User login
43-year-old male • fatigue • unintentional weight loss • pancytopenia • Dx?
THE CASE
A 43-year-old Black male presented to his primary care physician with an 8-month history of progressive fatigue, weakness, and unintentional weight loss. The patient’s history also included antiphospholipid antibody syndrome (APS) with prior deep venous thrombosis/pulmonary embolism for which he was taking warfarin.
At the time of presentation, he reported profound dyspnea on exertion, lightheadedness, dry mouth, low back pain, and worsening nocturia. The remainder of the review of systems was negative. He denied tobacco, alcohol, or illicit drug use or recent travel. His personal and family histories were negative for cancer.
Laboratory data collected during the outpatient visit were notable for a white blood cell count of 2300/mcL (reference range, 4000-11,000/mcL); hemoglobin, 8.6 g/dL (13.5-17.5 g/dL); and platelets, 44,000/mcL (150,000-400,000/mcL). Proteinuria was indicated by a measurement > 500 mg/dL on urine dipstick.
The patient was admitted to the hospital for further work-up of new pancytopenia. His vital signs on admission were notable for tachycardia and a weight of 237 lbs, decreased from 283 lbs 8 months prior. His physical exam revealed dry mucous membranes, bruising of fingertips, and marked lower extremity weakness with preserved sensation. No lymphadenopathy was noted on the admission physical exam.
THE DIAGNOSIS
Inpatient laboratory studies showed elevated inflammatory markers and a positive Coombs test with low haptoglobin. There was no evidence of bacterial or viral infection.
Autoimmune laboratory data included a positive antiphospholipid antibody (ANA) test (1:10,240, diffuse; reference < 1:160), an elevated dsDNA antibody level (800 IU/mL; reference range, 0-99 IU/mL), low complement levels, and antibody titers consistent with the patient’s known APS. Based on these findings, the patient was given a diagnosis of systemic lupus erythematosus (SLE).
DISCUSSION
Lymphadenopathy, revealed by exam or by imaging, in combination with systemic symptoms such as weight loss and fatigue, elicits an extensive differential diagnosis. In the absence of recent exposures, travel, or risk factors for infectious causes, our patient’s work-up was appropriately narrowed to noninfectious etiologies of pancytopenia and lymphadenopathy. At the top of this differential are malignancies—in particular, multiple myeloma and lymphoma—and rheumatologic processes, such as sarcoidosis, connective tissue disease, and SLE.1,2 Ultimately, the combination of autoimmune markers with the pancytopenia and a negative work-up for malignancy confirmed a diagnosis of SLE.
Continue to: SLE classification and generalized lymphadenopathy
SLE classification and generalized lymphadenopathy. SLE is a multisystem inflammatory process with a wide spectrum of clinical presentations. The American College of Rheumatology (ACR) has established validated criteria to aid in the diagnosis of SLE,3 which were most recently updated in 2012 to improve clinical utility. For a diagnosis to be made, at least 1 clinical and 1 immunologic criterion must be present or a renal biopsy must show lupus nephritis.3
Notably, lymphadenopathy is not included in this validated model, despite its occurrence in 25% to 50% of patients with SLE.1,3,4 With this in mind, SLE should be considered in the work-up of generalized lymphadenopathy.
ANA and SLE. Although it is estimated that 30% to 40% of patients with SLE test positive for ANA,5 the presence of ANA also is not part of the diagnostic criteria for SLE. Interestingly, the co-occurrence of the 2 has clinical implications for patients. In particular, patients with SLE and a positive ANA have higher prevalence of thrombosis, valvular disease, thrombocytopenia, and hemolytic anemia, among other complications.5 Although our patient’s presentation of thrombocytopenia and hemolysis clouded the initial work-up, such a combination is consistent with co-presentation of SLE and APS.
