TO THE EDITOR:
TEMPI (telangiectasias, elevated erythropoietin levels with erythrocytosis, monoclonal gammopathy, perinephric fluid collections, and intrapulmonary shunting) syndrome is a rare disorder named as such for its clinical characteristics.1 In cases reported worldwide, other clinical findings have been documented, including additional cutaneous manifestations, serous cavity effusions, and thrombotic and hemorrhagic events.2 The currently suggested diagnostic criteria includes an “other criterion” of venous thromboembolism (VTE), although the available evidence regarding the true incidence of this finding remains limited.3
Currently, thrombosis is known to be associated with several other disorders characterized by erythrocytosis. Primary acquired causes of polycythemia, such as polycythemia vera and Chuvash polycythemia, are well documented to carry a high thrombotic risk.4,5 Furthermore, some studies have suggested an association between secondary or idiopathic erythrocytosis and thrombosis, although the data are more limited because of the numerous confounding variables often present in patients with secondary erythrocytosis.6,7
Growing evidence also indicates that monoclonal gammopathy is associated with thrombotic events. The term “monoclonal gammopathy of thrombotic significance” has been proposed to describe these disorders, characterized by a monoclonal protein that have been identified as being associated with venous and arterial thromboembolism. Both multiple myeloma, the malignant form of monoclonal gammopathy, and monoclonal gammopathy of undetermined significance, the nonmalignant form, have been associated with a statistically significant increase in VTE risk.8,9
To date, 48 patients with TEMPI syndrome or suspected TEMPI syndrome have been reported in the literature, but many case reports and series have not documented the presence or absence of thrombotic events, making it difficult to estimate the true incidence of thrombosis. This lack of data motivated us to contact the authors directly to gather more detailed information. We aim to further elucidate the incidence of VTE in known patients with TEMPI syndrome.
To obtain more detailed information regarding thrombosis in patients with TEMPI syndrome, we contacted all authors with listed emails to inquire whether they and their coauthors would be interested in contributing clinical information about their reported cases. Because information on the patients under study had already been published according to their respective institutions’ consent policies and approval processes, our Institutional Review Board determined this project exempt from informed consent.
Authors who agreed to participate were sent a questionnaire asking for basic demographic information and general questions about TEMPI syndrome symptoms and clot information, if present. A determined effort was made to reach out to all authors multiple times, and complete thrombosis-related information was obtained directly from the care teams for 23 patients. An additional 2 case reports were deemed to contain sufficient thrombosis information to be included, resulting in a total cohort of 25 patients.
After data cleaning and range checks, numeric variables were presented as mean and standard deviation as well as median and interquartile range (IQR), whereas categorical variables were presented as count with frequency. We tested for differences between those with and without a venous clot using the Wilcoxon rank-sum test for numeric variables and Fisher exact test for categorical variables.
Characteristics of each patient are presented in Table 1 and comparisons between the VTE and no VTE groups are presented in Table 2. The average age of the cohort was 55.9 ± 10.6 years (median, 57 years [IQR, 51-60]) and was not significantly different between patients who had a venous clot vs those who did not (P = .36). Overall, 15 of 25 (60%) patients were female and 10 of 25 (40%) were male, with no significant differences according to venous clot status (P = .69). No differences between groups were observed for hematocrit (P = .91), hemoglobin (P = .63), or monoclonal gammopathy (M-protein) concentration (P = .83), with overall levels of 56.4% ± 4.1% (median, 57.0% [IQR, 53%-58.9%]), 17.3 ± 2.4 g/dL (median, 18 g/dL [IQR, 15.6-19 g/dL]), and 12.8± 7.7 g/L (median, 10.5 g/L [IQR, 7.4-16.5 g/L]), respectively. All patients experienced monoclonal gammopathy and erythrocytosis, and there were no statistically significant differences in telangiectasias and perinephric fluid (P > .99 for both). Although not statistically significant, there was an observable difference in intrapulmonary shunting, with 4 of 16 (25%) participants in the group without venous clots experiencing this complication compared with 5 of 9 (55.6%) participants in the group experiencing venous clots (P = .20). Finally, there were no differences in plasma cell concentration between groups, with 13 of 25 (52%) of the cohort in the <10% category and 12 of 25 (48%) in the ≥10% category (P = .69).
