AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Thrombocytopenia-absent radius (TAR) syndrome is a rare condition in which thrombocytopenia is associated with bilateral radial aplasia. TAR syndrome was first described in 1951. An autosomal recessive inheritance pattern was proposed because TAR affected more than 1 member of some families. In 1969, TAR was defined as a syndrome and further classified as the association of hypomegakaryocytic thrombocytopenia and absent radii. The expression varies and includes abnormalities in the GI, skeletal, hematologic, and cardiac systems.

Pathophysiology

Some have proposed that the association of seemingly disparate skeletal and hematologic abnormalities is related to the simultaneous development of the heart, the radii, and the megakaryocytes at 6-8 weeks' gestation. The similarity of TAR syndrome to congenital rubella suggests intrauterine injury when the involved systems develop, but a common etiologic agent has not been identified. As an alternative, the contiguous gene model is based on the premise that phenotypic findings are related when genes responsible for each defect are geographically related in a chromosome. This mechanism, if true, would be independent of the anatomic association and the degree of involvement in either system.

The exact pathophysiology of the thrombocytopenia is still unclear. The platelet abnormality reflects platelet hypoproduction, for which numerous explanatory theories have been proposed. One suggestion is that a failure in production of humoral or cellular stimulators of megakaryocytopoiesis (eg, thrombopoietin) is responsible for inhibiting platelet production. However, studies by Ballmaier et al (1997) and Sekine et al (1998) showed comparable or increased levels of thrombopoietin in patients with TAR compared with healthy control subjects. These findings suggest that the thrombocytopenia is due to a lack of response to thrombopoietin, especially given the observation of normal thrombopoietin receptor expression on megakaryocytes. In 2000, Letestu et al suggested that the defect was a blockage in cell differentiation at an early stage.

Other theories for platelet hypoproduction include an abnormal response to stimulators of megakaryocytopoiesis involving an abnormal signal-transduction pathway, decreased numbers and sizes of megakaryocytic progenitor cells (Sekine et al, 1998), abnormal progenitor cells with a maturational defect or receptor defect, and the presence of humoral or cellular inhibitors of megakaryocytopoiesis.

No causative mutation has been identified despite investigations of the c-mpl gene in patients with TAR. Another proposed candidate gene is a HOX gene. The HOX family of genes plays a major role in embryogenesis and cell differentiation, including differentiation of hematopoietic cell lines. However, Fleischman et al (2002) did not detect mutations in the coding sequence of HOX genes known to affect radial development. Although no mutation is known, the observation that platelet counts improve during infancy and that they may even normalize with age, has led to the suggestion that abnormal genes may be developmentally regulated.

TAR syndrome is generally considered an autosomal recessive disease. Some have suggested that the inheritance pattern may be autosomal dominant with variable penetrance. Urban et al (1998) postulated that, given the phenotypic overlap between Roberts syndrome and TAR syndrome, allelic heterogeneity might cause both. In this postulate, TAR syndrome is the compound heterozygous form, with a mild and a severe mutation, whereas Roberts syndrome is the homozygous form with the severe mutation. However, genetic heterogeneity and environmental factors cannot be completely ruled out.

Frequency

United States

TAR syndrome rarely occurs in the United States.

International

The frequency of TAR syndrome is 0.42 case per 100,000 live births in Spain.

Mortality/Morbidity

The major cause of mortality in TAR is hemorrhage. The incidence of hemorrhage is limited to the first 14 months of life. Of 20 deaths in 76 patients whom Hedberg et al reported in 1998, 18 were due to hemorrhagic events; most of patients who died had platelet counts <10 X 10⁹/L.

Bleeding and hemorrhage can also result in clinically significant morbidity, especially intracranial hemorrhage. Hand and upper-extremity function is usually good if radial aplasia is the only skeletal abnormality. However, patients require plastic surgery, occupational therapy, and physiotherapy.

Race

No ethnic or racial predilection is reported.

Sex

The male-to-female ratio is 1:1.

