ANGIOFOLLICULAR LYMPH NODE TRANSFORMATION IN HODGKIN’S LYMPHOMA
Ricardo Drut, MD, and Adriana Larregina, MD
0
Servicio de Patologia, Hospital
Fetal Pediatr Pathol Downloaded from informahealthcare.com by V U L Periodicals Rec on 12/30/14 For personal use only.
de Niiios, 1900 La Plata, Rep6blica Argentina
We present four examples of lymph nodes that have Hodgkin’s disease between nodules of angiofollicular hyperplasia, three hyaline-vascular and one plasma cell in type, suEesting the concurrence of the lymphoma with Castleman’s disease. Angiofollicular hyperplasia is claimed to be an immune derangement, and its presence in Hodgkin ’s disease may represent such a situation. KEY WORDS: angiofollicular hyperplasia, Hodgkin ’s lymphoma.
INTRODUCTION Angiofollicular lymph node hyperplasia (ALNH), Castleman’s disease (CD), is a reactive lymphoid proliferation of unknown cause and pathogenesis. Originally reported as a localized mediastinal tumor (l), the disorder has been expanded to include other sites, systemic manifestations, and multicentric lesions. Four reviews on the subject give a clear perspective of the biological spectrum of the process and speculate on the possible pathogenesis (2-5). Histologically, two types are recognized, hyaline-vascular and plasma cell. Intermediate forms may also be seen (6). Although most cases of ALNH are sporadic, plasma cell-type lesions have been said to occur in acquired immunodeficiency syndrome (AIDS), Kaposi’s sarcoma, Wiskott-Aldrich syndrome, rheumatoid arthritis, and other ill-defined autoimmune syndromes (2); in therapeutically immunosuppressed patients (7); and in lymph nodes draining carcinoma, lymphomas (Hodgkin’s and non-Hodgkin’s), vaccination sites, and skin lesions with urticaria (2). We report four children who had lymph nodes that combined histologic features of angiofollicular transformation (hyperplasia), hyaline-vascular in three and plasma cell type in one, and Hodgkin’s disease in the interangiofollicular areas. Address reprint requests to Ricardo Drut, M . D . , Servicio de Patologia, Hospital de Nifios, 1900 La Plata, Repliblica Argentina.
Pedtatric Pathology, 11 :903-908, 1991 Copyright 0 1991 by Hemisphere PublishinE Corporation
903
904
R. DRUT AND A. LARREGINA
Fetal Pediatr Pathol Downloaded from informahealthcare.com by V U L Periodicals Rec on 12/30/14 For personal use only.
CASE REPORTS Table 1 presents the clinical data. All patients had biopsies that revealed microscopic features in common. The lymph nodes of all four exhibited peripheral areas containing remnants of cortex with small but recognizable normal follicles. Deeper-seated areas had angiofollicular nodes of different diameters that contained a penetrating or central small vessel, associated in some with hyaline material and large germinal center-like cells with a concentric arrangement. These cells were surrounded by a mantle of variable thickness composed of mature lymphocytes frequently displaying an onion-skin arrangement. The interangiofollicular tissue contained capillaries with high endothelium, frequent UCHL- 1 reacting T lymphocytes, and diagnostic and nondiagnostic ReedSternberg cells. Many stained for the presence of the Leu-Ml and Ki-1 markers (Figs. 1 and 2). The CD4SRO T cell marker UCHL-1 also revealed the presence of some T cells within the angiofollicular nodes, among the central cells. The lymphocytes of the mantle were unstained. Case 3 also had many plasma cells in some interfollicular areas, hyalinized septa that partially compartmentalized the lymph node, and fibrosis of the capsule. Finally, some lymph nodes showed completely effaced areas occupied by Hodgkin’s lymphoma, mixed cellularity in type (Fig. 3).