Differences in sex, age, and race. SLE is more common in women than in men, with a prevalence ratio of 7:1.6 It is estimated that 65% of patients with SLE experience disease onset between the ages of 16 and 55 years.7
The median age of diagnosis also differs based on sex and race: According to Rus et al,8 the typical age ranges are 37 to 50 years for White women; 50 to 59 for White men; 15 to 44 for Black women; and 45 to 64 for Black men. These estimates of incidence stratified by race, sex, and age can be helpful when evaluating patients with confusing clinical presentations. Our patient’s age was consistent with the median for his sex and race.
Continue to: Our patient
Our patient was started on oral prednisone 60 mg/d with plans for a prolonged taper over 6 months under the close supervision of Rheumatology. His weakness and polyuria began to improve within a month, and lupus-related symptoms resolved within 3 months. His cytopenia also significantly improved, with the exception of refractory thrombocytopenia.
THE TAKEAWAY
SLE is a common diagnosis with multiple presentations. Although lymphadenopathy is not part of the clinical criteria for the diagnosis of SLE, multiple case studies have highlighted its prevalence among affected patients.1,2,4,9-17 APS and antiphospholipid antibodies are also absent in the diagnostic criteria despite being highly associated with SLE. Thus, co-presentation (as well as age and sex) can be helpful with both disease stratification and risk assessment once a diagnosis is made.
CORRESPONDENCE
Isabella Buzzo Bellon Brout, MD, 409 West Broadway, Boston, MA 02127; [email protected]
1. Afzal W, Arab T, Ullah T, et al. Generalized lymphadenopathy as presenting features of systemic lupus erythematosus: case report and review of literature. J Clin Med Res. 2016;8:819-823. doi: 10.14740/jocmr2717w
2. Smith LW, Petri M. Diffuse lymphadenopathy as the presenting manifestation of systemic lupus erythematosus. J Clin Rheumatol. 2013;19:397-399. doi: 10.1097/RHU.0b013e3182a6a924
3. Petri M, Orbai A, Graciela S, et al. Derivation and validation of the Systemic Lupus International Collaborating Clinics classification criteria for systemic lupus erythematosus. Arthritis Rheum. 2012;64:2677-2686. doi: 10.1002/art.34473
4. Kitsanou M, Adreopoulou E, Bai MK, et al. Extensive lymphadenopathy as the first clinical manifestation in systemic lupus erythematosus. Lupus. 2000;9:140-143. doi: 10.1191/096120300678828037
5. Unlu O, Zuily S, Erkan D. The clinical significance of antiphospholipid antibodies in systemic lupus erythematosus. Eur J Rheumatol. 2016;3:75-84. doi: 10.5152/eurjrheum.2015.0085
6. Lahita RG. The role of sex hormones in systemic lupus erythematosus. Curr Opin Rheumatol. 1999;11:352-356. doi: 10.1097/00002281-199909000-00005
7. Rothfield N. Clinical features of systemic lupus erythematosus. In: Kelley WN, Harris ED, Ruddy S, Sledge CB (eds). Textbook of Rheumatology. WB Saunders; 1981.
8. Rus V, Maury EE, Hochberg MC. The epidemiology of systemic lupus erythematosus. In: Wallace DJ, Hahn BH (eds). Dubois’ Lupus Erythematosus. Lippincott Williams and Wilkins; 2002.
9. Biner B, Acunas B, Karasalihoglu S, et al. Systemic lupus erythematosus presenting with generalized lymphadenopathy: a case report. Turk J Pediatr. 2001;43:94-96.
10. Gilmore R, Sin WY. Systemic lupus erythematosus mimicking lymphoma: the relevance of the clinical background in interpreting imaging studies. BMJ Case Rep. 2014;2014:bcr2013201802. doi: 10.1136/bcr-2013-201802
11. Shrestha D, Dhakal AK, Shiva RK, et al. Systemic lupus erythematosus and granulomatous lymphadenopathy. BMC Pediatr. 2013;13:179. doi: 10.1186/1471-2431-13-179
12. Melikoglu MA, Melikoglu M. The clinical importance of lymphadenopathy in systemic lupus erythematosus. Acta Rheumatol Port. 2008;33:402-406.
