Clinical audit of antiphospholipid antibody testing in tertiary practice: towards improved relevance in thrombophilia investigations.

BACKGROUND: The antiphospholipid syndrome (APS) is an autoimmune condition characterised by vascular thromboses and/or pregnancy morbidity. Diagnosis of APS typically requires laboratory evidence of antiphospholipid antibodies (aPL). Depending on their clinical presentation, affected individuals might be seen by a variety of clinical specialities. AIM: To evaluate clinical ordering patterns for aPL/APS at a tertiary level public facility. METHODS: We performed an audit of internal clinical requests for aPL tests at our institution for a 6-month period. RESULTS: We identified a wide variety of clinical ordering background for aPL, of predominantly obstetric (72/268; 26.9%) or thrombophilic (78/268; 29.1%) patients. Only 11/268 samples (4.1%) were positive for lupus anticoagulant (LA) and 14/268 (5.2%) were positive for anticardiolipin antibody (aCL). The percentage of aCL positivity in the LA-positive group was 46% (5/11). None of the 72 obstetric patients tested was identified to have aPL. Of the 11 LA-positive patients, the reasons identified for testing comprised: prolonged Activated Partial Thromboplastin Time (assay) (n= 3), thrombosis (n= 3), APS (n= 2), systemic lupus erythematosus (n= 2), vasculitis (n= 1). CONCLUSION: We determined a wide variety of clinical ordering background for aPL at a tertiary level institution, with an overall low rate (<10%) of aPL positivity among a hospital population of predominantly obstetric or thrombophilic patients. That no positive obstetric aPL cases were identified suggests local clinical ordering guidelines may need review, as also potentially practised at other institutions. We also observed a moderate rate (46%) of coincidence of aCL and LA, in agreement with guidelines indicating that multiple tests are required to identify APS.

Distinguishing types 1 and 2M von Willebrand disease.

Discrimination of types 1 and 2M von Willebrand disease (VWD) is problematic. Type 1 VWD represents a quantitative deficiency of von Willebrand factor and type 2M a qualitative disorder. 2M VWD is considered a potentially more serious bleeding disorder than type 1 VWD and may also require a differential management approach given the higher bleeding risk and that desmopressin may be less effective. We describe a case of 2M VWD 'masquerading' as type 1 and show how the differential diagnosis can be obtained using standard laboratory assays. The case was genetically confirmed as a 3943C>T mutation, leading to R1315C.

Two cases of refractory warm autoimmune hemolytic anemia treated with rituximab.

Autoimmune hemolytic anemia is thought to be mediated via auto-antibodies produced by lymphoid B cells. This may be an idiopathic process or secondary to an underlying infection or lymphoproliferative disorder. Conventional treatment comprises immunosuppression with corticosteroids and, in some cases, splenectomy. A proportion of patients require lifelong immunosuppression to maintain disease remission. Monoclonal antibody rituximab has gained widespread acceptance in the management of B-cell malignancies. Additionally, it has been used to treat disorders associated with auto-antibody production, such as cold hemagglutinin disease, immune thrombocytopenia, and Evans syndrome. Its use in the treatment of patients with autoimmune hemolytic anemia in the setting of allogeneic bone marrow transplantation as well as in patients with an underlying lymphoproliferative disease has also been reported. We report herein the successful use of rituximab in the treatment of two patients with idiopathic refractory warm autoimmune hemolytic anemia, who are still in remission at 15 and 9 months following treatment.

Hypodiploidy of 37 chromosomes in an adult patient with acute lymphoblastic leukemia.

We present a 42-year-old man with acute lymphoblastic leukemia and hypodiploidy at diagnosis. Chromosome count was 37, with a mixture of numerical and structural abnormalities. The patient died 9 months post diagnosis, during which time three further cytogenetic tests were performed. The core abnormalities seen upon diagnosis were present at 7 and 9 months after diagnosis, with a duplication of the abnormal hypodiploid karyotype on the last specimen. While considerable imbalances were present as a result of whole chromosome aneuploidy, no region was obviously nullisomic.

Laboratory diagnosis of von Willebrand disorder (vWD) and monitoring of DDAVP therapy: efficacy of the PFA-100 and vWF:CBA as combined diagnostic strategies.