Table 1.
Patient and venous and arterial clot characteristics
| ID | Reference | Age, y | Sex | Venous clot | Arterial clot | Characteristics of venous and arterial clots |
|||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| Time of occurrence since diagnosis | TEMPI syndrome treatment at the time of occurrence | Locations of clot(s) | VTE treatment | VTE prophylaxis before clot | Postthrombotic complications | ||||||
| 1 | 10 | 65 | F | Yes | No | 1 mo | No | Iliofemoral vein and pulmonary embolism | Warfarin | No | |
| 2 | 11 | 66 | M | Yes | No | At diagnosis | No | L lower extremity, pulmonary embolism | Direct factor Xa inhibitor | No | Postthrombotic syndrome |
| 3 | 1 | 36 | F | Yes | No | 1 y | No | Cerebral sinus | Warfarin | No | |
| 4 | 12 | 48 | M | Yes | No | 3 mo | No | Extending from peritoneovenous shunt in superior vena cava to R atrium | Warfarin | No | |
| 5 | 13 | 67 | F | Yes | No | 2 wk | Yes (CyBorD) | L jugular vein | LMWH | No | |
| 6 | 14 | 52 | F | Yes | No | 2 mo | Yes (CyBorD) | Cerebral sinus, R internal jugular vein | LMWH | No | Intracranial hemorrhage, death |
| 7 | 1 | 39 | F | Yes | No | 19 y | No | Common femoral vein, cerebral sinus | LMWH | No | Intracranial hemorrhage |
| 8 | 1 | 42 | M | Yes | No | ∗ | No | R internal jugular vein | Warfarin | ∗ | |
| 9 | 15 | 58 | F | Yes | No | ∗ | No | L apical thrombus | Warfarin | ∗ | |
| 10 | 16 | 49 | M | No | Yes | 1 y before diagnosis | No | Coronary artery | Stenting, antiplatelet therapy | No | |
| 11 | 17 | 53 | F | No | Yes | ∗ | No | L subclavian artery, L brachialis artery | Thrombectomy, unknown anticoagulation | Aspirin | Finger ischemia |
| 12 | 18 | 51 | F | No | Yes | At diagnosis | No | Splenic artery | Direct factor Xa inhibitor | No | |
| 13 | 19 | 57 | M | No | No | ||||||
| 14 | 20 | 40 | F | No | No | ||||||
| 15 | 21 | 75 | F | No | No | ||||||
| 16 | 22 | 58 | M | No | No | ||||||
| 17 | 23 | 58 | M | No | No | ||||||
| 18 | 24 | 53 | F | No | No | ||||||
| 19 | 25 | 60 | M | No | No | ||||||
| 20 | 25 | 57 | M | No | No | ||||||
| 21 | 25 | 57 | F | No | No | ||||||
| 22 | 26 | 56 | F | No | No | ||||||
| 23 | 27 | 75 | F | No | No | ||||||
| 24 | 28 | 52 | F | No | No | ||||||
| 25 | 29 | 73 | M | No | No | ||||||
F, female; ID, identification number; L, left; M, male; R, right.
Unknown or not provided.
Table 2.
