From: Subject: Idiopathic Thrombocytopenic Purpura -- Chu et al. 21 (3): 95 -- Pediatrics in Review Date: Tue, 16 Sep 2008 11:37:55 +0800 MIME-Version: 1.0 Content-Type: multipart/related; type="text/html"; boundary="----=_NextPart_000_0000_01C917F0.A9672970" X-MimeOLE: Produced By Microsoft MimeOLE V6.00.2900.3350 This is a multi-part message in MIME format. ------=_NextPart_000_0000_01C917F0.A9672970 Content-Type: text/html; charset="Windows-1252" Content-Transfer-Encoding: quoted-printable Content-Location: http://pedsinreview.aappublications.org/cgi/content/full/21/3/95?nfstatusdescription=SUCCESS%3A+Login+worked&nfstatus=200&HITS=10&sortspec=relevance&hits=10&FIRSTINDEX=0&resourcetype=HWCIT&fulltext=idiopathic+thrombocytopenia&searchid=1 Idiopathic Thrombocytopenic Purpura -- Chu et al. 21 = (3): 95 -- Pediatrics in Review
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(Pediatrics in Review. = 2000;21:95-104.)
=A9 2000 America= n Academy=20 of Pediatrics

Idiopathic Thrombocytopenic Purpura=20


Yu-Waye Chu, MD*
James = Korb,=20 MD3D{dagger}=20
Kathleen M. Sakamoto,=20 MD*

* = Division of=20 Hematology-Oncology, Department of Pediatrics.

3D{dagger}=20=20 Division of General Pediatrics, Department of Pediatrics, UCLA School of = Medicine, Los Angeles, CA. This work was supported by a Resident = Research Grant=20 from the American Academy of Pediatrics (Y-WC). KMS is a Scholar of the = Leukemia=20 Society of America.


3D"   =20 OBJECTIVES
Top
3D"OBJECTIVES
Epidemiology and Pathophysiology
Clinical and Laboratory Features
The Role of Bone...
Differential Diagnosis
Management of Acute ITP
IVIG and Steroids
Neonatal Thrombocytopenia
Management of Chronic ITP
Suggested=20 Reading
 
After = completing=20 this article, readers should be able to:

  1. Describe the clinical and laboratory features of idiopathic=20 thrombocytopenic purpura (ITP) and explain how they differ = in acute and chronic ITP.
  2. List the features of ITP that distinguish it from other = causes of thrombocytopenia.
  3. Explain the role of bone marrow examination in the=20 diagnosis of ITP.
  4. Describe the advantages and disadvantages of the = primary=20 therapies for ITP.
  5. Delineate the differences in therapeutic strategies for=20 ITP and neonatal alloimmune thrombocytopenia.
  6. Describe the role of splenectomy in the treatment of = ITP.=20


3D"   =20 Epidemiology and Pathophysiology
Top
OBJECTIVES
3D"Epidemiology and = Pathophysiology
Clinical and Laboratory Features
The Role of Bone...
Differential Diagnosis
Management of Acute ITP
IVIG and Steroids
Neonatal Thrombocytopenia
Management of Chronic ITP
Suggested=20 Reading
 
Idiopathic thrombocytopenic purpura = (ITP) is an=20 acquired hemorrhagic disorder characterized by: 1) = thrombocytopenia that is defined as a=20 platelet count less than 150 x=20 109/L ( 150,000/mcL), 2) a purpuric rash, 3) = normal bone=20 marrow, and 4) the absence of signs of other identifiable causes = of=20 thrombocytopenia. ITP is classified as = acute or=20 chronic, with the latter defined as the persistence of = thrombocytopenia for more = than 6 months=20 from the initial presentation of signs and symptoms. =

ITP is estimated to be one of the most common acquired bleeding=20 disorders encountered by pediatricians, with the incidence of = symptomatic disease being approximately 3 to 8 per 100,000 = children=20 per year. Acute ITP is more prevalent among children younger=20 than 10 years of age, affects males and females equally, and = is=20 more prevalent during the late winter and spring. Chronic ITP = affects adolescents more often than younger children, with = females=20 being affected more frequently than males. Unlike acute ITP, = it=20 does not show a seasonal predilection. Patients who have = chronic=20 ITP are more likely to exhibit an underlying autoimmune = disorder,=20 with up to one third having clinical and laboratory = manifestations=20 of collagen-vascular disease.

Although the focus of this article is on the clinical presentation,=20 diagnosis, and management of ITP, the pathophysiology of this = condition deserves mention because the mechanisms = contributing to=20 thrombocytopenia are more = complex than=20 originally thought. It is widely believed that the = destruction of=20 platelets in ITP involves autoantibodies to glycoproteins = normally=20 expressed on platelet membranes. The spleen and other organs = of the=20 reticuloendothelial system subsequently destroy these = antibody-coated=20 platelets in a manner analogous to what is observed in = autoimmune=20 hemolytic anemia. In addition to increased immune-mediated=20 destruction of platelets, there is evidence that platelet = production=20 in ITP is altered, especially in chronic ITP. Although the = number of=20 megakaryocytes in the bone marrow are normal or increased in = ITP,=20 plasma thrombopoietin levels, which are a measure of = proliferation=20 and maturation of megakaryocytic progenitors, are = significantly=20 decreased. In chronic ITP, platelet turnover is markedly = lower=20 despite decreased platelet survival, and megakaryocytes = isolated from=20 affected patients demonstrate suppressed growth in = vitro.

The clinical and epidemiological differences between acute and = chronic=20 ITP suggest that the resulting thrombocytopenia may have different = pathophysiologic mechanisms. In acute ITP, it has been postulated=20 that platelet destruction arises from antibodies generated=20 during the immune response to a viral or bacterial infection = that=20 cross-react with platelet antigens. Other mediators of the = immune=20 response arising from infection may play an additional role = in=20 suppressing platelet production. Chronic ITP, on the other = hand, may=20 be a consequence of an inherent defect in immune regulation, = as=20 is seen in other autoimmune disorders, resulting in the = generation=20 of platelet-specific antibodies. To date, a number of = platelet=20 surface glycoproteins (GPs) have been identified as specific=20 targets for autoantibodies in ITP, including GP IIb-IIIa, GP=20 Ib, and GP V. How these antiplatelet antibodies arise in ITP, = their significance in distinguishing the pathophysiology of=20 acute versus chronic ITP, and the cellular and biochemical = components=20 that are involved in their regulation remain unknown. Current = therapeutic regimens used in the management of ITP, therefore, = are=20 limited in their efficacy because they fail to target specific=20 immunologic pathways responsible for alteration of platelet=20 production and destruction.


