in 28 adult patients (from four centers Cambridge, UK Amsterdam Prague and Jerusalem) naive to enzyme therapy, with mild to moderate type I Gaucher disease, who were unable or unwilling to receive enzyme treatment. There was significant reduction in spleen and liver, although amelioration of anemia and thrombocytopenia lagged behind. There were side effects, including diarrhea, abdominal pains, weight loss, tremor, and peripheral neuropathy, which were reversible with dose reduction or withdrawal. 15 A low-dose trial showed dose dependency for clinical improvement but no reduction in severity or frequency of side effects. Finally, using SRT as a maintenance regimen (i.e., switching from ERT or in combination with ERT), at 6 months, there were no clinically significant differences among groups.

AID deficiency and autoimmunity in humans

Unlike its mouse counterpart, AID deficiency in humans is associated with an increase in the incidence of certain autoimmune disorders, particularly the immune cytopenias, such as autoimmune hemolytic anemia, autoimmune thrombocytopenia or autoimmune neutropenia (Quartier et al., 2004). Interestingly, these autoimmunities are also associated with other primary immunodeficiencies such as common variable immune deficiency, and rarely, severe combined immunodeficiency (Arkwright et al., 2002). The common denominator appears to be the inability of the immunodeficient individual to clear persisting pathogens (Arkwright et al., 2002). It is possible that in those individuals with a residual lymphocyte population, there is compensation by relaxing tolerance checkpoints in order to deal with the pressure from persisting infection, allowing expansion and activation of autoreactive lymphocytes that would otherwise be prevented from participating in the immune response. It was also suggested...


If a patient presents with at least two of the criteria listed in Table 3.5, but lacks evidence for infection, the conditions for a systemic inflammatory response syndrome (SIRS) are met. The SIRS is the uniform answer of the body to a variety of diseases such as pancreatitis, major operation, severe trauma, or ischemia. Additionally a drop in the platelet count and the antithrombin-III levels (AT-III) is usually seen (Fresenius and Heck 2001). The definition for severe sepsis includes the standard sepsis criteria in conjunction with signs of organ dysfunction, hypoperfusion, or sepsis-induced hypotension, which present as lactate acidosis, oliguria, en-cephalopathy, or thrombocytopenia.


Perioperative heparin prophylaxis can cause thrombo-cytopenia. There are two types of heparin-induced thrombocytopenia (HIT). HIT I is characterized by a transitory, slight, and asymptomatic reduction in platelet count during the first 1-2 days of treatment. It resolves spontaneously and does not require discontinuation of the drug. The origin of HIT I is not completely understood, but may be caused by a heparin-induced platelet clumping. The immunologic etiology of HIT II is largely accepted platelet factor 4 (PF4) displaced from endothelial heparin sulphate or directly from the platelets binds to the heparin molecule to form an immunogenic complex. The IgG anti-heparin PF4 immunocomplexes activate platelets and provoke an immunologic endotheli-al lesion with thrombocytopenia and or thrombosis. Cutaneous allergic manifestation at the heparin injection sites and skin necrosis may be present as well. Interestingly, hemorrhagic events are not frequent, while the major clinical...

History And Exam

After a few days of flu-like illness, this 39-yr-old man was brought to the emergency room because of confusion. An MR venogram showed a cerebral venous thrombosis. Hematologic investigations uncovered a platelet count of 700,000 and a prothrombin gene mutation. He was started on coumadin. On evaluation 6 months later, his acuity was 20 20


Towards the end of pregnancy < 5 of women have a platelet count < 150 x 109 l. This gestational thrombocytopaenia carries no significance, but requires exclusion of other disorders (Table 29.4). If the platelet count is < 100 x 109 l, further investigations are required (Table 29.5). Spontaneous bleeding is unlikely with platelets > 20 x 109 l and monitoring of the patient and platelet count Immune thrombocytopaenic purpura (ITP) Heparin-induced thrombocytopaenia (HIT) Post-transfusion purpura (PTP) Acute fatty Liver of pregnancy Pre-eclampsia (PET) HELLP syndrome Thrombotic thrombocytopaenic purpura (TTP) Haemolytic uraemic syndrome (HUS) Disseminated intravascular coagulation (DIC) Drug induced thrombocytopenia Systemic lupus erythematosis (SLE) antiphospholipid are often all that is required, with the aim often attaining an adequate platelet count for delivery. A spontaneous vaginal delivery or Caesarean Section can take place when platelets are > 50 x 109 l. If the woman...