DISCUSSION Morphologic features of these four cases appear to have characteristics of two lymphoid lesions. Hodgkin’s disease is a much more heterogeneous process
than was initially thought and is just now beginning to be understood (8). If classical criteria are followed (9) and special subtypes are kept in mind (8, 9), TABLE 1. Angiofollicular Hyperplasia Associated with Hodgkin’s Disease: Clinical Data of Four Patients
Patient
Age, sex
Location
1
12, M
2 3
4, M 11, M
Axilla, retroperitoneum, spleen hilus, appendix, spleen’ Left cervical Right cervical
4
6, F
Right cervical
Evolution time
Stage
Follow-up
18 mo
IIIB
AW,*8 yr
6-7 wk 2 Y’
IA IIIA
2 ma
IIB
AW, 4 yr Recent; good response to chemotherapy Unknown (consultation)
“Nephrotic syndrome due to minimal change disease treated with steroids at the time of axillary lymph node biopsy. Spleen with Hodgkin’s disease only (spleen biopsy). bAW, alive and well.
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CASTLEMAN’S AND HODGKIN‘S DISEASE
905
FIGURE 1. Area of the lymph node showing the association of an angiofollicular node (left) and Hodgkin’s disease (right). Inset: high-power view of Reed-Sternberg cells. Case 2. X40; inset X400.
the histologic diagnosis of Hodgkin’s disease can be relatively easy. Immunohistochemistry may contribute to a more secure diagnosis (10-12). Although Hodgkin’s disease has been included in the differential diagnosis of ALNH (3, 6), our cases demonstrate that both lesions may be present simultaneously in the same node. Whether one lesion favors the development of the other is unknown. The angiofollicular pattern may not represent “true” ALNH but merely an angiofollicular transformation adjacent to the lymphoma (according to the scheme of Fig. 3). The differential diagnosis of Hodgkin’s disease between ALNH angiofollicular nodules from interfollicular Hodgkin’s disease (13) is difficult. The original descriptions of interfollicular Hodgkin’s disease almost fit our cases but do not mention the characteristic angiofollicular transformation, that is, the follicular nodules around a central vessel or penetrated by small vessels. This feature is characteristic of Castleman’s disease (6) and has not been described in studies of the vascular pattern of Hodgkin’s disease (14, 15). The rest of the findings of Doggett et al. (13) may overlap with those of ALNH. Their figure 2 clearly presents a low-power view of a lymph node with hyperplastic follicles different from the remnants of normal follicles that appear compressed below the capsule (13). Doggett’s cases may also represent examples of angiofollicular transforma-
Fetal Pediatr Pathol Downloaded from informahealthcare.com by V U L Periodicals Rec on 12/30/14 For personal use only.
906
R. DRUT AND A. LARREGINA
FIGURE 2. Angiofollicular node with a penetrating capillary is surrounded by Hodgkin’s disease. Inset: Ki-1 (upper) and Leu-M1 (lower) reactive Reed-Sternberg cells. X 400.
X 40.
FIGURE 3. Schema depicting areas recognized in the lymph nodes. 1, Remaining normal lymph node; 2 , area with the angiofollicular transformation (hyperplasia); 3, area with Hodgkin’s disease; 4, angiofollicular node surrounded by Hodgkin’s disease. The dashed line represents the advancing edge of Hodgkin’s lymphoma.
Fetal Pediatr Pathol Downloaded from informahealthcare.com by V U L Periodicals Rec on 12/30/14 For personal use only.