3D"   =20 Clinical and Laboratory Features
Top
OBJECTIVES
Epidemiology and Pathophysiology
3D"Clinical and Laboratory = Features
The Role of Bone...
Differential Diagnosis
Management of Acute ITP
IVIG and Steroids
Neonatal Thrombocytopenia
Management of Chronic ITP
Suggested=20 Reading
 
  &nb= sp;  CLINICAL FINDINGS
ITP is diagnosed = largely on=20 clinical findings. Familiarity with the features of acute ITP = plays=20 an important role in determining the extent of the diagnostic = evaluation. The typical clinical presentation is that of an = otherwise=20 healthy child who develops easy bruising and a purpuric rash. = Bleeding from mucous membranes, such as nosebleeds or = gingival=20 bleeding, is seen in about one third of cases. Other sites of = bleeding include the gastrointestinal tract, vaginal mucosa, = the=20 urinary tract, the retina, and conjunctivae. In acute ITP, = the onset=20 of signs and symptoms often is preceded by a viral illness. = Except=20 for the manifestations of bleeding, findings on the physical=20 examination are otherwise completely normal. Pertinent = negatives of=20 the examination include the absence of lymphadenopathy and=20 hepatosplenomegaly. The presence of either should raise the=20 consideration of other diseases, particularly leukemia. = Similarly,=20 the presence of pallor, hyperbilirubinemia, and splenomegaly = are=20 features of a concomitant hemolytic anemia, which can be seen = in=20 conjunction with thrombocytopenia in Evans syndrome = and=20 other autoimmune diseases. In chronic ITP, the presentation = may be=20 more insidious, and often the patient may be asymptomatic.

The distribution of the patient=92s bruises and bleeding = sites=20 provides additional clues to the etiology. In disorders of = primary=20 hemostasis such as ITP and other platelet disorders, bruises = are=20 generalized and occur in areas not exposed to trauma. Bruises = found=20 in these areas are distinctly abnormal and warrant further=20 investigation. In contrast, bruising in a healthy, active child=20 occurs in exposed areas, especially over hard bony surfaces. = Bruising=20 also can be a feature of child abuse, which should be = considered=20 in a child who has generalized bruising and a normal platelet = count.

     LABORATORY=20 FINDINGS
The laboratory features of ITP help to = distinguish=20 it from other causes of thrombocytopenia. Key to the laboratory=20 diagnosis of acute ITP is the presence of a low platelet = count=20 (usually, 20 to 30 x=20 109/L [20,000 to 30,000/mcL]), generally with normal=20 values for age in all other cell lines. In about 15% of = patients,=20 mild anemia due to bleeding is present, but red blood cell = indices=20 are normal. If results of the complete blood count (CBC) are=20 consistent with ITP, coagulation studies are not warranted. = The=20 prothrombin time and partial thromboplastin time are = invariably=20 normal, but the bleeding time, which is a direct test of = platelet=20 function, almost always is prolonged. Abnormal leukocyte or = red blood=20 cell counts should prompt further diagnostic investigation to = exclude=20 the possibility of an underlying leukemia or aplastic = anemia.=20

In addition to the CBC, it is essential to examine a peripheral = blood=20 smear under light microscopy for several reasons. First, it=20 serves to rule out "pseudothrombocytopenia," an in vitro = artifact=20 caused by the clumping of platelets in tubes containing the=20 anticoagulant ethylene-diamine-tetraacetic acid, which = results=20 in low platelet counts when measured on an automated cell = counter.=20 Second, characterization of red blood cell morphology enables = the=20 examiner to detect the presence of a concomitant hemolytic process = (eg, hemolytic-uremic syndrome, disseminated intravascular=20 coagulation, or Evans syndrome) or hypoproliferative anemia = (eg,=20 anemia due to nutritional deficiencies). Third, abnormal = white blood=20 cell counts or the presence of immature nucleated forms may = indicate=20 an underlying primary or secondary bone marrow neoplasm. = Fourth,=20 examination of individual platelets aids in the diagnosis of = ITP.=20 Platelet size is increased noticeably in acute ITP, = reflecting=20 increased platelet turnover and the release of younger, = larger=20 platelets from the bone marrow, while it may be reduced in = other=20 thromboctyopenic entities (see Differential Diagnosis). =

An examination of the bone marrow is indicated in certain situations=20 (see following section). Megakaryocytes usually are present = in normal=20 or increased numbers in acute ITP. Bone marrow examination = also=20 is useful in confirming normal morphologies in other cell = types=20 and in ascertaining the presence of blast cells suggestive of = leukemia or other lymphoproliferative disorders. Finally, it=20 can help to determine the presence of metastatic disease, such = as=20 neuroblastoma.

In chronic ITP, the platelet count at presentation is generally=20 between 20 and 70 x = 109/L=20 (20,000 and 70,000/mcL). Additional tests should be performed = before=20 making the diagnosis of chronic ITP, including a evaluation = for=20 autoimmune disease, infection, and immunodeficiency (Table = 1 ). Thyroid studies are = obtained=20 to rule out autoimmune thyroid disease, which has been = associated=20 with chronic ITP. A Coombs test and measurement of the=20 reticulocyte count are employed to exclude Evans syndrome = (immune=20 thrombocytopenia with = autoimmune=20 hemolytic anemia). Numerous viral infections have been = implicated in=20 causing thrombocytopenia. Isolated thrombocytopenia can be the = presenting=20 symptom of human immunodeficiency virus infection and may be = seen=20 after immunization with measle-mumps-rubella vaccine.