13. Tamaki K, Morishima S, Nakachi S, et al. An atypical case of late-onset systemic lupus erythematosus with systemic lymphadenopathy and severe autoimmune thrombocytopenia/neutropenia mimicking malignant lymphoma. Int J Hematol. 2017;105:526-531. doi: 10.1007/s12185-016-2126-8
14. Hyami T, Kato T, Moritani S, et al. Systemic lupus erythematosus with abdominal lymphadenopathy. Eur J Dermatol. 2019;29:342-344. doi: 10.1684/ejd.2019.3589
15. Mull ES, Aranez V, Pierce D, et al. Newly diagnosed systemic lupus erythematosus: atypical presentation with focal seizures and long-standing lymphadenopathy. J Clin Rheumatol. 2019;25:e109-e113. doi: 10.1097/RHU.0000000000000681
16. Kassan SS, Moss ML, Reddick RL. Progressive hilar and mediastinal lymphadenopathy in systemic lupus erythematosus on corticosteroid therapy. N Engl J Med. 1976;294:1382-1383. doi: 10.1056/NEJM197606172942506
17. Tuinman PR, Nieuwenhuis MB, Groen E, et al. A young woman with generalized lymphadenopathy. Systemic lupus erythematosus. Neth J Med. 2011;69:284-288.
THE CASE
A 43-year-old Black male presented to his primary care physician with an 8-month history of progressive fatigue, weakness, and unintentional weight loss. The patient’s history also included antiphospholipid antibody syndrome (APS) with prior deep venous thrombosis/pulmonary embolism for which he was taking warfarin.
At the time of presentation, he reported profound dyspnea on exertion, lightheadedness, dry mouth, low back pain, and worsening nocturia. The remainder of the review of systems was negative. He denied tobacco, alcohol, or illicit drug use or recent travel. His personal and family histories were negative for cancer.
Laboratory data collected during the outpatient visit were notable for a white blood cell count of 2300/mcL (reference range, 4000-11,000/mcL); hemoglobin, 8.6 g/dL (13.5-17.5 g/dL); and platelets, 44,000/mcL (150,000-400,000/mcL). Proteinuria was indicated by a measurement > 500 mg/dL on urine dipstick.
The patient was admitted to the hospital for further work-up of new pancytopenia. His vital signs on admission were notable for tachycardia and a weight of 237 lbs, decreased from 283 lbs 8 months prior. His physical exam revealed dry mucous membranes, bruising of fingertips, and marked lower extremity weakness with preserved sensation. No lymphadenopathy was noted on the admission physical exam.
THE DIAGNOSIS
Inpatient laboratory studies showed elevated inflammatory markers and a positive Coombs test with low haptoglobin. There was no evidence of bacterial or viral infection.
Autoimmune laboratory data included a positive antiphospholipid antibody (ANA) test (1:10,240, diffuse; reference < 1:160), an elevated dsDNA antibody level (800 IU/mL; reference range, 0-99 IU/mL), low complement levels, and antibody titers consistent with the patient’s known APS. Based on these findings, the patient was given a diagnosis of systemic lupus erythematosus (SLE).
DISCUSSION
Lymphadenopathy, revealed by exam or by imaging, in combination with systemic symptoms such as weight loss and fatigue, elicits an extensive differential diagnosis. In the absence of recent exposures, travel, or risk factors for infectious causes, our patient’s work-up was appropriately narrowed to noninfectious etiologies of pancytopenia and lymphadenopathy. At the top of this differential are malignancies—in particular, multiple myeloma and lymphoma—and rheumatologic processes, such as sarcoidosis, connective tissue disease, and SLE.1,2 Ultimately, the combination of autoimmune markers with the pancytopenia and a negative work-up for malignancy confirmed a diagnosis of SLE.