Age

TAR syndrome is congenital, and patients usually present with symptomatic thrombocytopenia in the first week of life.

CLINICAL

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History

• Episodes of thrombocytopenia begin in the neonatal period.
• • About 50% of affected infants are symptomatic in the first week of life, and 90% are symptomatic by the age of 4 months.
  • Thrombocytopenia can fluctuate over time. Therefore, if TAR syndrome is strongly suspected on the basis of one normal platelet count, repeating the blood work is recommended.
  • Thrombocytopenic episodes are most frequent during the first 2 years of life, when they increase the mortality rate secondary to intracranial hemorrhage.
  • With increasing age, the recurrence of thrombocytopenic episodes decreases. Thrombocytopenia can improve to a near-normal state.
  • Nonspecific stress, infection, and diet (eg, allergy to cow's milk) may precipitate episodes.
  • Symptoms include purpura, petechiae, epistaxis, melena, hemoptysis, hematuria, hematemesis, and, rarely, intracranial hemorrhage.
• Symptomatic cow's-milk allergy is associated with 47% of all cases of TAR syndrome, and patients may present as vomiting, bloody diarrhea, and failure to thrive.
• Mental retardation is associated with about 7% of all cases of TAR syndrome.
• • The association of TAR with mental retardation is presumed to be secondary to complications from intracranial hemorrhage precipitated by thrombocytopenia.
  • Symptoms of acute intracranial hemorrhage in an infant are associated with poor feeding, lethargy, irritability, and fluctuating levels of consciousness.
  • Structural causes that predispose the patient to mental retardation and other neuropsychiatric disorders (psychosis) have been suggested (Sachdev, 2005).
  • Hypoplasia of the cerebellar vermis and corpus callosum has been reported in this syndrome (Skorka, 2005).

Physical

• Upper-extremity abnormalities range from isolated absent radii to phocomelia. Abnormalities include the following:
• • Bilateral radial aplasia
  • Radial club hand
  • Hypoplastic carpals and phalanges
  • Hypoplastic ulnae, humeri, and shoulder girdles
  • Syndactyly and clinodactyly of fingers and toes
  • Selective hypoplasia of middle phalanx, fifth digit
  • Altered palmar contours
• Greenhalgh et al (2002) examined 34 patients with TAR syndrome. Their findings demonstrated how the length of the upper limb can affect the patient's functional ability. They divided upper-limb defects into 3 categories of severity, as follows:
  • The first group (71%) had mild defects consisting of radial aplasia with various degrees of ulnar and humeral hypoplasia. The patients also had normal shoulder girth and, hence, near-normal upper-body strength, but splints were still useful for periods of prolonged activity of the upper limbs.
  • The second group (18%) had increased degrees of limb shortening, humeral hypoplasia, and underdevelopment of the shoulder girth with decreased upper-body strength. Splints were also useful in this group.
  • The last group was the most affected, with severe ulnar and humeral shortening and phocomelia.
• Lower-extremity anomalies occur in 46% of patients and vary from clinically undetectable changes to phocomelia. These anomalies are usually less severe than those of the upper limbs. Abnormalities include the following:
• • Hip dislocation
  • Femoral torsion
  • Tibial torsion
  • Valgus and varus foot deformities
  • Deformity of the knee (eg, absence of the patella, patellar dislocation)
  • Absent tibiofibular joint
  • Abnormal toe placement
  • Fifth toe overlapping the fourth
• Cardiac anomalies occur in 15-33% of patients and include the following:
• • Tetralogy of Fallot
  • Atrial septal defect
  • Ventricular septal defect (VSD)
• Facial anomalies (which occur in 53% of patients) include the following:
• • Micrognathia (3-30% of patients)
  • Tall, broad forehead
  • Facial hemangiomas
  • Hypertelorism
  • Low, posteriorly rotated ears
• Other abnormalities are numerous and include the following:
• • Asymmetric first rib
  • Cervical rib, cervical spina bifida, fused cervical spine, and nuchal folds
  • Meckel diverticulum
  • Uterine anomalies
  • Dorsal pedal edema
  • Hyperhidrosis
  • Short stature (95% of patients at or below the 50th percentile)
  • Skeletal malformations
  • Renal anomalies (23% of patients), eg, duplex ureter, mild renal pelvis dilatation, horseshoe kidneys
  • Intracranial vascular malformation
  • Sensorineural loss
  • Cleft palate
  • Scoliosis
  • GI anomalies (eg, esophageal atresia, tracheoesophageal fistula, anal atresia)
  • Annular pancreas
• Only patients with TAR syndrome consistently have bilateral absence of the radii with the presence of thumbs and 4 digits. In distinguishing TAR from other syndromes involving skeletal abnormalities of the upper extremities, the following features may be of assistance:
• • Patients with TAR syndrome always have thumbs, but thumbs may be hypoplastic or absent in patients with Fanconi anemia. Fanconi anemia is also associated with chromosomal abnormalities, a rare onset of thrombocytopenia before age 1 year, and pancytopenia in children aged 5-10 years. A reliable diagnostic test is a chromosomal breakage study.
  • Thumb abnormalities include absent, hypoplastic, and triphalangeal thumbs in Holt-Oram syndrome, and blood counts are normal. The patient often has a family history of heart and limb defects due to the autosomal dominant pattern of inheritance.
  • Thrombocytopenia is not often observed in Roberts syndrome (Roberts-SC phocomelia). Most patients with this syndrome have microcephaly and mental retardation.
  • Radial hypoplasia is found in patients with Aase syndrome, but the thumb is triphalangeal. Hypoplastic anemia is the usual presentation, similar to that of Blackfan-Diamond syndrome. Thrombocytopenia is not a feature.