View = this=20 table:
[in=20 this window]
[in a new window]
  		Table 1. Laboratory Tests = in the=20 Evaluation of Chronic Immune Thrombocytopenic Purpura =


3D"    The=20 Role of Bone Marrow Aspirations in Diagnosis =
Top
OBJECTIVES
Epidemiology and Pathophysiology
Clinical and Laboratory Features
3D"The Role of Bone...
Differential Diagnosis
Management of Acute ITP
IVIG and Steroids
Neonatal Thrombocytopenia
Management of Chronic ITP
Suggested=20 Reading
 
Whether bone = marrow=20 should be examined routinely in patients who have suspected = ITP is=20 controversial. Historically, such examinations were common to = rule=20 out diseases such as leukemia and aplastic anemia as causes = of the=20 thrombocytopenia. However, = there is=20 increasing argument against performing bone marrow = aspirations to=20 diagnose acute ITP. As stated previously, acute ITP is = largely a=20 clinical diagnosis that is confirmed relatively easily by = routine=20 blood tests. A growing number of studies have demonstrated = that the=20 likelihood of a newly diagnosed leukemia presenting as an = isolated=20 thrombocytopenia is extremely low. = Among=20 2,239 patients newly diagnosed with acute lymphoblastic = leukemia=20 in a recent Pediatric Oncology Group study population, for = example,=20 none exhibited isolated thrombocytopenia in the presence of = an=20 otherwise normal CBC and cell morphologies on peripheral smear. = In=20 a retrospective review of 127 cases of children who had an initial = diagnosis of acute ITP and in whom confirmatory bone marrow=20 aspirations were performed, only five cases were identified = where=20 examination of the bone marrow led to a different diagnosis = from ITP.=20 In each of these five cases, features on initial clinical=20 presentation were atypical for acute ITP. A more recent = review of 322=20 cases of children who had provisional diagnoses of acute ITP=20 confirmed by bone marrow aspiration also failed to reveal a = single=20 case of leukemia. Furthermore, the decision to perform a bone = marrow aspiration can be deferred if a patient is to be = treated=20 initially with intravenous immunoglobulins (IVIG) pending the = response to treatment. This approach avoids the concern of=20 interfering with the diagnosis of leukemia by partially = treating a=20 patient who presumably has ITP with steroids.

Even though bone marrow examinations have apparent limited value = in=20 the diagnosis of acute ITP, they must be performed in situations=20 where the diagnosis does not absolutely correlate with the = expected=20 clinical and laboratory findings (see Differential = Diagnosis). These=20 include: 1) unusual findings on history and physical = examination (eg,=20 history of fevers, weight loss, fatigue, bone pain, and = presence of=20 lymphadenopathy or splenomegaly on physical examination); 2) = the=20 presence of abnormal white or red blood cell counts and = indices on=20 the CBC; and 3) cases in which steroids are to be used for=20 treatment, either as a first-line drug or as a second option = when=20 IVIG fails to resolve the thrombocytopenia. Bone marrow = examination=20 is also important in evaluating chronic ITP and in cases of=20 thrombocytopenia that are refractory to = multiple=20 treatment modalities. The importance of performing bone = marrow=20 aspirations in these circumstances is highlighted by case = reports in=20 which the diagnosis of leukemia or aplastic anemia not only = was=20 delayed, but it was masked by the partial treatment with = steroids of=20 patients initially diagnosed as having ITP.

Although examination of the bone marrow is the "gold standard" = in=20 diagnosing acute ITP, noninvasive tests to distinguish acute=20 ITP from other thrombocytopenic disorders continue to be = developed=20 and may decrease further the need to perform bone marrow = aspirations.=20 None is in general clinical use to date, but they show = promise=20 as useful adjuncts to other laboratory tests for diagnosing = ITP.=20 One such method involves measurement of the reticulated = platelet=20 count. As mentioned previously, platelets on the peripheral = blood=20 smear from patients who have acute ITP are larger, indicating=20 increased platelet turnover and a higher percentage of young=20 platelets in the circulation. These platelets contain a = higher RNA=20 content than do more mature platelets, as do immature red = blood=20 cells (ie, reticulocytes). These platelets have been termed=20 "reticulated platelets." By employing fluorescent dyes that = bind=20 nucleic acid and measuring dye fluorescence by flow = cytometry, it is=20 possible to quantitate reticulated platelets and distinguish=20 between a hyperproliferative (eg, acute ITP) and a=20 hypoproliferative (eg, leukemia, aplastic anemia) process. = Comparison=20 of the reticulated platelet count in 15 patients who had = acute ITP,=20 20 patients who had acute lymphoblastic leukemia, 10 patients = who had=20 aplastic anemia, and 27 healthy children revealed a = significantly=20 higher count among those who had acute ITP compared with the = other=20 groups. Importantly, the degree of elevation in the = reticulated=20 platelet count in acute ITP is such that there was no overlap = with=20 the hypoproliferative groups, providing a positive predictive = value,=20 sensitivity, and specificity approaching 100% when the = reticulated=20 platelet count exceeded 13.7% and the total platelet count = was less=20 than 50 x = 109/L=20 (50,000/mcL). Tests such as this potentially can assist in = the=20 diagnosis of ITP without the need to perform more invasive=20 procedures. Its utility in distinguishing acute ITP from = other=20 non-neoplastic causes of thrombocytopenia and its role = in the=20 diagnosis of chronic ITP, however, warrant further investigation. =


3D"   =20 Differential Diagnosis
Top
OBJECTIVES
Epidemiology and Pathophysiology
Clinical and Laboratory Features
The Role of Bone...
3D"Differential = Diagnosis
Management of Acute ITP
IVIG and Steroids
Neonatal Thrombocytopenia
Management of Chronic ITP
Suggested=20 Reading
 
The = differential=20 diagnosis for thrombocytopenia is very broad. = A low=20 platelet count can result from immunologic and nonimmunologic = entities.=20 Table 2 lists selected causes of thrombocytopenia and the = clinical and=20 laboratory associations that distinguish them from ITP. It is = worth=20 stressing again that the diagnosis of ITP is based on the = presence of=20 an isolated thrombocytopenia in the absence = of=20 clinical and laboratory features suggestive of other disorders. = The=20 distinction of these diseases from ITP is based almost entirely = on=20 findings from the history and physical examination and = interpretation=20 of the CBC. As stated previously, ordering additional tests = or=20 examining the bone marrow usually is not necessary to establish = the=20 diagnosis of ITP.


View = this=20 table:
[in=20 this window]
[in a new window]
  		Table 2. Differential = Diagnosis of=20 Thrombocytopenia =


View = this=20 table:
[in=20 this window]
[in a new window]
  		Table 3. Common Drugs and = Thrombocytopenia =


3D"   =20 Management of Acute ITP
Top
OBJECTIVES
Epidemiology and Pathophysiology
Clinical and Laboratory Features
The Role of Bone...
Differential Diagnosis
3D"Management of Acute = ITP
IVIG and Steroids
Neonatal Thrombocytopenia
Management of Chronic ITP
Suggested=20 Reading
 
Acute ITP = generally=20 can be diagnosed and managed in an outpatient setting by the = primary=20 care pediatrician. Referral to a hematologist-oncologist is = warranted=20 if there is evidence of concurrent disease, such as malignancy, = bone=20 marrow failure, autoimmune disease, or immunodeficiency.