We have coevaluated a combination of test processes for diagnosing von Willebrand disease (vWD) and monitoring deamino-delta-D-arginine vasopressin (DDAVP) therapy. Using normal controls (n = 23), closure time (CT) ranges measured by PFA-100(R) were (mean +/- 2SD): (i) collagen/ADP cartridge (C/ADP): 67-127 s (ii) collagen/epinephrine (C/Epi): 94-162 s. From a panel of 125 patients undergoing evaluation for clinical haemostatic defects, 29/30 samples from patients with vWD [17/18 type 1, 1/1 type 3, 3/3 type 2A, 7/7 type 2B and 1/1 pseudo-vWD] gave prolonged CTs using C/Epi. The C/ADP was less sensitive, being normal in 7/18 of the type 1 vWD individuals, with higher sensitivity to more severe vWD. Individuals with haemophilia (six factor VIII-deficient, one factor XI-deficient) gave normal CTs, while those with clinical thrombocytopenia (n=13) gave normal or prolonged CTs, somewhat dependent on platelet count. The PFA-100 was also evaluated as a part of the laboratory monitoring procedure in patients with either vWD or haemophilia undergoing a DDAVP trial as a therapeutic management process. For vWD, correction of an initially prolonged CT by DDAVP, accompanied by normalization of von Willebrand factor (vWF) measurable by von Willebrand factor antigen, vWF collagen binding activity and vWF ristocetin cofactor assays (vWF:Ag, vWF:CBA and vWF:RCof), was achieved in type 1 vWD (n=5). In an individual with type 2A vWD, DDAVP normalized vWF:Ag and vWF:RCof, but had no apparent effect on the baseline maximally prolonged CT. In an individual with type 2B vWD, factor VIII/vWF concentrate also normalized vWF:Ag and vWF:RCof, but similarly had no apparent effect on the baseline maximally prolonged CT. vWF:CBA did not normalize for either of these individuals, potentially suggesting that normalization of vWF:CBA might be required for normalization of CT. This concept is supported by correlation analysis undertaken between CT and various vWF parameters. Among these, vWF:CBA held the strongest relationship in our data set, which showed an inverse progressive rise in CT for falling vWF:CBA. Based on these results, we would conclude that the PFA-100 is highly sensitive to the presence of vWD, and may thus provide a valuable screening test for vWD. Furthermore, the combined utility of the PFA-100 and vWF:CBA as markers of DDAVP responsiveness may prove to be simple, quick but powerful, predictors for its clinical efficacy.

Laboratory testing for von Willebrand's disease: an assessment of current diagnostic practice and efficacy by means of a multi-laboratory survey. RCPA Quality Assurance Program (QAP) in Haematology Haemostasis Scientific Advisory Panel.