Comparison between groups with and without VTE
| Variables∗ | N | Cohort | n | No VTE | n | VTE | P value† |
|---|---|---|---|---|---|---|---|
| Demographics | |||||||
| Age, y | 25 | 55.9 ± 10.6 | 16 | 57.8 ± 9.5 | 9 | 52.6 ± 12.1 | .36 |
| 57 (51-60) | 57 (52.5-59) | 52 (42-65) | |||||
| Sex | 25 | 16 | 9 | .69 | |||
| Female | 15 (60.0) | 9 (56.3) | 6 (66.7) | ||||
| Male | 10 (40.0) | 7 (43.8) | 3 (33.3) | ||||
| Clinical characteristics | |||||||
| Light chain | 25 | 16 | 9 | .23 | |||
| Κ | 15 (60.0) | 8 (50.0) | 7 (77.8) | ||||
| λ | 10 (40.0) | 8 (50.0) | 2 (22.2) | ||||
| M-protein | 25 | 16 | 9 | .17 | |||
| IgG | 17 (68.0) | 10 (62.5) | 7 (77.8) | ||||
| IgA | 7 (28.0) | 6 (37.5) | 1 (11.1) | ||||
| IgM | 1 (4.0) | 0 (0) | 1 (11.1) | ||||
| M-protein + light chain | 25 | 16 | 9 | .20 | |||
| IgG κ | 14 (56.0) | 7 (43.8) | 7 (77.8) | ||||
| IgG λ | 3 (12.0) | 3 (18.8) | 0 (0) | ||||
| IgM λ | 1 (4.0) | 0 (0) | 1 (11.1) | ||||
| IgA κ | 1 (4.0) | 1 (6.3) | 0 (0) | ||||
| IgA λ | 6 (24.0) | 5 (31.3) | 1 (11.1) | ||||
| M-protein concentration, g/L | 20 | 12.8 ± 7.7 | 13 | 12.4 ± 7.7 | 7 | 13.7 ± 8.2 | .83 |
| 10.5 (7.4-16.5) | 11.0 (7.1-15.6) | 9.8 (7.6-23) | |||||
| Hemoglobin, g/dL | 21 | 17.3 ± 2.4 | 15 | 17.6 ± 2.1 | 6 | 16.8 ± 3.2 | .63 |
| 18 (15.6-19) | 18.1 (15.6-19) | 16.2 (15.3-19.7) | |||||
| Hematocrit, % | 18 | 56.4 ± 4.1 | 12 | 56.3 ± 4.1 | 6 | 56.7 ± 4.6 | .91 |
| 57.0 (53-58.9) | 56.5 (54.5-59.0) | 57.5 (51.7-58) | |||||
| EPO level, mIU/mL | 25 | 2046.9 ± 2601.0 | 16 | 1441.8 ± 1988.3 | 9 | 3122.7 ± 3293.8 | .38 |
| 676 (165.8-4371) | 560 (143-1917.5) | 2620 (165.8-5000) | |||||
| Telangiectasias | 25 | 16 | 9 | >.99 | |||
| No | 1 (4.0) | 1 (6.3) | 0 (0) | ||||
| Yes | 24 (96.0) | 15 (93.8) | 9 (100) | ||||
| Erythrocytosis | 25 | 16 | 9 | n/a | |||
| No | 0 (0) | 0 (0) | 0 (0) | ||||
| Yes | 25 (100) | 16 (100) | 9 (100) | ||||
| Perinephric fluid | 25 | 16 | 9 | >.99 | |||
| No | 5 (20.0) | 3 (18.8) | 2 (22.2) | ||||
| Yes | 20 (80.0) | 13 (81.3) | 7 (77.8) | ||||
| Intrapulmonary shunting | 25 | 16 | 9 | .20 | |||
| No | 9 (36.0) | 4 (25.0) | 5 (55.6) | ||||
| Yes | 16 (64.0) | 12 (75.0) | 4 (44.4) | ||||
| Plasma cells | 25 | 16 | 9 | .69 | |||
| <10% | 13 (52.0) | 9 (56.3) | 4 (44.4) | ||||
| ≥10% | 12 (48.0) | 7 (43.8) | 5 (55.6) | ||||
EPO, erythropoietin; n/a, not applicable.
Numeric variables are presented as mean ± standard deviation and median (IQR), whereas categorical variables are presented as count (frequency).
P values were obtained using the Wilcoxon rank-sum test for numeric variables and Fisher exact test for categorical variables.