Continue to: SLE classification and generalized lymphadenopathy
SLE classification and generalized lymphadenopathy. SLE is a multisystem inflammatory process with a wide spectrum of clinical presentations. The American College of Rheumatology (ACR) has established validated criteria to aid in the diagnosis of SLE,3 which were most recently updated in 2012 to improve clinical utility. For a diagnosis to be made, at least 1 clinical and 1 immunologic criterion must be present or a renal biopsy must show lupus nephritis.3
Notably, lymphadenopathy is not included in this validated model, despite its occurrence in 25% to 50% of patients with SLE.1,3,4 With this in mind, SLE should be considered in the work-up of generalized lymphadenopathy.
ANA and SLE. Although it is estimated that 30% to 40% of patients with SLE test positive for ANA,5 the presence of ANA also is not part of the diagnostic criteria for SLE. Interestingly, the co-occurrence of the 2 has clinical implications for patients. In particular, patients with SLE and a positive ANA have higher prevalence of thrombosis, valvular disease, thrombocytopenia, and hemolytic anemia, among other complications.5 Although our patient’s presentation of thrombocytopenia and hemolysis clouded the initial work-up, such a combination is consistent with co-presentation of SLE and APS.
Differences in sex, age, and race. SLE is more common in women than in men, with a prevalence ratio of 7:1.6 It is estimated that 65% of patients with SLE experience disease onset between the ages of 16 and 55 years.7
The median age of diagnosis also differs based on sex and race: According to Rus et al,8 the typical age ranges are 37 to 50 years for White women; 50 to 59 for White men; 15 to 44 for Black women; and 45 to 64 for Black men. These estimates of incidence stratified by race, sex, and age can be helpful when evaluating patients with confusing clinical presentations. Our patient’s age was consistent with the median for his sex and race.
Continue to: Our patient
Our patient was started on oral prednisone 60 mg/d with plans for a prolonged taper over 6 months under the close supervision of Rheumatology. His weakness and polyuria began to improve within a month, and lupus-related symptoms resolved within 3 months. His cytopenia also significantly improved, with the exception of refractory thrombocytopenia.
THE TAKEAWAY
SLE is a common diagnosis with multiple presentations. Although lymphadenopathy is not part of the clinical criteria for the diagnosis of SLE, multiple case studies have highlighted its prevalence among affected patients.1,2,4,9-17 APS and antiphospholipid antibodies are also absent in the diagnostic criteria despite being highly associated with SLE. Thus, co-presentation (as well as age and sex) can be helpful with both disease stratification and risk assessment once a diagnosis is made.
CORRESPONDENCE
Isabella Buzzo Bellon Brout, MD, 409 West Broadway, Boston, MA 02127; [email protected]
THE CASE
A 43-year-old Black male presented to his primary care physician with an 8-month history of progressive fatigue, weakness, and unintentional weight loss. The patient’s history also included antiphospholipid antibody syndrome (APS) with prior deep venous thrombosis/pulmonary embolism for which he was taking warfarin.
At the time of presentation, he reported profound dyspnea on exertion, lightheadedness, dry mouth, low back pain, and worsening nocturia. The remainder of the review of systems was negative. He denied tobacco, alcohol, or illicit drug use or recent travel. His personal and family histories were negative for cancer.
Laboratory data collected during the outpatient visit were notable for a white blood cell count of 2300/mcL (reference range, 4000-11,000/mcL); hemoglobin, 8.6 g/dL (13.5-17.5 g/dL); and platelets, 44,000/mcL (150,000-400,000/mcL). Proteinuria was indicated by a measurement > 500 mg/dL on urine dipstick.
The patient was admitted to the hospital for further work-up of new pancytopenia. His vital signs on admission were notable for tachycardia and a weight of 237 lbs, decreased from 283 lbs 8 months prior. His physical exam revealed dry mucous membranes, bruising of fingertips, and marked lower extremity weakness with preserved sensation. No lymphadenopathy was noted on the admission physical exam.
