SLIDE SEMINAR NON NEOPLASTIC LYMPH NODE DISORDERS DR SHEILA NAIR CMC, VELLORE

SLIDE SEMINAR NON NEOPLASTIC LYMPH NODE DISORDERS DR SHEILA NAIR CMC, VELLORE

Case 1 34 year old male, mass right cervical region, for 4 years. No other significant findings. Grossly, the mass was well encapsulated, 5cms in diameter, cut surface was homogenous tan brown and slightly lobulated.

CASTLEMANS DISEASE HYALINE VASCULAR VARIANT

Castlemans Disease Unicentric or multicentric Hyaline Vascular variant (HV) Plasma cell variant ( PC) Hyaline Vascular variant : 80-90% of unicentric CD M=F, No symptoms except for compressive symptoms if mass is large. Sites: - Mediastinum, and other sites including abdominal lymph nodes Etiology: unknown. Treatment :Surgical excision and RT, if incompletely excised.

Case 2 62 year old male with a large swelling left side of neck, biopsy from which was taken. Investigations revealed normal haemoglobin and blood counts. Total protein 7.4 g%, Albumin 4.4g%. Serum electrophoresis - normal pattern.

Kappa lambda

CASTLEMANS DISEASE PLASMA CELL VARIANT

CASTLEMANS DISEASE PLASMA CELL VARIANT 10-20% of localized CD and majority of multicentric CD. Patients usually older than HV type Can be symptomatic, can be associated with POEMS syndrome. Symptomatic patients require steroids and chemotherapy.

Multicentric CD HIV infection, POEMS syndrome. Associated with HHV-8 infection. Most cases are PC variant. B- type symptoms common. Raised ESR, anemia, thrombocytopenia, elevated IL6, LDH and CRP, polyclonal hypergammaglobulinaemia. Higher incidence of Kaposi sarcoma and malignant lymphomas Glomeruloid haemangioma of skin.

Case 3 29 year old lady with low grade fever and left cervical lymphadenopathy. No other significant findings.

TOXOPLASMA LYMPHADENITIS

Lymphadenitis caused by infection with protozoan Toxoplasma gondii. Common in warm and humid climates. Definitive host is cat. Human beings are infected through contaminated soil or eating undercooked meat. Transplacental transfer can occur Chronic asymptomatic infection.

In intermediate hosts, oocysts rupture and trophozoites are released which are carried by lymphatics and blood within macrophages to internal organs In immunodefficient hosts: multiply within macrophages into clusters of crescent shaped bodies called Tachyzoites. Immunocompetent hosts: segregated in cysts Bradyzoites which multiply slowly

Toxoplasmosis-manifestations Toxoplasma lymphadenitis Systemic Toxoplasmosis in immunodefficient patients Fetal toxoplasmosis by trans placental infection.

Toxoplasma lymphadenitis Painless lymphadenopathy Posterior cervical or other lymph nodes Usually resolve spontaneously

Histology Triad: Toxoplasma trophozoites and cysts rarely seen. Immunohistochemical confirmation by toxoplasma antibodies permits easier recognition of the cysts in tissue sections

Positive correlation between histology and serology was obtained in 85% of cases. PCR targeting DNA is highly sensitive.

Case 4 14 year old girl with fever, cough and bilateral tender cervical lymph nodes of two months duration. No other significant findings.

KP1 KP1 MPO CD123

KIKUCHI DISEASE (KIKUCHI FUJIMOTO LYMPHADENOPATHY, HISTIOCYTIIC NECROTISING LYMPHADENITIS)

Described independently by Kikuchi and Fujimoto in 1972 Subacute necrotizing lymphadenitis Commonly in Asia Young adults with a slight female preponderance Unknown etiology

Usually unilateral cervical lymphadenopathy May have systemic symptoms Benign course with spontaneous regression in few weeks or months Rarely have recurrence.

Four histological subtypes: Lymphohisticytic type Phagocytic type Necrotic type Foamy cell type

Differential Diagnosis: Tuberculosis SLE Non Hodgkin lymphoma

SLE

Case 5 35 year old female with itchy skin lesions for 4 months and bilateral axillary lymphadenopathy.

DERMATOPATHIC LYMPHADENOPATHY

Usually associated with chronic dermatological lesions and represents a lymph node reaction to the drainage of melanin and various skin antigens Axillary and inguinal lymph nodes are most commonly involved

Immunohistochemistry: Both IDC and Langerhans cells are S100+ Langerhans cells also CD1a, langerin+ cf :phagocytic histiocytes CD68+,S100 weak+, CD1a-.

Most important in cases with minimal involvement by MF/SS, where the histological findings closely resemble DL. Can be distinguished by an aberrent T- cell immunophenotype or molecular studies to asses monoclonal T-cell receptor gene rearrangements