CASTLEMAN‘S AND HODGKIN‘S DISEASE
907
tion with interangiofollicular Hodgkin’s disease rather than “interfollicular” Hodgkin’s disease. Confirmation of this statement would require review of the original cases. Fisher et al. (16) describe a case of C D in an ll-year-old girl who had a tumor in the neck of 5 years duration that recurred three times after the first biopsy. Only the fourth biopsy revealed Reed-Sternberg cells. The authors do not analyze their case in depth, although they raise the possibility that it represents Hodgkin’s disease from the outset. This may be another example of the combination we are describing, of concomitant Hodgkin’s and Castleman’s diseases. Predominance of T lymphocytes in the interfollicular areas is a feature shared by C D (17, 18) and the “stroma” of Hodgkin’s disease (9). The development of nephrotic syndrome (case 1) has been reported in association with both diseases (19-21). The wide variety of circumstances under which the plasma cell variant of C D has been found has raised doubts about its specificity as a diagnostic entity (4, 5). We suspect that the many associations are related to an immunologic imbalance that may be favored by or even induced by the CD. The combination of angiofollicular transformation with Hodgkin’s disease may represent one more example. Hodgkin’s disease with angiofollicular transformation may eventually emerge as another variant of the lymphoma that develops in a peculiar immunologic setting. More cases are needed to define the association and establish its possible prognostic value. Addendum: While this paper was in press Pettit et al. (Mod Pathol 1991;4:81A) reported a similar association in three adult patients. Their conclusion that “angiofollicular change in lymph nodes involved in Hodgkin’s disease may be a local morphologic manifestation of an abnormal immune state associated with Hodgkin’s disease” is similar to ours. Maheswaran et al. (Histopathology 1991;18:249-53) report three instances in which an initial diagnosis of Castleman’s disease (plasma cell variant) was followed within a year by a diagnosis, in another lymph node, of Hodgkin’s disease. Atypical CD15 and CD30 reactive cells were demonstrable, in retrospect, in the “Castleman’s’’ nodes.
REFERENCES 1. Castleman B, Iverson L, Menendez VP. Localized mediastinal lymph node hyperplasia resembling
thymoma. Cancer 1956;9:822-30. 2. Frizzera G. Castleman’s disease: More questions than answers. Hum Pathol 1985;16:202-5. 3. Linares K , Rosas-Uribe A. Giant lymphoid hyperplasia (Castleman’s disease) simulating lymphoma and thymoma: Clinical and pathological featuresin 7 patients. Patologia (Mex City) 1988;26:99-106 (in Spanish). 4. Isaacson PG. Commentary: Castleman’s disease. Histopathology 1989; 14:429-32.
Fetal Pediatr Pathol Downloaded from informahealthcare.com by V U L Periodicals Rec on 12/30/14 For personal use only.
908
R. DRUT AND A. LARREGINA
5. Frizzera G. Castleman’s disease and related disorders. Semin Diagn Pathol 1988;5:346-64. 6. Keller AR, Hochholzer L, Castleman B. Hyaline-vascular and plasma cell types of giant lymph node hyperplasia of the mediastinum and other locations. Cancer 1972;29:670-83. 7. Francis ND, Hollowood K, Gabriel R . Angiofollicular lymph node hyperplasia (letter). J Clin Pathol 1988;41 :353-6. 8. Anastasi J , Variakojis D. Heterogeneity in Hodgkin’s disease: No simple answer for a complex disorder. Hum Pathol 1988;19:1251-4. 9. Grogan T M . Hodgkin’s disease. In: Jaffe ES, ed. Surgical pathology of the lymph nodes and related organs. Philadelphia: W. B. Saunders, 1985;86-134 (Major Problems in Pathology). 10. Dorfman RF, Gatter KC, Pulford KA, Mason DY. An evaluation of the utility of anti-granulocyte and anti-leukocyte monoclonal antibodies in the diagnosis of Hodgkin’s disease. Am J Pathol 1986;123:508-19. 11. Chittal SM, Cavariviere P, Schwarting R , et al. Monoclonal antibodies in the diagnosis of Hodgkin’s disease. The search for a rational panel. Am J Surg Pathol 1988;12:9-21. 