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Acute liver failure
BOOK REVIEW
malignant melanoma remains highly unusual. Indeed, LCH is classically reported in association with other subtypes of Hodgkin's disease, but to our knowledge has never been described with N-LPHD. It has been previously described only once in lymph nodes draining the cutaneous site of a malignant melanoma .4 The pathogeny of LCH associated with neoplastic disorders is still unclear, and in our case, its association with two i n d e p e n d e n t but neighboring tumors raises some interesting questions. LCs belong to the dendritic cell (DC) lineage which is specialized in the processing and the presentation of antigens to T cells. 1 They may be recruited in several skin disorders including inflammatory diseases and tumors such as malignant melanoma. :,4 It is tempting to speculate that, in our case, these cells might have migrated from the melanoma site (where tumor antigens are shedded and processed) via the afferent lymphati£s to the T-dependent areas of the axil!ary lymph nodes (where antigens are presented to T cells) and accumulated there with the help of cytokines locally secreted by the adjacent N-LPHD neoplastic process. There is evidence that during their migration, DCs undergo a process of maturation characterized by the upregulatio n of several adhesion molecules and the acquisition of the full capacity of T-cell sensitization.: It has also be shown that on CD40 triggering (which mimicks interaction with T cells), cultured LCs acquire surface CD25 (Interleukin-2 receptor, IL-2R). 5 On the other hand, we have recently shown that reactive CD4+CD45RO+ T cells in LPHD exhibit a THl-type profile by producing high amounts ofinterleukin-2 (IL-2) and interferon-'y. ~ Although the signal that IL-2 provide s to LCs
•
remains to be determined, we can speculate that, in our case, high levels of IL-2, produced locally by the reactive T cells associated with N-LPHD, might have contributed to the hyperactivation of LCs leading to LCH development. Although this explanation may appear too simplistic and still needs to be confirmed a n d / o r completed, we hope that our hypothesis contributes to a better understanding of the relationships between DCs and neoplastic disorders. CANDICEROUFOSSE,MD LAURENCE LESPAGNARD,PHD, FRANCOISSALI~S,MD, DOMINIQUE BRON, MD, JWXN-LOuISDARGENT,MD Department of Pathology C.H.U. Saint-Pierre/U.L.B. InstitutJules Bordet and the Departments of Hematology and Surgery, U.L.B. InstitutJules Bordet, Brussels, Belgium 1. Wright-Browne V, Mc Clain KL, Talpaz M, et al: Physiologyand pathophysio!ogyof dendriticcells.Ht~MPATHOL28:563-579,1997 2. Dargent JL, Schanden6 L, Kornreich A, et al: Nature of the T lymphocytesin lymphocytepredominanceHodgkin'sdisease.LeukLymphoma 24:545-551, 1997 3. EgelerRM, NegliaJP,PuccettiDM, et al: Associationof Langerhans cell histiocytosiswith malignantneoplasms.Cancer71:865-873,1993 4. Richmond I, Eyden BP, Baneljee SS: Intranodal Langerhans' cell histiocytosisassociatedwith malignant melanoma. Histopathology26:380-382, 1995 5. Caux C, Massacrier C, Vanbervliet B, et al: Activation of human dendriticcellsthrough CD40cross-linking.JExp Med 180, 1263-1272, 1994
I
BOOK REVIEWS Acute Liver Failure William M. Lee, Roger Williams (eds), Cambridge University Press, $100.00 As noted by the editors, this book represents the outgrowth of two prior efforts to review current thinking on the topic of acute liver failure. These earlier efforts were published in monograph and j o u r n a l form and hence the current multi-authored text claims the distinction of constituting the first book dedicated to this subject. The target audience consists of internists, surgeons, intensivists, and other clinicians involved in diagnosis and treatment of persons with the disorder. As a consequence, the six primary sections of the book are as follows: (1) the clinical syndromes and etiologies of acute liver failure (viral, drug, etc,); (2) mechanisms of disease and multisystem involvement; (3) intensive care management; (4) transplantation; (5) artificial and bioartificial liver devices; (6) other therapeutic strategies. Section two will be of particular interest to pathologists with chapters on the role of cytokines and immune phenomena in acute liver failure (Kevork M, Peltichian and Gary A. Levy), the pathology of acute liver failure (Bernard Portmann and Romie Saxena) and replication and regeneration (Nelson Fausto). The quality of the pathology photographs is general!y excellent. This is not a book that the generally penurious general pathologist may wish to purchase. However, it would be a valuable addition to the hospital library.-ROBERT E, ANDERSON, MD, Professor,Laboratory Medicine and Pathology, University