We report an evaluation of current laboratory practice for the diagnosis of von Willebrand's disease (VWD) by means of a multilaboratory survey. This assessment was undertaken with the RCPA Quality Assurance Program (QAP) in Haematology, which covers a wide geographic area encompassing Australia, New Zealand and Asia. A total of 25 laboratories actively involved in testing for VWD were selected to participate in a sample testing assessment exercise. Samples comprised 10 plasmas: (i) a normal plasma pool (in duplicate), (ii) this pool diluted to 50% (in duplicate), (iii) a normal individual (X1), (iv) severe Type 1 VWD (X1), (v) Type 2B VWD (x2 unrelated donors), (vi) Type 3 VWD (x1), (vii) Type 2A VWD (x1). Laboratories were asked to perform all tests available to them in order to establish a laboratory diagnosis of VWD, and then to comment on the possibility or otherwise of VWD. Overall findings indicated a wide variation in test practice, in the effectiveness of various test procedures in detecting VWD, and in the ability of various composite test panels to identify type 2 VWD subtypes. Firstly, while all laboratories (n = 25) performed tests for FVIII:C activity, von Willebrand factor 'antigen' (VWF:Ag) and a functional VWF assay [using the ristocetin cofactor assay (VWF:RCo; n = 23) and/or the collagen binding assay (VWF:CBA; n = 12)], only three laboratories carried out VWF:Multimer analysis. Secondly, for the three quantitative VWF assays, 10/25 (40%) laboratories performed all three, whereas 15/25 (60%) performed only two [VWF:Ag and VWF:RCo (n = 13); VWF:Ag and VWF:CBA (n = 2)]. Thirdly, a variety of assay methodologies were evident for VWF:Ag [ELISA, electro-immuno diffusion (EID), latex immuno-assay (LIA), and VIDAS assay] and VWF:RCo (platelet agglutination/'aggregometry' and a 'functional VWF:RCo-alternative' ELISA assay). Between method analysis for the quantitative VWF assays showed that the VWF:RCo yielded the greatest degree of inter-laboratory assay variation, and had the poorest overall performance with respect to sensitivity to low levels of VWF. The VWF:CBA also performed better than the VWF:RCo in terms of ability to detect functional VWF 'discordance' (i.e. Type 2 VWD). Within VWF:Ag method analysis showed that the EID assay procedure was associated with the greatest variation in assay results, while the EID and LIA test methods showed poorer sensitivity at low VWF levels compared to the ELISA method. Within the VWF:RCo assay procedure, greatest variation in assay results and poorest sensitivity to low VWF levels was obtained using the agglutination method; however, the agglutination procedure showed better performance than the 'functional VWF:RCo-alternative' ELISA assay in identifying Type 2 VWD plasma samples. Finally, despite identified variations, most laboratories appeared to understand the complexities involved in the VWD-diagnostic process, and made appropriate diagnostic predictions regarding tested samples. From a total possible 246 interpretation events, laboratories in most cases correctly identified normal samples as normal (67/75 events = 89%), and VWD samples as derived from individuals with VWD (117/121 events = 97%). Moreover, when VWD was suggested by laboratory findings, laboratories usually correctly predicted the general subtype of VWD present (96/109 events = 88%). When 'misinterpretations' occurred, these could often be linked to the test panels utilised by laboratories. That is, laboratories using the VWF:Ag and VWF:RCo combination were more likely to incorrectly identify samples derived from Type 2 VWD patients as being Type 1, Type 1 VWD patients as being Type 2, and normal plasma samples as potentially derived from patients with VWD, compared to those using the VWF:Ag and VWF:CBA.

Plasma fibrinogen and other cardiovascular disease risk factors and cataract.

PURPOSE: To determine whether associations exist between cataract and established cardiovascular risk factors (other than smoking) - hypertension, body mass index, serum lipids and plasma fibrinogen. METHODS: The Blue Mountains Eye Study is a large (n=3654) population-based cross-sectional study conducted among people aged 49-97 years residing in the Blue Mountains, a region west of Sydney, Australia. Risk factor data were collected using standardised clinical procedures. Lens photographs were taken and graded for presence and severity of cortical, nuclear, and posterior subcapsular cataracts. RESULTS: Cortical cataract was associated with a history of myocardial infarction, higher plasma fibrinogen, and higher serum cholesterol. Nuclear cataract was associated with a higher platelet count but hypertension was associated with lower prevalence of nuclear cataract. Posterior subcapsular cataract was associated with higher plasma fibrinogen and lower body mass index. Some of these associations appeared to be stronger in women than in men: fibrinogen and cortical cataract and body mass index and posterior subcapsular cataract. CONCLUSIONS: Several risk factors for cardiovascular disease are associated with presence of cataract, perhaps explaining the observation in several studies that people with cataract have increased mortality rates. The possibility of strong associations between plasma fibrinogen and cataract merits further epidemiological and laboratory research.

Identification and characterization of a novel mutation in von Willebrand factor causing type 2B von Willebrand's disease.

Type 2B von Willebrand's disease (VWD) is a variant in which the structurally abnormal von Willebrand factor (VWF) has an increased affinity for the platelet glycoprotein Ib-IX-V complex. Spontaneous binding of type 2B VWF to platelets and their subsequent clearance from the plasma appear to account for the characteristic phenotype of type 2B VWD. Several type 2B mutations have been described and shown to be grouped along the amino edge of the beta sheet of the VWF A1 domain. In this report we describe a novel missense mutation, Arg543Leu, in the VWF A1 domain in three members of a family with type 2B VWD. We have expressed and characterized the corresponding recombinant mutant VWF in transiently transfected COS-7 cells. Relative to wild-type VWF, recombinant Arg543Leu VWF showed a similar multimer composition but exhibited binding to fixed platelets both in the presence and absence of ristocetin, confirming the ability of this mutation to permit spontaneous interaction of VWF with platelets. These studies are consistent with a recently proposed model in which the VWF-A1 domain exists in either 'on' or 'off' states, with type 2B mutations switching VWF to an 'on' state to facilitate GPIb binding.