THE DIAGNOSIS
Inpatient laboratory studies showed elevated inflammatory markers and a positive Coombs test with low haptoglobin. There was no evidence of bacterial or viral infection.
Autoimmune laboratory data included a positive antiphospholipid antibody (ANA) test (1:10,240, diffuse; reference < 1:160), an elevated dsDNA antibody level (800 IU/mL; reference range, 0-99 IU/mL), low complement levels, and antibody titers consistent with the patient’s known APS. Based on these findings, the patient was given a diagnosis of systemic lupus erythematosus (SLE).
DISCUSSION
Lymphadenopathy, revealed by exam or by imaging, in combination with systemic symptoms such as weight loss and fatigue, elicits an extensive differential diagnosis. In the absence of recent exposures, travel, or risk factors for infectious causes, our patient’s work-up was appropriately narrowed to noninfectious etiologies of pancytopenia and lymphadenopathy. At the top of this differential are malignancies—in particular, multiple myeloma and lymphoma—and rheumatologic processes, such as sarcoidosis, connective tissue disease, and SLE.1,2 Ultimately, the combination of autoimmune markers with the pancytopenia and a negative work-up for malignancy confirmed a diagnosis of SLE.
Continue to: SLE classification and generalized lymphadenopathy
SLE classification and generalized lymphadenopathy. SLE is a multisystem inflammatory process with a wide spectrum of clinical presentations. The American College of Rheumatology (ACR) has established validated criteria to aid in the diagnosis of SLE,3 which were most recently updated in 2012 to improve clinical utility. For a diagnosis to be made, at least 1 clinical and 1 immunologic criterion must be present or a renal biopsy must show lupus nephritis.3
Notably, lymphadenopathy is not included in this validated model, despite its occurrence in 25% to 50% of patients with SLE.1,3,4 With this in mind, SLE should be considered in the work-up of generalized lymphadenopathy.
ANA and SLE. Although it is estimated that 30% to 40% of patients with SLE test positive for ANA,5 the presence of ANA also is not part of the diagnostic criteria for SLE. Interestingly, the co-occurrence of the 2 has clinical implications for patients. In particular, patients with SLE and a positive ANA have higher prevalence of thrombosis, valvular disease, thrombocytopenia, and hemolytic anemia, among other complications.5 Although our patient’s presentation of thrombocytopenia and hemolysis clouded the initial work-up, such a combination is consistent with co-presentation of SLE and APS.
Differences in sex, age, and race. SLE is more common in women than in men, with a prevalence ratio of 7:1.6 It is estimated that 65% of patients with SLE experience disease onset between the ages of 16 and 55 years.7
The median age of diagnosis also differs based on sex and race: According to Rus et al,8 the typical age ranges are 37 to 50 years for White women; 50 to 59 for White men; 15 to 44 for Black women; and 45 to 64 for Black men. These estimates of incidence stratified by race, sex, and age can be helpful when evaluating patients with confusing clinical presentations. Our patient’s age was consistent with the median for his sex and race.
Continue to: Our patient
Our patient was started on oral prednisone 60 mg/d with plans for a prolonged taper over 6 months under the close supervision of Rheumatology. His weakness and polyuria began to improve within a month, and lupus-related symptoms resolved within 3 months. His cytopenia also significantly improved, with the exception of refractory thrombocytopenia.
THE TAKEAWAY
SLE is a common diagnosis with multiple presentations. Although lymphadenopathy is not part of the clinical criteria for the diagnosis of SLE, multiple case studies have highlighted its prevalence among affected patients.1,2,4,9-17 APS and antiphospholipid antibodies are also absent in the diagnostic criteria despite being highly associated with SLE. Thus, co-presentation (as well as age and sex) can be helpful with both disease stratification and risk assessment once a diagnosis is made.