Causes

Causes of TAR syndrome are unknown. See Pathophysiology.

DIFFERENTIALS

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Other Problems to be Considered

RAPADILINO syndrome: RAPADILINO syndrome is a rare syndrome characterized by radial hypoplasia or aplasia, patellar hypoplasia or aplasia, cleft or highly arched palate, diarrhea, dislocated joints, small size (>2 standard deviations below the mean in height), limb malformation, slender nose, and normal intelligence.

Roberts syndrome: Roberts syndrome is characterized by prenatal and postnatal growth retardation; craniofacial anomalies, especially facial clefts; limb deficiencies, including tetraphocomelia in most patients; and genital hyperplasia. Parental consanguinity rate is high.

Thalidomide embryopathy: Thalidomide embryopathy is the teratogenic effect of thalidomide when the drug is taken during pregnancy. Affected infants can have limb and digit defects, craniofacial anomalies, hearing and vision defects, and improper formation of organs including the heart and kidneys.

Trisomy 18 (Edward syndrome): Patients with trisomy 18 may have craniofacial anomalies (eg, prominent occiput, short palpebral fissures, micrognathia, external ear variations); digit anomalies (eg, clenched fist with the index finger overlapping the third finger, the fifth finger overlapping the fourth, hypoplastic nails, thumb aplasia); short sternum (breastbone); rocker-bottom feet; and cardiac, pulmonary, GI, and genitourinary defects.

VACTERL association: This is a syndrome of congenital anomalies that includes vertebral dysgenesis, anal atresia with or without fistula, cardiac defects (VSD), tracheoesophageal fistula, and renal and limb anomalies.

WORKUP

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Lab Studies

• CBC count findings
• • The platelet count may be 15-30 X 10⁹/L.
  • Eosinophilia is observed in 50% of patients.
  • Leukocytosis may be present, with a WBC count >35 X 10⁹/L with a left shift and leukemoid reaction.
  • Anemia may be present secondary to bleeding.
• Genetic findings
• • Chromosomes are normal.
  • Findings on chromosomal breakage studies with clastogenic agents are normal.