Baker employed a sigmoidal Emax model (R2 0.80) to describe the relationship between the AUC of 5-FU and the neutropenia observed following the administration of eniluracil and 5-FU on a 5-d schedule every 28 d (27). This model was less predictive of the degree of thrombocytopenia (R2 0.51). Interpretation of the pharmacodynamic findings is limited by the small number of patients and heterogeneity in the amount of prior myelosuppressive chemotherapy (27). Similarly, Humerickhouse and colleagues observed an inverse correlation between absolute neutrophil count nadirs and average 5-FU plasma concentrations. They found no correlation with other toxicities (30).

Phase I Studies

It is noteworthy that minor increases in the 5-FU dose produced significant increases in toxicity. For example, 20 mg m2 of 5-FU given with eniluracil and leucovorin was well tolerated no patients experienced hematologic toxicity > grade 2. By contrast, of the six patients who were treated at a 5-FU dose of 25 mg m2 per day, only a 25 dose increase, four developed grade 4 neutropenia and one experienced grade 3 thrombocytopenia.


With the use of chemical prophylaxis, the risk of bleeding and associated complications is present (25,27-30). They include, but are not limited to, wound hematoma, wound dehiscence, infection, peripheral nerve palsy, internal bleeding, disseminated intravascular coagulopathy, heparin-induced thrombocytopenia, warfarin-induced skin necrosis, stroke, and death (31-33). With preoperative use of chemical agents, the patients should be monitored for a drop in their hemoglobin and platelet count.

Preliminary Results

Single patient dose escalation proceeded from 100 mg bid up to 800 mg bid. Dose-limiting neutropenia and thrombocytopenia were encountered in patients treated at the 650 and 800 mg bid, and a third patient treated at 600 mg bid experienced dose-limiting fatigue. A total of7 patients were accrued at the 400 mg level. Two ofthese patients experienced grade 4 thrombocytopenia, one with grade 4 neutropenia. Grade 4 granulocyte and platelet toxicity typically were detected at d 15, with nadirs at d 18-21 and recovery by d 28. Other toxic effects observed at 400 mg bid were reversible grade 3 bilirubin elevation in a patient with high volume liver metastases, grade 2 creatinine elevation in one patient, and grade 2 skin rash in another patient. Based on the toxicity observed at 400 mg bid, additional patients were treated at the 300 mg bid dose. None ofthese patients experienced grade 3 or 4 neutropenia or thrombocytopenia, including two patients treated for 7 and 8 cycles, respectively,...

Noncardiac toxicity

DXN group patients had grade 3 or worse thrombocytopenia, after cycle 1 (11 23 versus 3 18 p < 0.05), 5 (13 18 versus 2 11 p < 0.001) and 6 (9 14 versus 1 9 p < 0.001)and significantly lower platelet nadir after cycle 4 (42 X 109 l versus 112 X 109 l p < 0.001) and cycle 6 (26 X 109 l versus 99 X 109 l p < 0.05) but no significant differences in the ANC nadirs were seen.

Case Presentation

Echocardiography Hand Book

Initial echocardiogram showed sinus tachycardia with no signs of acute ischemia. Q-waves were seen in the inferior leads, but no S1Q3T3 pattern observed. Platelet count fell during admission, dropping from 118 K dL to 18 K dL and the diagnosis or heparin-induced thrombocytopenia entertained platelet factor four (PF4) antibodies were requested. Plasma D-dimer enzyme-linked immu-nosorbent assay test (ELISA) and serum troponin I levels were both mildly elevated. Arterial blood gases were reported at the lower limits of normal.

Leukemia Cutis

Eyelid Infiltrative Disorders

INTRODUCTION Leukemia is a result of neoplastic proliferation of bone marrow-derived leukocytes, the majority of which are of B-cell origin. The disease may be subdivided into acute or chronic forms. The acute form presents with anemia, thrombocytopenia, hemorrhage, adenopathy, hepatosplenomegaly, and a rapidly fatal course. The chronic indolent form is often incidentally diagnosed following prolonged episodes of fever, weight loss, and infection. The acute leukemias are more likely to show eye involvement than chronic leukemias. Leukemia cutis may occur concurrently with bone marrow involvement, as an isolated site of relapse, or as the initial manifestation of leukemia. Leukemia cutis occurs in 25 to 30 of infants with congenital leukemia. In older persons the incidence of leukemia cutis at diagnosis is approximately 10 in acute myeloid leukemia and 1 in acute lymphoblastic leukemia. Between 75 and 90 of patients with leukemia will show eye or adnexal involvement at some stage of...

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