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• W2970721928 abstract "Histiocytic necrotising lymphadenitis, also known as Kikuchi disease, usually affects young adults of Asian descent who present typically with fever and painless, unilateral cervical lymphadenopathy.1Deaver D. Horna P. Cualing H. et al.Pathogenesis, diagnosis, and management of Kikuchi-Fujimoto disease.Cancer Control. 2014; 21: 313-321Crossref PubMed Scopus (43) Google Scholar Most cases follow a benign, self-limited course with spontaneous remission within a few months. The aetiology remains unclear. Both autoimmune and infectious aetiologies, especially viral infection, have been suggested,1Deaver D. Horna P. Cualing H. et al.Pathogenesis, diagnosis, and management of Kikuchi-Fujimoto disease.Cancer Control. 2014; 21: 313-321Crossref PubMed Scopus (43) Google Scholar but an association with phenytoin administration has not been reported. Pathologically, Kikuchi disease is characterised by a mixed population of plasmacytoid dendritic cells, histiocytes, T cells and immunoblasts with many cells undergoing apoptosis.2Kuo T.T. Kikuchi's disease (histiocytic necrotizing lymphadenitis). A clinicopathologic study of 79 cases with an analysis of histologic subtypes, immunohistology, and DNA ploidy.Am J Surg Pathol. 1995; 19: 798-809Crossref PubMed Scopus (314) Google Scholar Three morphological patterns have been described, and a temporal relationship has been suggested from proliferative phase to necrotic and then xanthomatous phase.2Kuo T.T. Kikuchi's disease (histiocytic necrotizing lymphadenitis). A clinicopathologic study of 79 cases with an analysis of histologic subtypes, immunohistology, and DNA ploidy.Am J Surg Pathol. 1995; 19: 798-809Crossref PubMed Scopus (314) Google Scholar However, the full morphological spectrum of Kikuchi disease is found only rarely in a single biopsy specimen. Thus, the well-known differential diagnosis may include lymphadenopathy in systemic lupus erythematosus (SLE) and infectious lymphadenitis.3O'Malley D.P. George T.I. Orazi A. et al.Benign and Reactive Conditions of Lymph Node and Spleen. Atlas of Nontumor Pathology. American Registry of Pathology, Washington, DC2009Google Scholar Here, we report a case of phenytoin (Dilantin)-induced necrotising lymphadenitis which mimicked Kikuchi disease. A 23-year-old Taiwanese man presented with convulsive status epilepticus characterised by episodic focal seizures with intermittent secondary generalisation in the past 12 months. He carried the HLA-B*1502 allele and took levetiracetam and lacosamide as baseline anti-epileptic medication.4Chen P. Lin J.J. Lu C.S. et al.Carbamazepine-induced toxic effects and HLA-B*1502 screening in Taiwan.N Engl J Med. 2011; 364: 1126-1133Crossref PubMed Scopus (500) Google Scholar The status epilepticus was controlled initially with valproic acid and levetiracetam; medication was changed to phenytoin on admission to avoid the risk of liver failure. Three days later, intermittent low-grade fever developed which was followed by spiking fever (39.2°C) one week later. In addition, generalised maculopapules with petechiae (Fig. 1A) and tender lymphadenopathy developed in the neck and inguinal regions. Laboratory data showed a white blood cell count of 5.1 K/μL with a left shift in maturation: metamyelocytes 1%, bands 3%, segs 65%, monocytes 11%, lymphocytes 9%, and basophils 1%. Serum liver enzymes were normal and the serum phenytoin level was 40.8 μg/mL (therapeutic range 10–20 μg/mL). Other tests were negative, including serology for infection by Mycobacterium tuberculosis, herpes simplex virus, varicella-herpes zoster virus; and autoimmune testing including anti-nuclear antibody, anti-double stranded DNA antibody, rheumatoid factor, anti-SSA/SSB, anti-neutrophil cytoplasmic antibody, anti-Jo-1, anti-ribosomal-P and anti-Scl-70. A computed tomography (CT) scan revealed enlarged tonsils and bilateral neck lymphadenopathy (Fig. 1B). Phenytoin was stopped on the 14th day after admission and