Hematological indices in an older population sample: derivation of healthy reference values.

Factors affecting hematological values were explored, and healthy reference values were estimated from a cross-sectional survey of a population (n = 4433), ages 49 years or more, residing permanently in a defined geographic region. Nursing home residents were excluded. Details of medication use and medical history were obtained by interview, and participants were asked to return after an overnight fast for blood sampling. The participation rate was 82.4%, of whom 88.4% provided a fasting blood sample. Hemoglobin, hematocrit, and erythrocyte counts were higher in men, whereas platelet counts were higher in women. Statistical associations between each hematological index and smoking, alcohol intake, use of certain drugs, chronic disease, and high creatinine values were tested by unpaired t-tests. Separate reference groups were defined for each hematological index by excluding subjects with any of the factors found to be of importance. The resulting reference values are particularly appropriate for evaluating hematological test results in older individuals.

Laboratory assays for von Willebrand factor: relative contribution to the diagnosis of von Willebrand's disease.

Appropriate investigation of a patient with suspected von Willebrand's disease (VWD) involves a clinical assessment of the patient followed by laboratory testing. A variety of laboratory assays may be performed, not necessarily restricted to an assessment of von Willebrand factor (VWF). Due to the limitations of each assay, and because of VWD heterogeneity, no single test procedure is sufficiently robust to permit detection of all VWD variants. Indeed, these factors often lead to considerable confusion in the process of laboratory interpretation regarding the likelihood of VWD, and the subtype of VWD. This paper attempts to clarify some of the issues that lead to this confusion. It analyses the relative contribution of four separate assays for VWF [VWF:Multimer analysis, VWF:Antigen (VWF:Ag), VWF:Ristocetin Cofactor (VWF:RCof), and VWF:Collagen Binding Activity assay (VWF:CBA)] to the diagnosis and classification of VWD. Although each assay detects VWF, it is important to recognise that each assay provides different information on the VWF so detected. For example, while the VWF:Ag assay is a quantitative assay and provides a very good measure of the overall level of VWF present in a patient's plasma, it is not a functional assay and yields no information concerning the quality of the VWF present. Thus, the VWF:Ag on its own will not permit detection of many qualitative defects (consequently, use of this assay alone will lead to many Type 2 VWD patients being missed by the laboratory). In contrast, the VWF:CBA is a functional assay which provides very useful information on the quality of VWF present. Although the VWF:CBA is also a quantitative assay, it is less sensitive than the VWF:Ag assay in terms of its ability to measure the overall level of VWF (i.e.; the VWF:CBA detects only highly adhesive VWF, and therefore only a proportion of overall VWF). In essence, the VWF:Ag and VWF:CBA assays are complementary assays and should be used in combination. The VWF:Multimer assay is a qualitative procedure, but at best is only semi-quantitative. The VWF:Multimer assay essentially provides a snap-shot of the VWF present. Unfortunately considerable technical and interpretive problems limits its overall applicability and usefulness. The VWF:RCof assay is both a quantitative and qualitative assay that provides information about the presence of VWF that lies between that provided individually by the VWF:Ag and VWF:CBA assays. Unfortunately, the VWF:RCof suffers considerable technical problems, including considerable assay variability, that also limits its overall usefulness. Laboratories performing assays for VWF need to develop diagnostic strategies which include the use of appropriate multiple test combinations so as to ensure that VWD is properly detected.

Aminopeptidase-N (CD13; gp 150): contrasting patterns of enzymatic activity in blood from patients with myeloid or lymphoid leukemia.

We have investigated the compartmentalization of aminopeptidase-N-like activity in various blood fractions obtained from patients with acute lymphoid (ALL) or myeloid (AML) leukemia. The primary difference appears not to be the absolute level of overall activity, but rather the relative proportions of the different forms of activity detected. Thus, despite similar levels of total aminopeptidase-N-like activity detected in cells from different leukemic groups, true aminopeptidase-N/CD13 activity was only detected in cells derived from AML patients. Even in these patients, however, most of the detected aminopeptidase-N-like activity ( > 80%) could not be attributed to aminopeptidase-N/CD13. In marked contrast, plasma from leukemic patients also contained substantial total aminopeptidase-N-like activity, of which (irrespective of leukemic group) most could be attributed to aminopeptidase-N/CD13. Whilst slightly higher levels of total activity were obtained in plasma from AML patients compared to ALL patients, there was no difference in the relative proportion attributable to aminopeptidase-N/CD13 (approximately 80% of total aminopeptidase-N-like activity). Evaluation of total aminopeptidase-N-like activity present in whole blood gave differential patterns, and whilst only a proportion (20-40% of total aminopeptidase-N-like activity) could be attributed to true aminopeptidase-N/CD13, blood from patients with CD13+ AML showed the greatest activity so attributable. In total, our results outline the complexities of peptidase activities present within blood of leukemic individuals, and may, in part, explain the variability of previous studies attempting to associate prognostic features with phenotypic expression of CD13.