Although not statistically significant, there were observable differences in light chain distribution and M-protein levels. Specifically, those in the venous clot group were more likely to have κ (7/9 [77.8%]) vs λ light chains compared with patients with no clot (8/16 [50%]; P = .23). Immunoglobulin G (IgG) was the most common M-protein in both groups; however, there were more with IgA in the no-clot group compared to the clot group (6/16 [35.7%] vs 1/9 [11.1%], respectively), and more patients with IgM in the clot group compared to those who did not have a venous clot (1/9 [11.1%] vs 0%, respectively; P = .17). Finally, when evaluating differences in M-proteins and light chain combinations, 7 of (77.8%) patients in the clot group had IgG κ compared with 7 of 16 (43.8%) in the no-clot group. In the no-clot group, 3 of 16 (18.8%) (vs 0% in the clot group) had IgG λ, and 5 of 16 (31.3%) had IgA λ compared with 1 of 9 (11.1%) in the group experiencing a venous clot (P = .20).
Among the patients who experienced VTE events, none were receiving immunomodulatory medications at the time of the clot. Three patients were undergoing therapeutic phlebotomy, and only 1 had a clot likely associated with central venous access. None of the patients were receiving VTE prophylaxis at the time of their venous clot, although 1 patient with an arterial event was taking aspirin. All but one of the venous clots occurred within 1 year of diagnosis, and the 1 remaining event occurred during a recurrence of TEMPI syndrome 19 years after the first diagnosis.
Of the venous clots, 4 were in the cerebral sinus, 1 was in the right internal jugular vein, and 1 was a left apical clot. All patients who developed clots were treated with anticoagulation, which prevented recurrence or worsening in all cases.
Based on the collected data, a correlation exists between TEMPI syndrome and venous clotting events. Among the 25 patients with confirmed thrombosis status, 9 (36%) experienced a venous thrombotic event.
It is not surprising that clotting events were common among patients with TEMPI syndrome, given that both monoclonal gammopathy and erythrocytosis are independently known to increase thrombotic risk. However, additional factors related to the treatment of TEMPI syndrome may also influence thrombotic risk. Chemotherapy regimens used for TEMPI syndrome treatment, many of which borrowed from multiple myeloma protocols, increase the risk of thrombotic events.30,31
Moreover, many patients with TEMPI syndrome undergo therapeutic phlebotomy to manage erythrocytosis. Although phlebotomy is generally considered to reduce thrombosis risk, paradoxically, it has been shown to increase thrombotic risk in patients with Chuvash polycythemia.32 Because the mechanism underlying erythrocytosis in TEMPI syndrome remains unclear, the impact of phlebotomy on thrombosis risk in this population is unknown. Additionally, many patients with TEMPI syndrome have venous catheters placed to facilitate chemotherapy administration, which can serve as a nidus for thrombosis.33
Given the high incidence of VTE in this cohort, future studies should explore whether thromboprophylaxis should be routinely recommended for patients with TEMPI syndrome. As more patients with TEMPI syndrome are identified, it will be important for future reports to document the presence or absence of thromboembolic events. Only with complete case characterization will we better understand the true risk and mechanisms of thrombosis in this rare syndrome.
Conflict-of-interest disclosure: The authors declare no competing financial interests.
Acknowledgments
Acknowledgments: The authors thank Chunyan Sun and Hongxiao Han for contributing patient information for their respective patients to this study.
This work was supported by National Center for Advancing Translational Sciences, National Institutes of Health grants UL1TR001855 and UL1TR000130. This study was also supported by an educational grant from the Los Angeles County Medical Center Committee for Interns and Residents.
The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Contribution: G.P. wrote the manuscript; D.S., C. O'Neill, M.L.W., and C. O'Connell provided significant edits; G.P. and M.L.W. analyzed the data; J.C. provided significant assistance in collecting patient information; and L.T., J.S., S.K., E.C., J.H., M.-N.P., A.I., D.N., M.P., P.-Y.S., L.Ü., J.T., T.S., E.D., E.E., H.Y., D.F., T.C., and W.S. provided significant patient data and information and edited the manuscript.
Footnotes
Data are available from the corresponding author, Graham Parker (gblakeparker@gmail.com), on request.
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