of Minnesota, Minneapolis, MN 201
Lever's Histopathology of the Skin, Eighth Edition, David Elder with Rosalie Elenitsas, Christine Jaworsky, and Bernett Johnson, Jr., Philadelphia, PA, Lippincott-Raven Publishers, 1997, 1073 pages, $165.00. Histologic Diagnosis of Inflammatory Skin Diseases--An Algorithmic Method Based on Pattern Aualysis. Second Edition. A. Bernard Ackerman with Nidhi Chongchitnant, Jorge Sanchez, Ying Guo, Bruce Bennin, Martin Reichel, and M. Barry Randall. Baltimore, Williams & Wilkins, 1997, 943 pages, $250.00. The Eighth edition of Lever's Histopathology of the Shin represents a major metamorphosis from (1) a volume singularly published for almost 50 years by the late Walter E Lever with recent assistance by Gundula Schaumberg-Lever tO (2) a comprehensive tome with over 50 contributors. David Elder and the Editorial Board, the latter primarily from the University of Pennsylvania's Departments of Pathology and Dermato!ogy, have enlisted the assistance of an international group of distinguishe d pathologists and dermatopathologists to generate a well-written and up-to-date textbook that should cor!tinue to enjoy widespread use and authoritative respect. The 8th edition has been expanded from 34 to 37 chapters, covers more than 1,000 pages, cites more than 6,100 references and contains in excess of 800 photomicrographs. Although the current volume follows the previous edition's format and time-honored disease classfiication of both inflammatory and neoplastic process, the contributing authors have made significant attempts to reclassify selected entities into more biologi-
malignant melanoma remains highly unusual. Indeed, LCH is classically reported in association with other subtypes of Hodgkin's disease, but to our knowledge has never been described with N-LPHD. It has been previously described only once in lymph nodes draining the cutaneous site of a malignant melanoma .4 The pathogeny of LCH associated with neoplastic disorders is still unclear, and in our case, its association with two i n d e p e n d e n t but neighboring tumors raises some interesting questions. LCs belong to the dendritic cell (DC) lineage which is specialized in the processing and the presentation of antigens to T cells. 1 They may be recruited in several skin disorders including inflammatory diseases and tumors such as malignant melanoma. :,4 It is tempting to speculate that, in our case, these cells might have migrated from the melanoma site (where tumor antigens are shedded and processed) via the afferent lymphati£s to the T-dependent areas of the axil!ary lymph nodes (where antigens are presented to T cells) and accumulated there with the help of cytokines locally secreted by the adjacent N-LPHD neoplastic process. There is evidence that during their migration, DCs undergo a process of maturation characterized by the upregulatio n of several adhesion molecules and the acquisition of the full capacity of T-cell sensitization.: It has also be shown that on CD40 triggering (which mimicks interaction with T cells), cultured LCs acquire surface CD25 (Interleukin-2 receptor, IL-2R). 5 On the other hand, we have recently shown that reactive CD4+CD45RO+ T cells in LPHD exhibit a THl-type profile by producing high amounts ofinterleukin-2 (IL-2) and interferon-'y. ~ Although the signal that IL-2 provide s to LCs
•