12. Ree HJ, Neiman RS, Martin AW, Dallenbach F, Stein H . Paraffin section markers for Reed-Sternberg cells. A comparative study of peanut agglutinin, Leu-M1, LN-2, and Ber-H2. Cancer 1989;63:2030-6. 13. Doggett RS, Colby TV, Dorfman R E Interfollicular Hodgkin’s disease. Am J Surg Pathol 1983;7:145-9. 14. Soderstrom N, Norberg B. Observations regarding the specific post-capillary venules of lymph nodes in malignant lymphomas. Acta Pathol Microbiol Scand [A] 1974;82:71-9. 15. Moller P, Lennert K. On the angiostructure of lymph nodes in Hodgkin’s disease. An immunohistochemical study using the lectin I of Ulex europacus as endothelial marker. Virchows Arch [A] 1984;403:257-70. 16. Fisher ER, Sieracki JC, Goldenberg D M . Identity and nature of isolated lymphoid tumors (so-called nodal hyperplasia, hamartoma, and angiomatous hamartoma) as revealed by histologic, electron microscopic and heterotransplantation studies. Cancer 1970;25:1286-300. 17. van der Oord JJ, De Wolf-Peeters C, Tricot G , Desmet VJ. Distribution of lymphocyte subsets in a case of angiofollicular lymph node hyperplasia. Am J Clin Pathol 1984;82:491-5. 18. Carbone A, Manconi R , Volpe R , et al. Immunohistochemical, enzyme histochemical, and immunologic features of giant lymph node hyperplasia of the hyaline-vascular type. Cancer 1986;58:908- 16. 19. Chan WC, Hargreaves H , Keller J. Giant lymph node hyperplasia with unusual clinicopathologic features. Cancer 1984;53:2 135-9. 20. Powderly WG, Cantwell BM, Fennelly JJ, Warde P, McCabe M M , Towers RP. Renal glomerulopathies associated with Hodgkin’s disease. Cancer 1985;56:874-5. 21. Routledge RC, Hann I M , Jones P H . Hodgkin’s disease complicated by the nephrotic syndrome. Cancer 1976;38:1735-40. Received January 28, 1991 Revirion accepted April 18, 1991
Ricardo Drut, MD, and Adriana Larregina, MD
0
Servicio de Patologia, Hospital
Fetal Pediatr Pathol Downloaded from informahealthcare.com by V U L Periodicals Rec on 12/30/14 For personal use only.
de Niiios, 1900 La Plata, Rep6blica Argentina
We present four examples of lymph nodes that have Hodgkin’s disease between nodules of angiofollicular hyperplasia, three hyaline-vascular and one plasma cell in type, suEesting the concurrence of the lymphoma with Castleman’s disease. Angiofollicular hyperplasia is claimed to be an immune derangement, and its presence in Hodgkin ’s disease may represent such a situation. KEY WORDS: angiofollicular hyperplasia, Hodgkin ’s lymphoma.
INTRODUCTION Angiofollicular lymph node hyperplasia (ALNH), Castleman’s disease (CD), is a reactive lymphoid proliferation of unknown cause and pathogenesis. Originally reported as a localized mediastinal tumor (l), the disorder has been expanded to include other sites, systemic manifestations, and multicentric lesions. Four reviews on the subject give a clear perspective of the biological spectrum of the process and speculate on the possible pathogenesis (2-5). Histologically, two types are recognized, hyaline-vascular and plasma cell. Intermediate forms may also be seen (6). Although most cases of ALNH are sporadic, plasma cell-type lesions have been said to occur in acquired immunodeficiency syndrome (AIDS), Kaposi’s sarcoma, Wiskott-Aldrich syndrome, rheumatoid arthritis, and other ill-defined autoimmune syndromes (2); in therapeutically immunosuppressed patients (7); and in lymph nodes draining carcinoma, lymphomas (Hodgkin’s and non-Hodgkin’s), vaccination sites, and skin lesions with urticaria (2). We report four children who had lymph nodes that combined histologic features of angiofollicular transformation (hyperplasia), hyaline-vascular in three and plasma cell type in one, and Hodgkin’s disease in the interangiofollicular areas. Address reprint requests to Ricardo Drut, M . D . , Servicio de Patologia, Hospital de Nifios, 1900 La Plata, Repliblica Argentina.