Imaging Studies

• Characteristic skeletal involvement (ie, absent radii) is detectable during prenatal transvaginal ultrasonography as early as 13 weeks' gestation, when sufficient fetal skeletal ossification is present.
• Upper-limb abnormalities on prenatal sonograms suggest numerous syndromes in the differential diagnosis.
• After radial aplasia is observed, ultrasonography of the extremities, face, and kidneys is indicated.

Other Tests

• Sampling of the bone marrow reveals the following findings:
• • Normal or hypercellular bone marrow
  • Decreased, absent, or immature megakaryocytes
  • Small, basophilic, vacuolated megakaryocytes
  • Erythroid hyperplasia

Procedures

• Cordocentesis can be performed to confirm known genetic conditions. Cordocentesis poses a 1-2% risk of fetal loss and a risk of prolonged bleeding from the umbilical puncture site.
• In 1994, Weinblatt et al performed in utero platelet transfusion of a fetus with radial aplasia at 37 weeks' gestation after cordocentesis revealed a platelet count of 40 X 10⁹/L. The infant was delivered within 24 hours of the transfusion with no complications.

TREATMENT

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Medical Care

General thrombocytopenic precautions during times of clinically significant thrombocytopenia with a platelet count <80 X 10⁹/L (usually during the first year of life) should include avoidance of trauma (with use of a soft helmet if needed), avoidance of certain antiplatelet drugs (eg, aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs]), and prolonged pressure on injection sites (especially after intramuscular injections).

• Prehospital care should involve first aid for visible acute hemorrhage.
• • Apply firm steady pressure to the site of bleeding.
  • Keep the patient warm.
  • Elevate the bleeding limb.
• The mainstay of hospital treatment is supportive care. By far, the most important treatment is platelet transfusion.
• • The goal of platelet transfusion is to maintain a sufficient volume of platelet to prevent bleeding without adverse effects.
  • Prophylactic transfusions with leukocyte-reduced platelet concentrates are used in patients at high risk of clinically significant hemorrhage.
  • A transfusion target extrapolated from thrombocytopenia associated with acute leukemia is a platelet count <40 X 10⁹/L. Platelet counts greater than this level are associated with a decreased risk of major vascular bleeding. Melena, epistaxis, hematuria, mucosal bleeding, and hematemesis are controlled in 80% of patients with acute leukemia when a posttransfusion increment of >40 X 10⁹/L is used.
• Potential risks of platelet transfusion include infection, anaphylaxis, and hemolytic reactions.
  • Hepatitis viruses (B, C, other) and HIV are the most common infective pathogens potentially transmitted with the transfusion of blood products.
  • A further risk with transfusion is human leukocyte antigen (HLA) alloimmunization. However, platelets themselves are not highly immunogenic, and contaminating lymphocytes are most likely to cause HLA alloimmunization. Therefore, leukocyte-reduced platelet concentrates should always be used. Alloimmunization can be delayed by using random single-donor platelets and, ideally, by identifying a limited number of dedicated donors.
  • Treatment of conditions refractory or nonresponsive to transfusion is difficult but may include the use of HLA-matched platelets from family members. However, the refractory state can occur even in patients receiving HLA-matched platelets, a finding that suggests a non-HLA, platelet-specific antigen.
• Splenectomy is usually effective for the treatment of thrombocytopenia in adults.
• Bone marrow transplantation (BMT) is an option for patients who remain thrombocytopenic with bleeding despite platelet transfusions.

Surgical Care

Splinting of the hands (and legs, if indicated) during infancy improves future function. If surgical correction of the arm deformities is indicated, it should be undertaken after the patient is hemodynamically stable. If surgery is not a feasible option to manage deformities of the upper limb as patients age, adaptive devices to assist with activities of daily living (eg, dressing, toileting, feeding) are helpful. Prostheses are less useful than adaptive devices because the patient often has a weak upper extremity because of poorly developed musculature and because a functional 5-digit hand diminishes the need for a long limb.