remains to be determined, we can speculate that, in our case, high levels of IL-2, produced locally by the reactive T cells associated with N-LPHD, might have contributed to the hyperactivation of LCs leading to LCH development. Although this explanation may appear too simplistic and still needs to be confirmed a n d / o r completed, we hope that our hypothesis contributes to a better understanding of the relationships between DCs and neoplastic disorders. CANDICEROUFOSSE,MD LAURENCE LESPAGNARD,PHD, FRANCOISSALI~S,MD, DOMINIQUE BRON, MD, JWXN-LOuISDARGENT,MD Department of Pathology C.H.U. Saint-Pierre/U.L.B. InstitutJules Bordet and the Departments of Hematology and Surgery, U.L.B. InstitutJules Bordet, Brussels, Belgium 1. Wright-Browne V, Mc Clain KL, Talpaz M, et al: Physiologyand pathophysio!ogyof dendriticcells.Ht~MPATHOL28:563-579,1997 2. Dargent JL, Schanden6 L, Kornreich A, et al: Nature of the T lymphocytesin lymphocytepredominanceHodgkin'sdisease.LeukLymphoma 24:545-551, 1997 3. EgelerRM, NegliaJP,PuccettiDM, et al: Associationof Langerhans cell histiocytosiswith malignantneoplasms.Cancer71:865-873,1993 4. Richmond I, Eyden BP, Baneljee SS: Intranodal Langerhans' cell histiocytosisassociatedwith malignant melanoma. Histopathology26:380-382, 1995 5. Caux C, Massacrier C, Vanbervliet B, et al: Activation of human dendriticcellsthrough CD40cross-linking.JExp Med 180, 1263-1272, 1994
I
BOOK REVIEWS Acute Liver Failure William M. Lee, Roger Williams (eds), Cambridge University Press, $100.00 As noted by the editors, this book represents the outgrowth of two prior efforts to review current thinking on the topic of acute liver failure. These earlier efforts were published in monograph and j o u r n a l form and hence the current multi-authored text claims the distinction of constituting the first book dedicated to this subject. The target audience consists of internists, surgeons, intensivists, and other clinicians involved in diagnosis and treatment of persons with the disorder. As a consequence, the six primary sections of the book are as follows: (1) the clinical syndromes and etiologies of acute liver failure (viral, drug, etc,); (2) mechanisms of disease and multisystem involvement; (3) intensive care management; (4) transplantation; (5) artificial and bioartificial liver devices; (6) other therapeutic strategies. Section two will be of particular interest to pathologists with chapters on the role of cytokines and immune phenomena in acute liver failure (Kevork M, Peltichian and Gary A. Levy), the pathology of acute liver failure (Bernard Portmann and Romie Saxena) and replication and regeneration (Nelson Fausto). The quality of the pathology photographs is general!y excellent. This is not a book that the generally penurious general pathologist may wish to purchase. However, it would be a valuable addition to the hospital library.-ROBERT E, ANDERSON, MD, Professor,Laboratory Medicine and Pathology, University
of Minnesota, Minneapolis, MN 201
Lever's Histopathology of the Skin, Eighth Edition, David Elder with Rosalie Elenitsas, Christine Jaworsky, and Bernett Johnson, Jr., Philadelphia, PA, Lippincott-Raven Publishers, 1997, 1073 pages, $165.00. Histologic Diagnosis of Inflammatory Skin Diseases--An Algorithmic Method Based on Pattern Aualysis. Second Edition. A. Bernard Ackerman with Nidhi Chongchitnant, Jorge Sanchez, Ying Guo, Bruce Bennin, Martin Reichel, and M. Barry Randall. Baltimore, Williams & Wilkins, 1997, 943 pages, $250.00. The Eighth edition of Lever's Histopathology of the Shin represents a major metamorphosis from (1) a volume singularly published for almost 50 years by the late Walter E Lever with recent assistance by Gundula Schaumberg-Lever tO (2) a comprehensive tome with over 50 contributors. David Elder and the Editorial Board, the latter primarily from the University of Pennsylvania's Departments of Pathology and Dermato!ogy, have enlisted the assistance of an international group of distinguishe d pathologists and dermatopathologists to generate a well-written and up-to-date textbook that should cor!tinue to enjoy widespread use and authoritative respect. The 8th edition has been expanded from 34 to 37 chapters, covers more than 1,000 pages, cites more than 6,100 references and contains in excess of 800 photomicrographs. Although the current volume follows the previous edition's format and time-honored disease classfiication of both inflammatory and neoplastic process, the contributing authors have made significant attempts to reclassify selected entities into more biologi-