     SUPPORTIVE=20 MEASURES
Supportive measures are important in the = management=20 of acute ITP. These include restricting physical activity, = wearing=20 protective head-gear, lining the crib with protective = padding,=20 avoiding medications that suppress platelet production or = alter their=20 function (Table 3 ), and maintaining a low threshold for prompt=20 evaluation of the child who has thrombocytopenia and sustains blunt = head=20 or abdominal trauma.

     PHARMACOLOGIC=20 MANAGEMENT
The pharmacologic = management of=20 acute ITP continues to be the subject of much controversy = because=20 most cases of ITP are self-limited; 80% to 90% of patients = will make=20 a full and sustained recovery within 6 months without any=20 treatment. However, at present there are no definitive = diagnostic=20 predictors to enable the physician to identify the 10% to 20% = of=20 patients who will progress to chronic ITP. Moreover, patients = who=20 have extremely low platelet counts (ie, 10 to 20 x 109/L [10,000 to 20,000/mcL]) = are=20 at increased risk for significant bleeding, the most = devastating=20 of which is intracranial hemorrhage (ICH). ICH always should = be=20 considered in the patient who has thrombocytopenia and presents = with a=20 persistent headache. Although the incidence of ICH is = extremely low=20 (only 56 documented cases identified from 1975 to 1996), the=20 mortality rate is significant (46%), and virtually all = episodes have=20 been associated with platelet counts of less than 2 x 109/L (20,000/mcL). Thus, the = rationale=20 for aggressive treatment of severe ITP at the time of = diagnosis is to=20 raise the platelet count to a level that decreases the risk = of=20 significant bleeding events.


3D"    IVIG=20 and Steroids
Top
OBJECTIVES
Epidemiology and Pathophysiology
Clinical and Laboratory Features
The Role of Bone...
Differential Diagnosis
Management of Acute ITP
3D"IVIG and = Steroids
Neonatal Thrombocytopenia
Management of Chronic ITP
Suggested=20 Reading
 
Currently, the = mainstays of pharmacologic management for acute ITP are IVIG = and=20 corticosteroids. The ability of both of these agents to raise = platelet counts has been documented in multiple studies, with = mean=20 time to raise platelet counts 20 x=20 109/L (20,000/mcL) ranging from 24 to 72 hours = after=20 initiation of therapy. There currently are no clear criteria = for=20 selecting IVIG or steroids as a first-line agent. IVIG=20 has several advantages over steroids. First, it appears to = induce a=20 more rapid increase in platelet count. Second, the adverse = effects of=20 steroid use, including weight gain, hypertension, = hyperglycemia,=20 Cushing syndrome, osteoporosis, and psychological disorders, = are=20 avoided with IVIG. Third, the physician can begin a = therapeutic trial=20 with IVIG without bone marrow aspiration to rule out=20 leukemia.

The disadvantages of IVIG as a first-line agent include its = higher=20 cost and difficulty with administration. It requires = intravenous=20 access, and the infusion requires several hours of = observation. Moreover, IVIG is associated with a number of adverse=20 effects. An aseptic meningitis effect will produce symptoms = similar=20 to that of an acute ICH, leading to additional costly tests = to=20 differentiate these two diagnoses. In a recent study examining = 38=20 children who had acute ITP treated with IVIG, 34% had neurologic=20 complications, and virtually all of those affected required=20 hospitalizations for a period longer than what was required = for the=20 ITP alone. Twenty-four percent of these patients required = emergent=20 computed tomography to rule out ICH. The combination of = prolonged=20 hospitalization and additional diagnostic studies resulted in = an=20 increased cost of approximately $1,700 for each patient who=20 experienced neurologic side effects from IVIG.

     ANTI-Rh(D)
Another agent under = investigation=20 in the treatment of acute ITP is anti-Rh(D). It is less = expensive=20 than IVIG and has been shown to raise platelet counts = effectively.=20 However, it is useful only in patients who are Rh-positive, = and=20 hemolytic anemia can occur as a side effect. In some = published=20 reports, treatment with anti-Rh(D) resulted in a slower rise = in=20 platelet count than with steroids or IVIG, which = theoretically could=20 prolong the interval in which a patient is at risk for ICH. = However,=20 other studies have shown that an increased dose of anti-Rh(D) = raised=20 platelet counts as quickly as did IVIG; the length of = hospital stay=20 was identical for patients receiving anti-Rh(D) and = IVIG.

     DOSING
Dosing schedules for IVIG = and steroids=20 are highly variable (Table 4 ). IVIG in a dose of 0.25 to 1 g/kg per day = for two=20 consecutive days or as a single dose of 0.8 g/kg has been = shown to=20 increase platelet counts. Dosage recommendations for oral=20 prednisone vary even more, ranging from 4 mg/kg per day for 4 = days=20 with or without a subsequent taper to 2 mg/kg per day for 2 = to 3=20 weeks. Some investigators also have demonstrated a role for = high-dose=20 intravenous methylprednisone (30 mg/kg per day for 2 to 3 days) = in=20 raising platelet counts. Anti-Rh(D), in the comparison trials = with IVIG and prednisone, was administered intramuscularly in = doses of 25 to 50 mcg/kg per day for two consecutive days. It = is important to note that the schedules listed in Table 4 are based on studies involving = relatively few=20 patients. The results of large, randomized, and controlled = studies to=20 establish the optimal doses of IVIG, steroids, and anti-Rh(D) = have=20 yet to be published.


View = this=20 table:
[in=20 this window]
[in a new window]
  		Table 4. Selected Dosing = Schedules=20 for Therapy of Acute ITP =

Although IVIG, steroids, and anti-Rh(D) have been shown to = shorten=20 the duration of thrombocytopenia, it is essential to = realize=20 that they are not cures for ITP. They only have the = potential=20 to shorten the period of thrombocytopenia and minimize the = risk=20 of life-threatening bleeding events. As stated previously, = ITP=20 is a self-limited disease in most pediatric patients. All of=20 the studies performed to date on the treatment of acute ITP=20 have focused on a rise in platelet counts as the endpoint; no = studies have documented decreases in morbidity or mortality.=20 Accordingly, despite the existence of agents that can raise = the=20 platelet count, a number of important questions remain: 1) = Are there=20 factors other than platelet counts less than 20 x 109/L (20,000/mcL) that = contribute to=20 an increased risk of intracranial hemorrhage? 2) What is the=20 cost-effectiveness of treating patients who have acute ITP = with IVIG=20 versus steroids versus anti-Rh(D), given each agent=92s = advantages and=20 disadvantages? 3) How effective are these agents in the = prevention of=20 chronic ITP?