Pedtatric Pathology, 11 :903-908, 1991 Copyright 0 1991 by Hemisphere PublishinE Corporation
903
904
R. DRUT AND A. LARREGINA
Fetal Pediatr Pathol Downloaded from informahealthcare.com by V U L Periodicals Rec on 12/30/14 For personal use only.
CASE REPORTS Table 1 presents the clinical data. All patients had biopsies that revealed microscopic features in common. The lymph nodes of all four exhibited peripheral areas containing remnants of cortex with small but recognizable normal follicles. Deeper-seated areas had angiofollicular nodes of different diameters that contained a penetrating or central small vessel, associated in some with hyaline material and large germinal center-like cells with a concentric arrangement. These cells were surrounded by a mantle of variable thickness composed of mature lymphocytes frequently displaying an onion-skin arrangement. The interangiofollicular tissue contained capillaries with high endothelium, frequent UCHL- 1 reacting T lymphocytes, and diagnostic and nondiagnostic ReedSternberg cells. Many stained for the presence of the Leu-Ml and Ki-1 markers (Figs. 1 and 2). The CD4SRO T cell marker UCHL-1 also revealed the presence of some T cells within the angiofollicular nodes, among the central cells. The lymphocytes of the mantle were unstained. Case 3 also had many plasma cells in some interfollicular areas, hyalinized septa that partially compartmentalized the lymph node, and fibrosis of the capsule. Finally, some lymph nodes showed completely effaced areas occupied by Hodgkin’s lymphoma, mixed cellularity in type (Fig. 3).
DISCUSSION Morphologic features of these four cases appear to have characteristics of two lymphoid lesions. Hodgkin’s disease is a much more heterogeneous process
than was initially thought and is just now beginning to be understood (8). If classical criteria are followed (9) and special subtypes are kept in mind (8, 9), TABLE 1. Angiofollicular Hyperplasia Associated with Hodgkin’s Disease: Clinical Data of Four Patients
Patient
Age, sex
Location
1
12, M
2 3
4, M 11, M
Axilla, retroperitoneum, spleen hilus, appendix, spleen’ Left cervical Right cervical
4
6, F
Right cervical
Evolution time
Stage
Follow-up
18 mo
IIIB
AW,*8 yr
6-7 wk 2 Y’
IA IIIA
2 ma
IIB
AW, 4 yr Recent; good response to chemotherapy Unknown (consultation)
“Nephrotic syndrome due to minimal change disease treated with steroids at the time of axillary lymph node biopsy. Spleen with Hodgkin’s disease only (spleen biopsy). bAW, alive and well.
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CASTLEMAN’S AND HODGKIN‘S DISEASE
905
FIGURE 1. Area of the lymph node showing the association of an angiofollicular node (left) and Hodgkin’s disease (right). Inset: high-power view of Reed-Sternberg cells. Case 2. X40; inset X400.
the histologic diagnosis of Hodgkin’s disease can be relatively easy. Immunohistochemistry may contribute to a more secure diagnosis (10-12). Although Hodgkin’s disease has been included in the differential diagnosis of ALNH (3, 6), our cases demonstrate that both lesions may be present simultaneously in the same node. Whether one lesion favors the development of the other is unknown. The angiofollicular pattern may not represent “true” ALNH but merely an angiofollicular transformation adjacent to the lymphoma (according to the scheme of Fig. 3). The differential diagnosis of Hodgkin’s disease between ALNH angiofollicular nodules from interfollicular Hodgkin’s disease (13) is difficult. The original descriptions of interfollicular Hodgkin’s disease almost fit our cases but do not mention the characteristic angiofollicular transformation, that is, the follicular nodules around a central vessel or penetrated by small vessels. This feature is characteristic of Castleman’s disease (6) and has not been described in studies of the vascular pattern of Hodgkin’s disease (14, 15). The rest of the findings of Doggett et al. (13) may overlap with those of ALNH. Their figure 2 clearly presents a low-power view of a lymph node with hyperplastic follicles different from the remnants of normal follicles that appear compressed below the capsule (13). Doggett’s cases may also represent examples of angiofollicular transforma-
Fetal Pediatr Pathol Downloaded from informahealthcare.com by V U L Periodicals Rec on 12/30/14 For personal use only.