Hodgkins disease: clinical and radiological prognostic factors in a laparotomy series.

From July 1979 to June 1988, 62 patients managed at Westmead Hospital underwent a staging laparotomy (LAP) for Hodgkins disease. Fifty-four patients were clinical stage (CS) I or II and eight were CS III. The sensitivities of the imaging modalities of computed tomography (CT), Gallium and bipedal lymphangiogram (LAG) were assessed for their predictive value for abdominal disease in patients who underwent a LAP. The most sensitive combination for predicting a negative laparotomy (78%) was a negative abdominal CT and a negative Gallium scan. Upstaging occurred in two of 16 Stage I patients (13%) and nine of 38 Stage II patients (24%). Of the 11 patients upstaged, the spleen was involved in 10 (91%). Factors which predicted for upstaging in a univariate analysis were: age greater than 40 years (P = 0.02), mixed cellularity or lymphocyte depleted histology (P = 0.02), and more than three sites involved above the diaphragm (P = 0.008). In a multivariate analysis, the only significant predictor was the number of sites of involvement (P = 0.007). Two subgroups who had a low probability of upstaging were favourable histology patients with up to two sites of involvement (0%) and females with up to two sites of involvement (0%). We conclude that abdominal imaging is associated with a high false-negative rate, particularly for CS II disease.

von Willebrand's disease: use of collagen binding assay provides potential improvement to laboratory monitoring of desmopressin (DDAVP) therapy.

This report describes studies investigating the use of a collagen binding assay to improve the laboratory monitoring of desmopressin (DDAVP) therapy in patients with von Willebrand's disease (vWD). We evaluated the response of seven patients with vWD (four type I, three type IIA) to DDAVP, administered using a standard protocol, by assessing levels of von Willebrand factor (vWF) and factor VIII, as well as performing skin bleeding times (SBT) prior to, and at sequential time points following, DDAVP administration. The study employed the following assays: von Willebrand factor antigen assay (vWF:Ag; determined by ELISA); a novel functionally based collagen binding assay (CBA; determined by ELISA); ristocetin cofactor assay (RCof; determined by platelet aggregometry); von Willebrand factor multimer analysis (using SDS-agarose gels); factor VIII coagulant (FVIIIC; determined by clotting assay); and factor VIII antigen (FVIIICAG; determined by ELISA). All patients showed an initial incremental increase in vWF/FVIII levels using all assays above, and some showed some correction in SBT. Although the absolute levels of vWF/FVIII antigen or activity varied between patients, the CBA was found to provide consistently the greatest proportional incremental increases (i.e., -fold) compared to baseline (pre-DDAVP) levels. Accordingly, we consistently observed an increase in the CBA to vWF:Ag ratio for all patients evaluated. This supplements previous findings that have suggested a unique ability of our CBA procedure to bind preferentially to higher molecular weight (i.e., more functionally active) forms of vWF. We therefore propose that the use of the above test combination (e.g., vWF:Ag plus CBA) may provide the basis for more accurate estimation of a patient's functional responsiveness to DDAVP therapy in future studies.

The Western Sydney Stroke Risk in the Elderly Study. A 5-year prospective study.