3D"   =20 Neonatal Thrombocytopenia =
Top
OBJECTIVES
Epidemiology and Pathophysiology
Clinical and Laboratory Features
The Role of Bone...
Differential Diagnosis
Management of Acute ITP
IVIG and Steroids
3D"Neonatal Thrombocytopenia
Management of Chronic ITP
Suggested=20 Reading
 
Immune = thrombocytopenia can be manifested = during the=20 neonatal period in infants born to mothers who have ITP and, = much=20 more rarely, in neonatal alloimmune thrombocytopenia. In the latter, = which=20 occurs in approximately 1 in 5,000 newborns, the platelets of = the affected infant contain different antigens from those of=20 the mother, and the subsequent formation of maternal = alloantibodies=20 that cross the placenta result in platelet destruction. Both=20 diseases are self-limiting; in most cases, the thrombocytopenia resolves = within 6=20 weeks of birth. However, there are significant differences = between=20 the two diseases that deserve mentioning. First, determining = the=20 maternal history is essential in distinguishing between the = two=20 diagnoses. In maternal ITP, the mother=92s platelet count is = generally=20 below normal, and in most cases there is a well-documented = history of=20 chronic ITP. In neonatal alloimmune thrombocytopenia, the mother has a = normal platelet=20 count and has no history of immune thrombocytopenia. However, a = history of=20 a sibling who has neonatal thrombocytopenia is strongly = suggestive=20 of neonatal alloimmune thrombocytopenia because subsequent = affected=20 siblings are affected more severely than the first. Second, = neonatal=20 alloimmune thrombocytopenia is a far more serious = disorder.=20 Not only is the platelet count lower compared with that of = the infant=20 born to a mother who has ITP, but the incidence of ICH is=20 significantly higher (10% to 30% versus 1% in infants born to = mothers=20 who have ITP).

The management of the infant who has autoimmune or alloimmune = thrombocytopenia is similar. = IVIG,=20 steroids, platelet transfusions, and exchange transfusions = all have=20 been investigated. The important distinction = in=20 treatment is that in neonatal alloimmune thrombocytopenia, plasmapheresed = or=20 washed platelets from the mother should be used for transfusion=20 because they lack the alloantigen responsible for the = formation=20 of antiplatelet antibodies. In infants born to mothers who = have=20 ITP, transfusion with maternal platelets is avoided because = they=20 contain the antigens responsible for the formation of = platelet=20 autoantibodies. Furthermore, because most cases of neonatal=20 thrombocytopenia due to maternal ITP are = mild and=20 self-limiting, aggressive therapy usually is not = required.=20


3D"   =20 Management of Chronic ITP
Top
OBJECTIVES
Epidemiology and Pathophysiology
Clinical and Laboratory Features
The Role of Bone...
Differential Diagnosis
Management of Acute ITP
IVIG and Steroids
Neonatal Thrombocytopenia
3D"Management of Chronic = ITP
Suggested=20 Reading
 
In the = minority of=20 cases in which thrombocytopenia persists for = more than=20 6 months (ie, chronic ITP), management is highly = individualized and=20 depends primarily on the degree of thrombocytopenia and the need = to=20 preserve the patient=92s quality of life. Studies examining = the natural=20 course of chronic ITP suggest that most patients maintain = platelet=20 counts above 30 x 109/L=20 (30,000/mcL). In a significant percentage of patients (40% to = 79%),=20 complete remission (defined as a platelet count 100 x 109/L [100,000/mcL]) is = achieved=20 over the course of 3 months to 15 years. As in acute ITP, the = goal=20 of management is to minimize the risk of significant = bleeding.=20 Patients should be directed to avoid activities that increase = the risk of trauma and to avoid all medications that suppress = platelet production and function (Table 3 ). Platelet counts must be = monitored regularly=20 because this may determine the aggressiveness of further = treatment.=20 Finally, patients should be evaluated for autoimmune disease = as=20 previously described because a greater percentage of patients = who=20 have features of chronic ITP have an underlying autoimmune = disorder.=20 It is important to re-evaluate these patients over time if = the=20 initial evaluation fails to establish a diagnosis. In some = cases, the=20 diagnosis may not be apparent for years.

     PHARMACOLOGIC=20 OPTIONS
Pharmacologic approaches to the management of = chronic=20 ITP that have been studied to date include steroids, IVIG, = androgens,=20 anti-Rh(D), recombinant human interferon-alpha-2b, and=20 immunosuppressive agents used alone or in combination. = Although all=20 of these have been shown to induce a transient rise in = platelet=20 counts, none has demonstrated an ability to sustain a = desirable=20 platelet count; therefore, repeated treatments may be = required.=20 This not only potentiates chronic drug toxicity, but it = greatly=20 increases the cost of therapy. Whether any of these agents = alters the=20 natural course of chronic ITP, affects long-term morbidity or = mortality, or increases the rate of long-term remission = remains=20 unclear. Because the majority of cases of chronic ITP remit = either=20 spontaneously or with treatment and because the associated = mortality=20 and morbidity are low, a number of authors advocate = interventions=20 only when the platelet count is dangerously low or if the = patient is=20 symptomatic.

     SPLENECTOMY
Splenectomy has been = shown to=20 induce long-term remission in chronic steroid/IVIG-resistant = ITP. The=20 benefits of splenectomy over long-term drug therapy include = the=20 avoidance of chronic drug toxicity and potentially greater=20 cost-effectiveness. However, splenectomy entails inherent = risks of=20 morbidity and mortality. Postsurgical hemorrhage and = postsplenectomy=20 sepsis are two of the life-threatening complications. = Although the=20 risk of post-operative bleeding is surprisingly low, the risk = of=20 postsplenectomy sepsis is significant, with the incidence of = septic=20 mortality ranging from 3% to 11%. Furthermore, the incidence = of=20 postsplenectomy sepsis is highest among patients younger than = 5 years=20 of age. Causative organisms include pneumococcus, Haemophilus=20 influenzae, and meningococcus. Immunization with = pneumococcal,=20 Haemophilus, and meningococcal vaccines before = splenectomy,=20 administration of prophylactic antibiotic therapy, and delay = of=20 splenectomy for as long as possible for patients in the high-risk = age=20 group are recommended to minimize the risk of postsplenectomy=20 sepsis.