biopsy of a right posterior neck lymph node was performed the next day. The pathological diagnosis was necrotising lymphadenopathy with a differential diagnosis between Kikuchi disease and SLE lymphadenopathy; clinical evaluation was recommended. After withdrawal of phenytoin, fever resolved, skin rash gradually regressed, and lymphadenopathy disappeared within one week. The Naranjo adverse drug reaction probability scale was 8 (Supplementary Fig. 1, Appendix A), indicating a probable relationship between the patient's development of necrotising lymphadenitis and treatment with phenytoin.5Fleming P. Marik P.E. The DRESS syndrome: the great clinical mimicker.Pharmacotherapy. 2011; 31: 332Crossref PubMed Scopus (29) Google Scholar Pathologically, the lymph node showed interfollicular (T-zone) expansion with several residual lymphoid follicles. Other fields of interfollicular expansion contained several foci of necrosis composed of karyorrhectic debris and fibrin deposits surrounded by histiocytes (Fig. 1C). The interfollicular expansion revealed a polymorphic infiltrate characterised by small and large lymphocytes, histiocytes and some apoptotic cells indicative of plasmacytoid dendritic cells. Plasma cells and eosinophils were inconspicuous. Immunohistochemical analysis showed that the interfollicular areas were enriched by CD3+ T cells (Fig. 2A,B). CD20 was expressed predominantly by lymphoid follicles (Fig. 2C). Many plasmacytoid dendritic cells in the interfollicular areas were highlighted by CD123 (Fig. 2D). Histiocytes with crescentic (C-shaped) nuclei were positive for myeloperoxidase (Fig. 2E). In situ hybridisation for detection of Epstein–Barr virus was negative (Fig. 2F). Necrotising lymphadenitis, characterised by focal or geographic necrosis in a lymph node surrounded by an organised cellular response, can be the result of infectious and non-infectious aetiologies.3O'Malley D.P. George T.I. Orazi A. et al.Benign and Reactive Conditions of Lymph Node and Spleen. Atlas of Nontumor Pathology. American Registry of Pathology, Washington, DC2009Google Scholar The differential diagnoses may include Kikuchi–Fujimoto disease, systemic lupus erythematosus, cat-scratch disease, tularaemia, tuberculosis, lymphogranuloma venereum, and viral infections such as herpes simplex virus (HSV) and Epstein–Barr virus.3O'Malley D.P. George T.I. Orazi A. et al.Benign and Reactive Conditions of Lymph Node and Spleen. Atlas of Nontumor Pathology. American Registry of Pathology, Washington, DC2009Google Scholar Neoplastic conditions such as lymphoma and metastatic carcinoma may also contain foci reminiscent of necrotising lymphadenitis.3O'Malley D.P. George T.I. Orazi A. et al.Benign and Reactive Conditions of Lymph Node and Spleen. Atlas of Nontumor Pathology. American Registry of Pathology, Washington, DC2009Google Scholar In the current case, there was no granuloma and special studies including acid-fast, GMS stain, HSV immunostain and EBER in situ hybridisation were all negative. Thus, the initial morphological impression was Kikuchi disease and lupus lymphadenitis. After correlation with the clinical history, the morphological features were consistent with phenytoin-induced lymphadenopathy. Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, also known as drug-induced hypersensitivity syndrome (DIHS) or anti-epileptic hypersensitivity syndrome (AHS), is potentially life-threatening, and is characterised by morbilliform skin eruptions, fever, lymphadenopathy, haematological abnormalities, and manifestations of multiorgan dysfunction.6De A. Rajagopalan M. Sarda A. et al.Drug reaction with eosinophilia and systemic symptoms: an update and review of recent literature.Indian J Dermatol. 2018; 63: 30-40Crossref PubMed Scopus (29) Google Scholar DRESS syndrome is well-known to be caused by phenytoin (phenytoin hypersensitivity syndrome) and other medications, such as allopurinol, antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs).7Husain Z. Reddy B.Y. Schwartz R.A. DRESS syndrome: Part I. Clinical perspectives.J Am Acad Dermatol. 