Aging of the Australian population, as in other developed nations, will ensure that stroke remains one of the most important causes of death and disability. The Stroke Risk in the Elderly (SITE) study aims to measure prospectively the independent contribution of dietary, sociodemographic, blood lipid, blood pressure, and hemostatic factors to risk of stroke and other cardiovascular outcomes. The target population included all independently living men and women aged 65 years and over, residents in several retirement villages in western metropolitan Sydney, New South Wales, Australia. The study cohort consists of 225 men and 787 women, selected as a convenience sample from all eligible residents in the local government areas (LGAs) adjacent to Westmead Hospital. Participants attended a baseline session to complete dietary, life-style, medical, and sociodemographic questionnaires. Anthropomorphic variables and blood pressure were measured. Blood was taken for measurement of serum lipid, glucose, and hemostatic factors. Questionnaire results were compared with an age/sex-stratified, randomly selected sample drawn from the community (in the same LGAs), in order to quantify potential sampling and selection biases. The study cohort will be followed for a minimum of 5 years. The attendance rate of eligible residents for a baseline medical, dietary, life-style, and sociodemographic assessment was 72% for males and 69% for females. The study cohort was older, better educated, less ethnically diverse, and among women, less likely to have ever been married compared to people aged over 65 years in the comparison group. The baseline results suggest that hemostatic factors may be of importance in assessing risk of cardiovascular disease, (CVD), particularly in older men.(ABSTRACT TRUNCATED AT 250 WORDS)

Familial hypobetalipoproteinaemia: a rare presentation to the lipid clinic.

OBJECTIVE: To report a case of familial hypobetalipoproteinaemia in a woman who presented after the incidental finding of marked hypocholesterolaemia during laboratory tests. CLINICAL FEATURES: An asymptomatic 37-year-old Lebanese woman presented to the lipid clinic with a serum total cholesterol concentration of 1.1 mmol/L, high density lipoprotein (HDL) cholesterol of 1.0 mmol/L, and triglycerides of 0.28 mmol/L. No secondary cause for the hypocholesterolaemia was established. INVESTIGATION AND OUTCOME: Her serum apolipoprotein B (apo B) levels were markedly reduced at 0.07 g/L. Except for one daughter (IV-4), all other family members including her husband (her first cousin) had apo B levels about 25% of normal. Daughter IV-4 had undetectable apo B levels. Family studies confirmed an autosomal dominant pattern of inheritance consistent with familial hypobetalipoproteinaemia. CONCLUSION: Familial hypobetalipoproteinaemia is a rare condition that should be considered in the differential diagnosis of hypocholesterolaemia. Absence of clinical features, autosomal dominant pattern of inheritance, and reduced apo B levels suggest the diagnosis.

von Willebrand's disease: laboratory investigation using an improved functional assay for von Willebrand factor.

This report details extensive studies investigating an improved screening procedure for the laboratory confirmation of clinically suspected von Willebrand's disease (vWD). Over the past two years, over 400 plasma samples, comprising samples derived from both normal individuals (n = 112) and from patients undergoing investigation on clinical grounds, underwent analysis in this screening procedure, comprising three distinct assays: a standard ELISA assay for von Willebrand Factor (vWF) antigen levels (vWF:Ag), a standard ristocetin cofactor (R Cof) assay, and a functional collagen based ELISA assay for vWF ('CBA'). Normal individual plasma samples yielded normal reference values (mean +/- 2SD) approximating 50-200% (vWF:Ag, R Cof) or 50-250% (CBA). In order to permit comparative analysis, and based upon derived assay values, and subsequent multimer analysis, patient samples were either deemed to derive from persons unlikely to suffer vWD ('non-vWD' patient group) or those potentially suffering vWD. The latter group was further separated into subgroups based upon the likelihood, and probable subtype of vWD. In conjunction with the vWF:Ag assay, the CBA provides the basis by which an effective predictor system (likelihood and probable subtype of vWD) can be offered on the basis of preliminary screening procedures. To date, there has been no overlap in vWF:Ag to CBA ratios (vWF:CBA) between patients yielding Type II vWD like multimer patterns and those yielding Type I vWD, or normal, multimer patterns. Thus, high vWF:CBA (i.e. > or = 3.0) would suggest a Type II, or pseudo, -vWD like defect, whereas low vWF:CBA (< or = 2.5) would likely derive from either normal individuals, or persons suffering from Type I vWD.(ABSTRACT TRUNCATED AT 250 WORDS)

Thymic hyperplasia associated with Hodgkin disease and thyrotoxicosis.

A 19-year-old woman had a residual gallium-sequestering mediastinal mass after treatment for Hodgkin disease. Coincidentally, she also had hyperthyroidism. The initial concern was that the mass was residual Hodgkin disease. Thymic hyperplasia has been described in association with both these conditions. The mass disappeared after treatment of her hyperthyroidism.