Splenectomy does not ensure long-term remission in all patients; = only=20 60% to 90% of those who have chronic ITP respond to splenectomy. = The=20 need to identify patients who are likely to respond to splenectomy = is=20 abundantly clear. Results of several retrospective studies have = shown=20 that those who demonstrated a significant, although = transient,=20 rise in platelet count after treatment with either steroids = or=20 IVIG had a good response to splenectomy (ie, they did not = require any=20 subsequent medical therapy for their thrombocytopenia). In = contrast, those=20 who did not respond well initially to medical therapy had = relatively=20 poor responses to splenectomy and required continuing medical = management.

Splenectomy is reserved for those patients who have extremely = low=20 platelet counts (and, therefore, are at increased risk of = bleeding)=20 and who are refractory to pharmacologic management. In cases = of=20 life-threatening hemorrhage due to ITP, emergent splenectomy = may be=20 required to increase the platelet count rapidly. It is = important to=20 remember that platelet transfusions alone prior to = splenectomy,=20 although helpful, will not raise the platelet count. IVIG and = steroids also are required to disrupt the autoimmune destruction = of=20 platelets and maintain the platelet count at a level desirable for=20 surgery. A noninvasive alternative to splenectomy in the treatment = of=20 chronic ITP is the use of a short course of radiation = therapy,=20 which resulted in a sustained increase in platelet counts in = a=20 small group of older adult patients who were considered too = unstable=20 for surgery. Use of this therapeutic approach in the pediatric=20 population remains to be evaluated.

Acknowledgments The authors thank Dr Stephen Feig = for=20 helpful suggestions and Wendy Aft for preparation of the=20 manuscript.


3D"   =20 Suggested Reading
Top
OBJECTIVES
Epidemiology and Pathophysiology
Clinical and Laboratory Features
The Role of Bone...
Differential Diagnosis
Management of Acute ITP
IVIG and Steroids
Neonatal Thrombocytopenia
Management of Chronic ITP
3D"Suggested=20 Reading
 