Management of lower-extremity deformities must be individualized given the wide spectrum of anomalies. Intervention can range from no treatment if the deformity is mild (eg, mild varus deformity) and if it causes no functional impairment to the use of a power wheelchair or a motorized cart if the anomaly is severe and if it limits ambulation. Overall, the goal is to improve functioning and enhance independence.

Splenectomy is usually effective for the treatment of thrombocytopenia in adults.

Consultations

The patient with suspected TAR syndrome should be examined by a hematologist, orthopedic surgeon, plastic surgeon, and cardiologist, all of whom specialize in treating children.

Diet

Patients should avoid ingesting cow's milk for the first year of life because cow's milk allergy is associated with TAR and may precipitate thrombocytopenic episodes. The frequency of thrombocytopenic episodes and the risk of complications are typically highest during the first 2 years of life, and recurrences decrease as the child ages. Blood diarrhea is reported in 20% of patients. Removal of milk from the diet alleviates this symptom.

Activity

Careful handling of the patient, with padding his or her crib and with the application of soft helmets, can be used in the first year of life. Most patients are adequately hemostatic after the first year of life to allow them to perform normal activities. Patients should avoid trauma (eg, contact sports) during periods of thrombocytopenia.

MEDICATION

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Drug Category: Antifibrinolytic agents

Antifibrinolytic agents decrease bleeding and transfusion requirements and help establish hemostasis. They are especially useful for controlling bleeding or prolonged oozing from gingival surfaces (eg, during teething in infants).

Drug Category: Synthetic antidiuretic hormones

Synthetic antidiuretic hormones nonspecifically enhance hemostasis by stimulating the release of von Willebrand factor. Desmopressin stimulates the release of factor VIII, prostaglandins, and plasminogen. However, the mechanism of action is not clear, and it may not be common to all 3 substances. These agents affect vascular walls, increasing platelet adhesion. This local hemostatic action may account for their hemostatic properties.

FOLLOW-UP

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Further Inpatient Care

• Monitor response to platelet transfusions through observation of hemostasis and rise in platelet counts.

Further Outpatient Care

• Monitor the need for and response to platelet transfusions by measuring platelet counts.

Deterrence/Prevention

• While the patient is thrombocytopenic, injury-prevention strategies are indicated.
• Patients should avoid contact sports and use appropriate protective gear (eg, helmets, padding) when participating in sports or leisure activities.

Complications

• Complications arise from hemorrhage and hemorrhagic insults, especially intracranial hemorrhage.

Prognosis

• The clinical course is one of episodic, severe thrombocytopenia superimposed on a background of persistent thrombocytopenia. The frequency of thrombocytopenic episodes decreases with age. By school age, near-normal platelet counts are expected. If a patient survives the initial 2 years of life, life expectancy is normal.
• The risk of morbidity may be increased. Case reports describe acute leukemia in both pediatric and adult patients with TAR syndrome. This development is not entirely unexpected because other syndromes of bone marrow failure, such as Fanconi anemia and Shwachman-Diamond syndrome, are associated with an increased risk of malignancies. Given the rare incidence of this syndrome, identifying a chance association or a causal relationship is difficult.

Patient Education

• Patients and families must be educated about the risk of hemorrhagic injury during episodes of thrombocytopenia, about signs and symptoms indicative of thrombocytopenia (eg, bruising, petechiae, mucosal bleeding), and about the need to promptly seek medical attention during these episodes.
• For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patient education article Bone Marrow Biopsy.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failure to counsel families on the risks of hemorrhage associated with thrombocytopenia and the need for prompt management during thrombocytopenic episodes could expose the practitioner to liability.

Special Concerns

• Although no genetic anomaly is clearly associated with TAR syndrome, several patients with an apparent autosomal recessive pattern are reported in an extended family lineage.
• Families benefit from genetic counseling after one affected child is identified.