906
R. DRUT AND A. LARREGINA
FIGURE 2. Angiofollicular node with a penetrating capillary is surrounded by Hodgkin’s disease. Inset: Ki-1 (upper) and Leu-M1 (lower) reactive Reed-Sternberg cells. X 400.
X 40.
FIGURE 3. Schema depicting areas recognized in the lymph nodes. 1, Remaining normal lymph node; 2 , area with the angiofollicular transformation (hyperplasia); 3, area with Hodgkin’s disease; 4, angiofollicular node surrounded by Hodgkin’s disease. The dashed line represents the advancing edge of Hodgkin’s lymphoma.
Fetal Pediatr Pathol Downloaded from informahealthcare.com by V U L Periodicals Rec on 12/30/14 For personal use only.
CASTLEMAN‘S AND HODGKIN‘S DISEASE
907
tion with interangiofollicular Hodgkin’s disease rather than “interfollicular” Hodgkin’s disease. Confirmation of this statement would require review of the original cases. Fisher et al. (16) describe a case of C D in an ll-year-old girl who had a tumor in the neck of 5 years duration that recurred three times after the first biopsy. Only the fourth biopsy revealed Reed-Sternberg cells. The authors do not analyze their case in depth, although they raise the possibility that it represents Hodgkin’s disease from the outset. This may be another example of the combination we are describing, of concomitant Hodgkin’s and Castleman’s diseases. Predominance of T lymphocytes in the interfollicular areas is a feature shared by C D (17, 18) and the “stroma” of Hodgkin’s disease (9). The development of nephrotic syndrome (case 1) has been reported in association with both diseases (19-21). The wide variety of circumstances under which the plasma cell variant of C D has been found has raised doubts about its specificity as a diagnostic entity (4, 5). We suspect that the many associations are related to an immunologic imbalance that may be favored by or even induced by the CD. The combination of angiofollicular transformation with Hodgkin’s disease may represent one more example. Hodgkin’s disease with angiofollicular transformation may eventually emerge as another variant of the lymphoma that develops in a peculiar immunologic setting. More cases are needed to define the association and establish its possible prognostic value. Addendum: While this paper was in press Pettit et al. (Mod Pathol 1991;4:81A) reported a similar association in three adult patients. Their conclusion that “angiofollicular change in lymph nodes involved in Hodgkin’s disease may be a local morphologic manifestation of an abnormal immune state associated with Hodgkin’s disease” is similar to ours. Maheswaran et al. (Histopathology 1991;18:249-53) report three instances in which an initial diagnosis of Castleman’s disease (plasma cell variant) was followed within a year by a diagnosis, in another lymph node, of Hodgkin’s disease. Atypical CD15 and CD30 reactive cells were demonstrable, in retrospect, in the “Castleman’s’’ nodes.
REFERENCES 1. Castleman B, Iverson L, Menendez VP. Localized mediastinal lymph node hyperplasia resembling
thymoma. Cancer 1956;9:822-30. 2. Frizzera G. Castleman’s disease: More questions than answers. Hum Pathol 1985;16:202-5. 3. Linares K , Rosas-Uribe A. Giant lymphoid hyperplasia (Castleman’s disease) simulating lymphoma and thymoma: Clinical and pathological featuresin 7 patients. Patologia (Mex City) 1988;26:99-106 (in Spanish). 4. Isaacson PG. Commentary: Castleman’s disease. Histopathology 1989; 14:429-32.