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'XMLHttpRequest()' functionality in IE and Opera. Opera = requires=0A= the Sun Java Runtime Environment .=0A= =0A= by Andrew Gregory=0A= http://www.scss.com.au/family/andrew/webdesign/xmlhttprequest/=0A= =0A= This work is licensed under the Creative Commons Attribution License. To = view a=0A= copy of this license, visit = http://creativecommons.org/licenses/by-sa/2.5/ or=0A= send a letter to Creative Commons, 559 Nathan Abbott Way, Stanford, = California=0A= 94305, USA.=0A= =0A= Attribution: Leave my name and web address in this script intact.=0A= =0A= Not Supported in Opera=0A= ----------------------=0A= * user/password authentication=0A= * responseXML data member=0A= =0A= Not Fully Supported in Opera=0A= ----------------------------=0A= * async requests=0A= * abort()=0A= * getAllResponseHeaders(), getAllResponseHeader(header)=0A= =0A= */=0A= // IE support=0A= if (window.ActiveXObject && !window.XMLHttpRequest) {=0A= window.XMLHttpRequest =3D function() {=0A= var msxmls =3D new Array(=0A= 'Msxml2.XMLHTTP.5.0',=0A= 'Msxml2.XMLHTTP.4.0',=0A= 'Msxml2.XMLHTTP.3.0',=0A= 'Msxml2.XMLHTTP',=0A= 'Microsoft.XMLHTTP');=0A= for (var i =3D 0; i < msxmls.length; i++) {=0A= try {=0A= return new ActiveXObject(msxmls[i]);=0A= } catch (e) {=0A= }=0A= }=0A= return null;=0A= };=0A= }=0A= // Gecko support=0A= /* ;-) */=0A= // Opera support=0A= if (window.opera && !window.XMLHttpRequest) {=0A= window.XMLHttpRequest =3D function() {=0A= this.readyState =3D 0; // = 0=3Duninitialized,1=3Dloading,2=3Dloaded,3=3Dinteractive,4=3Dcomplete=0A= this.status =3D 0; // HTTP status codes=0A= this.statusText =3D '';=0A= this._headers =3D [];=0A= this._aborted =3D false;=0A= this._async =3D true;=0A= this._defaultCharset =3D 'ISO-8859-1';=0A= this._getCharset =3D function() {=0A= var charset =3D _defaultCharset;=0A= var contentType =3D = this.getResponseHeader('Content-type').toUpperCase();=0A= val =3D contentType.indexOf('CHARSET=3D');=0A= if (val !=3D -1) {=0A= charset =3D contentType.substring(val);=0A= }=0A= val =3D charset.indexOf(';');=0A= if (val !=3D -1) {=0A= charset =3D charset.substring(0, val);=0A= }=0A= val =3D charset.indexOf(',');=0A= if (val !=3D -1) {=0A= charset =3D charset.substring(0, val);=0A= }=0A= return charset;=0A= };=0A= this.abort =3D function() {=0A= this._aborted =3D true;=0A= };=0A= this.getAllResponseHeaders =3D function() {=0A= return this.getAllResponseHeader('*');=0A= };=0A= this.getAllResponseHeader =3D function(header) {=0A= var ret =3D '';=0A= for (var i =3D 0; i < this._headers.length; i++) {=0A= if (header =3D=3D '*' || this._headers[i].h =3D=3D header) {=0A= ret +=3D this._headers[i].h + ': ' + this._headers[i].v + '\n';=0A= }=0A= }=0A= return ret;=0A= };=0A= this.getResponseHeader =3D function(header) {=0A= var ret =3D getAllResponseHeader(header);=0A= var i =3D ret.indexOf('\n');=0A= if (i !=3D -1) {=0A= ret =3D ret.substring(0, i);=0A= }=0A= return ret;=0A= };=0A= this.setRequestHeader =3D function(header, value) {=0A= this._headers[this._headers.length] =3D {h:header, v:value};=0A= };=0A= this.open =3D function(method, url, async, user, password) {=0A= this.method =3D method;=0A= this.url =3D url;=0A= this._async =3D true;=0A= this._aborted =3D false;=0A= this._headers =3D [];=0A= if (arguments.length >=3D 3) {=0A= this._async =3D async;=0A= }=0A= if (arguments.length > 3) {=0A= opera.postError('XMLHttpRequest.open() - user/password not = supported');=0A= }=0A= this.readyState =3D 1;=0A= if (this.onreadystatechange) {=0A= this.onreadystatechange();=0A= }=0A= };=0A= this.send =3D function(data) {=0A= if (!navigator.javaEnabled()) {=0A= alert("XMLHttpRequest.send() - Java must be installed and = enabled.");=0A= return;=0A= }=0A= if (this._async) {=0A= setTimeout(this._sendasync, 0, this, data);=0A= // this is not really asynchronous and won't execute until the = current=0A= // execution context ends=0A= } else {=0A= this._sendsync(data);=0A= }=0A= }=0A= this._sendasync =3D function(req, data) {=0A= if (!req._aborted) {=0A= req._sendsync(data);=0A= }=0A= };=0A= this._sendsync =3D function(data) {=0A= this.readyState =3D 2;=0A= if (this.onreadystatechange) {=0A= this.onreadystatechange();=0A= }=0A= // open connection=0A= var url =3D new java.net.URL(new = java.net.URL(window.location.href), this.url);=0A= var conn =3D url.openConnection();=0A= for (var i =3D 0; i < this._headers.length; i++) {=0A= conn.setRequestProperty(this._headers[i].h, this._headers[i].v);=0A= }=0A= this._headers =3D [];=0A= if (this.method =3D=3D 'POST') {=0A= // POST data=0A= conn.setDoOutput(true);=0A= var wr =3D new = java.io.OutputStreamWriter(conn.getOutputStream(), this._getCharset());=0A= wr.write(data);=0A= wr.flush();=0A= wr.close();=0A= }=0A= // read response headers=0A= // NOTE: the getHeaderField() methods always return nulls for me :(=0A= var gotContentEncoding =3D false;=0A= var gotContentLength =3D false;=0A= var gotContentType =3D false;=0A= var gotDate =3D false;=0A= var gotExpiration =3D false;=0A= var gotLastModified =3D false;=0A= for (var i =3D 0; ; i++) {=0A= var hdrName =3D conn.getHeaderFieldKey(i);=0A= var hdrValue =3D conn.getHeaderField(i);=0A= if (hdrName =3D=3D null && hdrValue =3D=3D null) {=0A= break;=0A= }=0A= if (hdrName !=3D null) {=0A= this._headers[this._headers.length] =3D {h:hdrName, = v:hdrValue};=0A= switch (hdrName.toLowerCase()) {=0A= case 'content-encoding': gotContentEncoding =3D true; break;=0A= case 'content-length' : gotContentLength =3D true; break;=0A= case 'content-type' : gotContentType =3D true; break;=0A= case 'date' : gotDate =3D true; break;=0A= case 'expires' : gotExpiration =3D true; break;=0A= case 'last-modified' : gotLastModified =3D true; break;=0A= }=0A= }=0A= }=0A= // try to fill in any missing header information=0A= var val;=0A= val =3D conn.getContentEncoding();=0A= if (val !=3D null && !gotContentEncoding) = this._headers[this._headers.length] =3D {h:'Content-encoding', v:val};=0A= val =3D conn.getContentLength();=0A= if (val !=3D -1 && !gotContentLength) = this._headers[this._headers.length] =3D {h:'Content-length', v:val};=0A= val =3D conn.getContentType();=0A= if (val !=3D null && !gotContentType) = this._headers[this._headers.length] =3D {h:'Content-type', v:val};=0A= val =3D conn.getDate();=0A= if (val !=3D 0 && !gotDate) this._headers[this._headers.length] = =3D {h:'Date', v:(new Date(val)).toUTCString()};=0A= val =3D conn.getExpiration();=0A= if (val !=3D 0 && !gotExpiration) = this._headers[this._headers.length] =3D {h:'Expires', v:(new = Date(val)).toUTCString()};=0A= val =3D conn.getLastModified();=0A= if (val !=3D 0 && !gotLastModified) = this._headers[this._headers.length] =3D {h:'Last-modified', v:(new = Date(val)).toUTCString()};=0A= // read response data=0A= var reqdata =3D '';=0A= var stream =3D conn.getInputStream();=0A= if (stream) {=0A= var reader =3D new java.io.BufferedReader(new = java.io.InputStreamReader(stream, this._getCharset()));=0A= var line;=0A= while ((line =3D reader.readLine()) !