CORRESPONDENCE
Isabella Buzzo Bellon Brout, MD, 409 West Broadway, Boston, MA 02127; [email protected]
1. Afzal W, Arab T, Ullah T, et al. Generalized lymphadenopathy as presenting features of systemic lupus erythematosus: case report and review of literature. J Clin Med Res. 2016;8:819-823. doi: 10.14740/jocmr2717w
2. Smith LW, Petri M. Diffuse lymphadenopathy as the presenting manifestation of systemic lupus erythematosus. J Clin Rheumatol. 2013;19:397-399. doi: 10.1097/RHU.0b013e3182a6a924
3. Petri M, Orbai A, Graciela S, et al. Derivation and validation of the Systemic Lupus International Collaborating Clinics classification criteria for systemic lupus erythematosus. Arthritis Rheum. 2012;64:2677-2686. doi: 10.1002/art.34473
4. Kitsanou M, Adreopoulou E, Bai MK, et al. Extensive lymphadenopathy as the first clinical manifestation in systemic lupus erythematosus. Lupus. 2000;9:140-143. doi: 10.1191/096120300678828037
5. Unlu O, Zuily S, Erkan D. The clinical significance of antiphospholipid antibodies in systemic lupus erythematosus. Eur J Rheumatol. 2016;3:75-84. doi: 10.5152/eurjrheum.2015.0085
6. Lahita RG. The role of sex hormones in systemic lupus erythematosus. Curr Opin Rheumatol. 1999;11:352-356. doi: 10.1097/00002281-199909000-00005
7. Rothfield N. Clinical features of systemic lupus erythematosus. In: Kelley WN, Harris ED, Ruddy S, Sledge CB (eds). Textbook of Rheumatology. WB Saunders; 1981.
8. Rus V, Maury EE, Hochberg MC. The epidemiology of systemic lupus erythematosus. In: Wallace DJ, Hahn BH (eds). Dubois’ Lupus Erythematosus. Lippincott Williams and Wilkins; 2002.
9. Biner B, Acunas B, Karasalihoglu S, et al. Systemic lupus erythematosus presenting with generalized lymphadenopathy: a case report. Turk J Pediatr. 2001;43:94-96.
10. Gilmore R, Sin WY. Systemic lupus erythematosus mimicking lymphoma: the relevance of the clinical background in interpreting imaging studies. BMJ Case Rep. 2014;2014:bcr2013201802. doi: 10.1136/bcr-2013-201802
11. Shrestha D, Dhakal AK, Shiva RK, et al. Systemic lupus erythematosus and granulomatous lymphadenopathy. BMC Pediatr. 2013;13:179. doi: 10.1186/1471-2431-13-179
12. Melikoglu MA, Melikoglu M. The clinical importance of lymphadenopathy in systemic lupus erythematosus. Acta Rheumatol Port. 2008;33:402-406.
13. Tamaki K, Morishima S, Nakachi S, et al. An atypical case of late-onset systemic lupus erythematosus with systemic lymphadenopathy and severe autoimmune thrombocytopenia/neutropenia mimicking malignant lymphoma. Int J Hematol. 2017;105:526-531. doi: 10.1007/s12185-016-2126-8
14. Hyami T, Kato T, Moritani S, et al. Systemic lupus erythematosus with abdominal lymphadenopathy. Eur J Dermatol. 2019;29:342-344. doi: 10.1684/ejd.2019.3589
15. Mull ES, Aranez V, Pierce D, et al. Newly diagnosed systemic lupus erythematosus: atypical presentation with focal seizures and long-standing lymphadenopathy. J Clin Rheumatol. 2019;25:e109-e113. doi: 10.1097/RHU.0000000000000681
16. Kassan SS, Moss ML, Reddick RL. Progressive hilar and mediastinal lymphadenopathy in systemic lupus erythematosus on corticosteroid therapy. N Engl J Med. 1976;294:1382-1383. doi: 10.1056/NEJM197606172942506
17. Tuinman PR, Nieuwenhuis MB, Groen E, et al. A young woman with generalized lymphadenopathy. Systemic lupus erythematosus. Neth J Med. 2011;69:284-288.