Fetal Pediatr Pathol Downloaded from informahealthcare.com by V U L Periodicals Rec on 12/30/14 For personal use only.
908
R. DRUT AND A. LARREGINA
5. Frizzera G. Castleman’s disease and related disorders. Semin Diagn Pathol 1988;5:346-64. 6. Keller AR, Hochholzer L, Castleman B. Hyaline-vascular and plasma cell types of giant lymph node hyperplasia of the mediastinum and other locations. Cancer 1972;29:670-83. 7. Francis ND, Hollowood K, Gabriel R . Angiofollicular lymph node hyperplasia (letter). J Clin Pathol 1988;41 :353-6. 8. Anastasi J , Variakojis D. Heterogeneity in Hodgkin’s disease: No simple answer for a complex disorder. Hum Pathol 1988;19:1251-4. 9. Grogan T M . Hodgkin’s disease. In: Jaffe ES, ed. Surgical pathology of the lymph nodes and related organs. Philadelphia: W. B. Saunders, 1985;86-134 (Major Problems in Pathology). 10. Dorfman RF, Gatter KC, Pulford KA, Mason DY. An evaluation of the utility of anti-granulocyte and anti-leukocyte monoclonal antibodies in the diagnosis of Hodgkin’s disease. Am J Pathol 1986;123:508-19. 11. Chittal SM, Cavariviere P, Schwarting R , et al. Monoclonal antibodies in the diagnosis of Hodgkin’s disease. The search for a rational panel. Am J Surg Pathol 1988;12:9-21. 12. Ree HJ, Neiman RS, Martin AW, Dallenbach F, Stein H . Paraffin section markers for Reed-Sternberg cells. A comparative study of peanut agglutinin, Leu-M1, LN-2, and Ber-H2. Cancer 1989;63:2030-6. 13. Doggett RS, Colby TV, Dorfman R E Interfollicular Hodgkin’s disease. Am J Surg Pathol 1983;7:145-9. 14. Soderstrom N, Norberg B. Observations regarding the specific post-capillary venules of lymph nodes in malignant lymphomas. Acta Pathol Microbiol Scand [A] 1974;82:71-9. 15. Moller P, Lennert K. On the angiostructure of lymph nodes in Hodgkin’s disease. An immunohistochemical study using the lectin I of Ulex europacus as endothelial marker. Virchows Arch [A] 1984;403:257-70. 16. Fisher ER, Sieracki JC, Goldenberg D M . Identity and nature of isolated lymphoid tumors (so-called nodal hyperplasia, hamartoma, and angiomatous hamartoma) as revealed by histologic, electron microscopic and heterotransplantation studies. Cancer 1970;25:1286-300. 17. van der Oord JJ, De Wolf-Peeters C, Tricot G , Desmet VJ. Distribution of lymphocyte subsets in a case of angiofollicular lymph node hyperplasia. Am J Clin Pathol 1984;82:491-5. 18. Carbone A, Manconi R , Volpe R , et al. Immunohistochemical, enzyme histochemical, and immunologic features of giant lymph node hyperplasia of the hyaline-vascular type. Cancer 1986;58:908- 16. 19. Chan WC, Hargreaves H , Keller J. Giant lymph node hyperplasia with unusual clinicopathologic features. Cancer 1984;53:2 135-9. 20. Powderly WG, Cantwell BM, Fennelly JJ, Warde P, McCabe M M , Towers RP. Renal glomerulopathies associated with Hodgkin’s disease. Cancer 1985;56:874-5. 21. Routledge RC, Hann I M , Jones P H . Hodgkin’s disease complicated by the nephrotic syndrome. Cancer 1976;38:1735-40. Received January 28, 1991 Revirion accepted April 18, 1991