MULTIMEDIA

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Media file 1:  Infant with thrombocytopenia-absent radius syndrome. The arms and forearms are shortened, with radial deviation of both hands because of the absence of bilateral radii. The legs are normal. See also Images 2 and 3.
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Media type:  Photo

Media file 2:  Same infant as in Images 1 and 3. Close-up photograph of arm and forearm (volar aspect). Note the petechiae.
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Media type:  Photo

Media file 3:  Same infant as in Images 1 and 2. Close-up photograph of arm and forearm (dorsal aspect).
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Media type:  Photo

REFERENCES

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• Ballmaier M, Schulze H, Strauss G, et al. Thrombopoietin in patients with congenital thrombocytopenia and absent radii: elevated serum levels, normal receptor expression, but defective reactivity to thrombopoietin. Blood. Jul 15 1997;90(2):612-9. [Medline]. [Full Text].
• Fadoo Z, Naqvi SM. Acute myeloid leukemia in a patient with thrombocytopenia with absent radii syndrome. J Pediatr Hematol Oncol. Feb 2002;24(2):134-5. [Medline].
• Fleischman RA, Letestu R, Mi X, et al. Absence of mutations in the HoxA10, HoxA11 and HoxD11 nucleotide coding sequences in thrombocytopenia with absent radius syndrome. Br J Haematol. Feb 2002;116(2):367-75. [Medline].
• Greenhalgh KL, Howell RT, Bottani A, et al. Thrombocytopenia-absent radius syndrome: a clinical genetic study. J Med Genet. Dec 2002;39(12):876-81. [Medline]. [Full Text].
• Hall JG, Levin J, Kuhn JP, et al. Thrombocytopenia with absent radius (TAR). Medicine (Baltimore). Nov 1969;48(6):411-39. [Medline].
• Hedberg VA, Lipton JM. Thrombocytopenia with absent radii. A review of 100 cases. Am J Pediatr Hematol Oncol. Spring 1988;10(1):51-64. [Medline].
• Letestu R, Vitrat N, Masse A, et al. Existence of a differentiation blockage at the stage of a megakaryocyte precursor in the thrombocytopenia and absent radii (TAR) syndrome. Blood. Mar 1 2000;95(5):1633-41. [Medline]. [Full Text].
• MacDonald MR, Schaefer GB, Olney AH, Patton DF. Hypoplasia of the cerebellar vermis and corpus callosum in thrombocytopenia with absent radius syndrome on MRI studies. Am J Med Genet. Mar 1 1994;50(1):46-50. [Medline].
• McLaurin TM, Bukrey CD, Lovett RJ, Mochel DM. Management of thrombocytopenia-absent radius (TAR) syndrome. J Pediatr Orthop. May-Jun 1999;19(3):289-96. [Medline].
• Sachdev P. Brief psychosis in thrombocytopenia-absent radius syndrome: a case report. Aust N Z J Psychiatry. Sep 2005;39(9):841-2. [Medline].
• Sekine I, Hagiwara T, Miyazaki H, et al. Thrombocytopenia with absent radii syndrome: studies on serum thrombopoietin levels and megakaryopoiesis in vitro. J Pediatr Hematol Oncol. Jan-Feb 1998;20(1):74-8. [Medline].
• Skorka A, Bielicka-Cymermann J, Gieruszczak-Bialek D, Korniszewski L. Thrombocytopenia-absent radius (tar) syndrome: a case with agenesis of corpus callosum, hypoplasia of cerebellar vermis and horseshoe kidney. Genet Couns. 2005;16(4):377-82. [Medline].
• Urban M, Opitz C, Bommer C, et al. Bilaterally cleft lip, limb defects, and haematological manifestations: Roberts syndrome versus TAR syndrome. Am J Med Genet. Sep 23 1998;79(3):155-60. [Medline].
• Weinblatt M, Petrikovsky B, Bialer M, et al. Prenatal evaluation and in utero platelet transfusion for thrombocytopenia absent radii syndrome. Prenat Diagn. Sep 1994;14(9):892-6. [Medline].

Article Last Updated: Dec 14, 2006