=3D null) {=0A= if (this.readyState =3D=3D 2) {=0A= this.readyState =3D 3;=0A= if (this.onreadystatechange) {=0A= this.onreadystatechange();=0A= }=0A= }=0A= reqdata +=3D line + '\n';=0A= }=0A= reader.close();=0A= this.status =3D 200;=0A= this.statusText =3D 'OK';=0A= this.responseText =3D reqdata;=0A= this.readyState =3D 4;=0A= if (this.onreadystatechange) {=0A= this.onreadystatechange();=0A= }=0A= if (this.onload) {=0A= this.onload();=0A= }=0A= } else {=0A= // error=0A= this.status =3D 404;=0A= this.statusText =3D 'Not Found';=0A= this.responseText =3D '';=0A= this.readyState =3D 4;=0A= if (this.onreadystatechange) {=0A= this.onreadystatechange();=0A= }=0A= if (this.onerror) {=0A= this.onerror();=0A= }=0A= }=0A= };=0A= };=0A= }=0A= // ActiveXObject emulation=0A= if (!window.ActiveXObject && window.XMLHttpRequest) {=0A= window.ActiveXObject =3D function(type) {=0A= switch (type.toLowerCase()) {=0A= case 'microsoft.xmlhttp':=0A= case 'msxml2.xmlhttp':=0A= case 'msxml2.xmlhttp.3.0':=0A= case 'msxml2.xmlhttp.4.0':=0A= case 'msxml2.xmlhttp.5.0':=0A= return new XMLHttpRequest();=0A= }=0A= return null;=0A= };=0A= }=0A= ------=_NextPart_000_0000_01C917F0.A9672970 Content-Type: application/octet-stream Content-Transfer-Encoding: quoted-printable Content-Location: http://pedsinreview.aappublications.org/javascript/ajax/utility.js /************************************************************************= *****=0A= * javascript/ajax/utility.js=0A= *=0A= * Utility functions for working with XMLHttpRequest data.=0A= *=0A= * Copyright 2006 Board of Trustees of the Leland Stanford Junior = University.=0A= = *************************************************************************= ***/=0A= =0A= /*=0A= * Copy XML nodes into an HTMLElement. This effectively=0A= * clones XML markup which uses XHTML naming conventions=0A= * into an HTML DOM.=0A= */=0A= function copy_xml_to_html(src, dst) {=0A= if (src.nodeType =3D=3D 1) { /* Node.ELEMENT_NODE */=0A= var e =3D document.createElement(src.nodeName);=0A= for (var i =3D 0; i < src.childNodes.length; i++) {=0A= copy_xml_to_html(src.childNodes[i], e);=0A= }=0A= for (var i =3D 0; i < src.attributes.length; i++) {=0A= var n =3D src.attributes[i].name;=0A= var v =3D unescape_xml_string(src.attributes[i].value); =0A= e.setAttribute(n, v);=0A= if (n =3D=3D "class") {=0A= e.className =3D v;=0A= }=0A= else if (n =3D=3D "style") {=0A= set_css_style(v, e, "");=0A= }=0A= }=0A= dst.appendChild(e);=0A= }=0A= else if (src.nodeType =3D=3D 3) { /* Node.TEXT_NODE */=0A= dst.appendChild(document.createTextNode(src.nodeValue));=0A= }=0A= }=0A= =0A= /* =0A= * It is unclear that this is the right thing to be calling=0A= * from copy_xml_to_html, but it appears that Safari decides=0A= * to convert & to the NCR #, and then encodes that=0A= * NCR to &%26%2338;. So, I'm going to treat the DOM Attr=0A= * value as a plain string, and run our XML string input=0A= * through the decoding routine below.=0A= */=0A= function unescape_xml_string(s) {=0A= return s.replace(/'/g, "'")=0A= .replace(/'/g, "'")=0A= .replace(/"/g, "\"")=0A= .replace(/"/g, "\"")=0A= .replace(/>/g, ">")=0A= .replace(/>/g, ">")=0A= .replace(/</g, "<")=0A= .replace(/</g, "<")=0A= .replace(/&/g, "&")=0A= .replace(/&/g, "&");=0A= }=0A= =0A= /*=0A= * Parse set of CSS rules and apply them to an element.=0A= * This is quite horrifying, but I'm unable to determine=0A= * how else to handle this with IE 6. 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if (name =3D=3D "background-position") {=0A= e.style.backgroundPosition =3D value;=0A= }=0A= else if (name =3D=3D "background-position-x") {=0A= e.style.backgroundPositionX =3D value;=0A= }=0A= else if (name =3D=3D "background-position-y") {=0A= e.style.backgroundPositionY =3D value;=0A= }=0A= else if (name =3D=3D "background-repeat") {=0A= e.style.backgroundRepeat =3D value;=0A= }=0A= else if (name =3D=3D "behavior") {=0A= e.style.behavior =3D value;=0A= }=0A= else if (name =3D=3D "border") {=0A= e.style.border =3D value;=0A= }=0A= else if (name =3D=3D "border-bottom") {=0A= e.style.borderBottom =3D value;=0A= }=0A= else if (name =3D=3D "border-bottom-color") {=0A= e.style.borderBottomColor =3D value;=0A= }=0A= else if (name =3D=3D "border-bottom-style") {=0A= e.style.borderBottomStyle =3D value;=0A= }=0A= else if (name =3D=3D "border-bottom-width") {=0A= e.style.borderBottomWidth =3D value;=0A= }=0A= else if (name =3D=3D "border-collapse") {=0A= e.style.borderCollapse =3D value;=0A= 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"vertical-align") {=0A= e.style.verticalAlign =3D value;=0A= }=0A= else if (name =3D=3D "visibility") {=0A= e.style.visibility =3D value;=0A= }=0A= else if (name =3D=3D "white-space") {=0A= e.style.whiteSpace =3D value;=0A= }=0A= else if (name =3D=3D "width") {=0A= e.style.width =3D value;=0A= }=0A= else if (name =3D=3D "word-break") {=0A= e.style.wordBreak =3D value;=0A= }=0A= else if (name =3D=3D "word-spacing") {=0A= e.style.wordSpacing =3D value;=0A= }=0A= else if (name =3D=3D "word-wrap") {=0A= e.style.wordWrap =3D value;=0A= }=0A= else if (name =3D=3D "writing-mode") {=0A= e.style.writingMode =3D value;=0A= }=0A= else if (name =3D=3D "z-index") {=0A= e.style.zIndex =3D value;=0A= }=0A= else if (name =3D=3D "zoom") {=0A= e.style.zoom =3D value;=0A= }=0A= }=0A= catch (e) {=0A= /* ignore error on attempt to set e.style.[property] */=0A= }=0A= }=0A= }=0A= }=0A= ------=_NextPart_000_0000_01C917F0.A9672970 Content-Type: application/octet-stream Content-Transfer-Encoding: quoted-printable Content-Location: http://pedsinreview.aappublications.org/javascript/entrez/callback.js /************************************************************************= *****=0A= * javascript/entrez/callback.js=0A= *=0A= * Entrez Linking callback to populate content box.=0A= *=0A= * Copyright 2006 Board of Trustees of the Leland Stanford Junior = University.=0A= = *************************************************************************= ***/=0A= =0A= /*=0A= * Execute callback to fill content box with Entrez Linking information.=0A= */=0A= function entrez_callback(pmid, callback_url) {=0A= /*=0A= * MSIE 5.5 and below have issues with the JavaScript=0A= * used for Entrez Linking. For now we have to disable=0A= * the callback until we can track down a proper fix=0A= * (or everybody sanely upgrades to version 6 or 7!).=0A= */=0A= if (navigator) {=0A= var appname =3D navigator.appName;=0A= if (appname =3D=3D "Microsoft Internet Explorer") {=0A= var userAgent =3D navigator["userAgent"];=0A= var s =3D "MSIE ";=0A= var n =3D -1; =0A= if ((n =3D userAgent.indexOf(s)) !=3D -1) {=0A= var v =3D parseFloat(userAgent.substring(n+s.length));=0A= if (v < 6) {=0A= return;=0A= }=0A= }=0A= }=0A= }=0A= =0A= /*=0A= * Acquire table row element to update, initiate callback=0A= * to update table with Entrez Links.=0A= */=0A= var tr =3D document.getElementById('entrez_callback_'+pmid);=0A= if (!tr) {=0A= return;=0A= }=0A= var req =3D new XMLHttpRequest();=0A= if (!req) {=0A= return;=0A= }=0A= req.onreadystatechange =3D function() {=0A= if (req.readyState =3D=3D 4 && (req.status =3D=3D 200 || req.status = =3D=3D 304)) {=0A= var src =3D req.responseXML.documentElement;=0A= var dst =3D document.createDocumentFragment();=0A= for (var i =3D 0; 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