1. Afzal W, Arab T, Ullah T, et al. Generalized lymphadenopathy as presenting features of systemic lupus erythematosus: case report and review of literature. J Clin Med Res. 2016;8:819-823. doi: 10.14740/jocmr2717w
2. Smith LW, Petri M. Diffuse lymphadenopathy as the presenting manifestation of systemic lupus erythematosus. J Clin Rheumatol. 2013;19:397-399. doi: 10.1097/RHU.0b013e3182a6a924
3. Petri M, Orbai A, Graciela S, et al. Derivation and validation of the Systemic Lupus International Collaborating Clinics classification criteria for systemic lupus erythematosus. Arthritis Rheum. 2012;64:2677-2686. doi: 10.1002/art.34473
4. Kitsanou M, Adreopoulou E, Bai MK, et al. Extensive lymphadenopathy as the first clinical manifestation in systemic lupus erythematosus. Lupus. 2000;9:140-143. doi: 10.1191/096120300678828037
5. Unlu O, Zuily S, Erkan D. The clinical significance of antiphospholipid antibodies in systemic lupus erythematosus. Eur J Rheumatol. 2016;3:75-84. doi: 10.5152/eurjrheum.2015.0085
6. Lahita RG. The role of sex hormones in systemic lupus erythematosus. Curr Opin Rheumatol. 1999;11:352-356. doi: 10.1097/00002281-199909000-00005
7. Rothfield N. Clinical features of systemic lupus erythematosus. In: Kelley WN, Harris ED, Ruddy S, Sledge CB (eds). Textbook of Rheumatology. WB Saunders; 1981.
8. Rus V, Maury EE, Hochberg MC. The epidemiology of systemic lupus erythematosus. In: Wallace DJ, Hahn BH (eds). Dubois’ Lupus Erythematosus. Lippincott Williams and Wilkins; 2002.
9. Biner B, Acunas B, Karasalihoglu S, et al. Systemic lupus erythematosus presenting with generalized lymphadenopathy: a case report. Turk J Pediatr. 2001;43:94-96.
10. Gilmore R, Sin WY. Systemic lupus erythematosus mimicking lymphoma: the relevance of the clinical background in interpreting imaging studies. BMJ Case Rep. 2014;2014:bcr2013201802. doi: 10.1136/bcr-2013-201802
11. Shrestha D, Dhakal AK, Shiva RK, et al. Systemic lupus erythematosus and granulomatous lymphadenopathy. BMC Pediatr. 2013;13:179. doi: 10.1186/1471-2431-13-179
12. Melikoglu MA, Melikoglu M. The clinical importance of lymphadenopathy in systemic lupus erythematosus. Acta Rheumatol Port. 2008;33:402-406.
13. Tamaki K, Morishima S, Nakachi S, et al. An atypical case of late-onset systemic lupus erythematosus with systemic lymphadenopathy and severe autoimmune thrombocytopenia/neutropenia mimicking malignant lymphoma. Int J Hematol. 2017;105:526-531. doi: 10.1007/s12185-016-2126-8
14. Hyami T, Kato T, Moritani S, et al. Systemic lupus erythematosus with abdominal lymphadenopathy. Eur J Dermatol. 2019;29:342-344. doi: 10.1684/ejd.2019.3589
15. Mull ES, Aranez V, Pierce D, et al. Newly diagnosed systemic lupus erythematosus: atypical presentation with focal seizures and long-standing lymphadenopathy. J Clin Rheumatol. 2019;25:e109-e113. doi: 10.1097/RHU.0000000000000681
16. Kassan SS, Moss ML, Reddick RL. Progressive hilar and mediastinal lymphadenopathy in systemic lupus erythematosus on corticosteroid therapy. N Engl J Med. 1976;294:1382-1383. doi: 10.1056/NEJM197606172942506
17. Tuinman PR, Nieuwenhuis MB, Groen E, et al. A young woman with generalized lymphadenopathy. Systemic lupus erythematosus. Neth J Med. 2011;69:284-288.