2013; 68 (693e1–14; 706–8)Abstract Full Text Full Text PDF Scopus (169) Google Scholar DRESS syndrome has a latency interval of 2–6 weeks from drug administration to syndrome onset. The pathogenesis of DRESS syndrome remains to be clarified, but reactivation of human herpes virus 6 (HHV6) with lymphocytic activation may play a role.5Fleming P. Marik P.E. The DRESS syndrome: the great clinical mimicker.Pharmacotherapy. 2011; 31: 332Crossref PubMed Scopus (29) Google Scholar, 7Husain Z. Reddy B.Y. Schwartz R.A. DRESS syndrome: Part I. Clinical perspectives.J Am Acad Dermatol. 2013; 68 (693e1–14; 706–8)Abstract Full Text Full Text PDF Scopus (169) Google Scholar Withdrawal of the offending agent was the most important part of treatment. Supportive care may be adequate for patients with mild DRESS syndrome. Glucocorticoids, intravenous immunoglobulin (IVIG), plasmapheresis and N-acetylcysteine have been used for severe DRESS cases.8Cumbo-Nacheli G. Weinberger J. Alkhalil M. et al.Anticonvulsant hypersensitivity syndrome: is there a role for immunomodulation?.Epilepsia. 2008; 49: 2108-2112Crossref PubMed Scopus (23) Google Scholar The morphological spectrum of phenytoin (Dilantin)-associated lymphadenopathy is broad and may include lymphoid hyperplasia with or without immunoblastic hyperplasia,9Abbondazo S.L. Irey N.S. Frizzera G. Dilantin-associated lymphadenopathy. Spectrum of histopathologic patterns.Am J Surg Pathol. 1995; 19: 675-686Crossref PubMed Scopus (45) Google Scholar granulomatous lymphadenopathy,10Ovallath S. Remya R.K. Kumar C. et al.Granulomatous lymphadenopathy secondary to phenytoin therapy.Seizure. 2013; 22: 240-241Abstract Full Text Full Text PDF PubMed Scopus (5) Google Scholar immunoblastic lymphadenopathy,11Lapes M.J. Vivacqua R.J. Antoniades K. Immunoblactic lymphadenopathy associated with phenytoin (diphenylhydantoin).Lancet. 1976; 1: 198Abstract PubMed Scopus (30) Google Scholar and necrotising lymphadenitis.12Subbannan K. Gujral J.S. Necrotizing lymphadenitis associated with the phenytoin-induced hypersensitivity syndrome.South Med J. 2005; 98: 937-939Crossref PubMed Scopus (7) Google Scholar Cases of Hodgkin lymphoma and non-Hodgkin lymphoma also have been reported.9Abbondazo S.L. Irey N.S. Frizzera G. Dilantin-associated lymphadenopathy. Spectrum of histopathologic patterns.Am J Surg Pathol. 1995; 19: 675-686Crossref PubMed Scopus (45) Google Scholar The finding of necrotising lymphadenitis is the least frequent and has been reported only once.12Subbannan K. Gujral J.S. Necrotizing lymphadenitis associated with the phenytoin-induced hypersensitivity syndrome.South Med J. 2005; 98: 937-939Crossref PubMed Scopus (7) Google Scholar In the previous case, the patient presented with a similar clinical picture of fever, lymphadenopathy, and mucocutaneous rashes. Both patients showed no atypical lymphocytosis or eosinophilia. The previously reported patient had prominent liver enzyme elevation. Interestingly, carbamazepine, another anti-epileptic drug may produce lymphadenopathy resembling Kikuchi disease as we reported here.13Ganga A. Corda D. Gallo Carrabba G. et al.A case of carbamazepine-induced lymphadenopathy resembling Kikuchi disease.Eur Neurol. 1998; 39: 247-248PubMed Google Scholar In conclusion, we report this case to emphasise that phenytoin exposure uncommonly causes necrotising lymphadenitis and should be included in the differential diagnosis of this finding. Withdrawal of the offending agent, in this case phenytoin, was the key to successful management of this patient. This current case also alerts pathologists that drug-associated lymphadenopathy may be occasionally reminiscent of Kikuchi disease. The authors state that there are no conflicts of interest to disclose." @default.
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• W2970721928 title "Phenytoin-associated necrotising lymphadenitis mimicking Kikuchi disease" @default.
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