PATTERN OF INFLAMMATORY DISEASES IN LYMPH NODE BIOPSY

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Dr.MUSA EZEKIEL REGISTRAR, ABUTH ZARIA

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PATTERNS OF INFLAMMATORY DISEASES IN LYMPH NODE BIOPSIES IN ABUTH ,ZARIA . A FIVE YEAR REVIEW(2006-2010):

PATTERNS OF INFLAMMATORY DISEASES IN LYMPH NODE BIOPSIES IN ABUTH ,ZARIA . A FIVE YEAR REVIEW(2006-2010) BY DR.MUSA EZEKIEL DEPT.OF MEDICINE

SYNOPSIS :

SYNOPSIS Lymph node Anatomy. Patterns of inflammatory diseases affecting lymph nodes. Discussion. Recommendation Conclusion References.

Anatomy Of the Lymph Node:

Anatomy Of the Lymph Node .

The Lymph Nodes:

The Lymph Nodes Anatomy oval, bean shaped structures scattered throughout body along lymph vessels may be deep or superficial concentrated along the respiratory tree and GI tract, in the mammary glands, axillae, and groin filter lymph fluid to trap foreign organisms, cell debris, and tumor cells

PowerPoint Presentation:

Lymphatic Organs – Lymph Nodes Covered by a fibrous connective tissue capsule Trabeculae extend from cortex to medulla Stroma – the internal supportive connective tissue network of reticular fibers

Structure of a Lymph Node:

Structure of a Lymph Node outer cortex - filled with lymph follicles outer edge of follicle contains more T cells inner germinal center is the site of B-cell proliferation inner medulla - medullary cords of lymphocytes, macrophages, plasma cells (activated B cells) Cortex Medulla

:

follicles with germinal centers Histology of Lymph Nodes

Circulation in the Lymph Nodes:

Circulation in the Lymph Nodes Lymph enters via a number of afferent lymphatic vessels It then enters a large subcapsular sinus and travels into a number of smaller sinuses It meanders through these sinuses and exits the node at the hilus via efferent vessels The node acts as a “settling tank,” because there are fewer efferent vessels, lymph stagnates somewhat in the node This allows lymphocytes and macrophages time to carry out their protective functions Only lymph nodes filter lymph!

Lymph Flow Through Lymph Nodes:

Lymph Flow Through Lymph Nodes fluid enters cortex through afferent vessels filter and trap damaged cells, microorganisms, foreign substances, tumor cells by reticular fibers macrophages phagocytize some, lymphocytes destroy some by immune defenses exits medulla by efferent vessels at hilus

Patterns Of Inflammatory Diseases In ABUTH,2006-2010:

Patterns Of Inflammatory Diseases In ABUTH,2006-2010

Prevalence of Age-related TB Adenitis:

Prevalence of Age-related TB Adenitis

Prevalence of Sex-related Inflammatory Diseases in ABUTH:

Prevalence of Sex-related Inflammatory Diseases in ABUTH

PAEDIATRIC VS ADULT TB :

PAEDIATRIC VS ADULT TB

TB:

TB

Toxoplasmosis:

Toxoplasmosis

HIV:

HIV

HIV:

HIV

:

DISCUSSION

TB ADENITIS:

TB ADENITIS TB adenitis refers to involvement of lymph nodes by members of the M.tuberculosis complex which include M.tuberculosis , M.bovis , M.africanum , M.canetti and M.caprae . It may be associated with pulmonary TB or other organ involvement but is usually an isolated finding - 20% of all TB cases are extrapulmonary TB

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Most common EPTB In the US, non - tuberculous mycobacteria are the most common cause of mycobacterial lymphadenitis in children extrapulmonary TB ( EPTB) rates have not declined in the US HIV positive patients with MTB are more likely to have EPTB than HIV negative patients 45 - 70% Vs 15%

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In HIV positive patients TBLN is associated with CD4 < 300 ( usually <100) A US based study in Houston revealed the following characteristics in HIV negative patients – Predictive factors: Female ,birth in Africa/SE Asia Protective factors: White Race and Diabetes Mellitus

Pathogenesis:

Pathogenesis 3 suspected routes: 1) Reactivation of PTB or hilar extension is most common 2)Deep cervical involvement from laryngeal infection 3) hematogenous

Histo-pathology:

Histo -pathology 4 distinct cytological patterns noted on aspirate, ranging from - Pattern 1: occasional granulomas with early epitheloid cells, extensive necrosis and foam cells, numerous AFB - seen in HIV positive patients with TBLN - Pattern 4: Numerous granulomata with most epitheloid cells and minimal necrosis + absence of AFB mostly - seen in HIV negative patients with TBLN

Clinical features :

Clinical features Pediatric TBLN is mostly an isolated infection in the anterior cervical chain Adult infection is similar with 70% anterior cervical chain - 58% of which is in the jugulodigastric region HIV co - infection is associated with a more severe/disseminated disease

Clinical Features:

Clinical Features Abnormal CXR did not correlate with sputum positivity but wt loss did Disease associations: Chronic granulomatous disease, lymphoma, HIV diabetes,Renal Insufficiency and Alcoholism and low iron and Vitamin D levels are also associated with MTB

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Pathological types: (1) Caseous type: low immunity, common in child (2) Fibrous type: marked fibrosis with minimal caseation or lymphoid hyperplasia. (3) Lymphadenoid type: Marked lymphoid hyperplasia with no caseation or fibrosis Fate of T.B. Lymphadenitis: 1- Resolution. 2- Calcification 3- Caseation - cold abscess or sinus formation. 4- General dissemination

Diagnosis:

Diagnosis About 20% have positive sputum cultures but only 9 - 15% had positive AFB sputum smears. Biopsy is the gold standard for diagnosis FNA biopsy lead to TB diagnosis in 79% of cases compared to surgical biopsy in 83% Histology more sensitive than culture

Diagnosis:

Diagnosis Nucleic acid amplification tests(PCR) for TB lymphadenitis are rapid but yield variable and inconsistent results Immune based blood tests include: - T cell based cellular response ( IGRA - Interferon Gamma Release Assay) and - humoral antibody response

Treatment:

Treatment Drug resistance in 13% of 147 cases of TBLN in Manitoba only in foreign born Standard per British Thoracic Society for uncomplicated TBLN Rifampin + Isoniazid + Ethambutol for 2 months followed by Isonizid and Ethambutol for 6 months Standard abbreviations include: S = streptomycin, H or INH= isoniazid , R or RFM= Rifampin , Z or PZA= Pyrazinamide , E= Ethambutol

Treatment:

Treatment Extend to 6 - 12 months if LN persists , rebiopsy and place on a CAT II regimen: 2 months of SHRZE then 1 month of RHZE followed by 5 months of RHE Alternate regimen is 4RHZE +2 RH: 5 year remission rate was 89% Steroids not recommended by IDSA currently ( Evidence DIII) however has had anecdotal benefit

Treatment:

Treatment Steroids decrease pain and discomfort anecdotally though these outcomes have not been studied in larger trials . Surgery has no role for MTB unlike non TB mycobacteria ( Evidence BIII per IDSA) Interferon gamma and GCSF are under investigation

Paradoxical Response (PR):

Paradoxical Response (PR) Defined as development of enlarging nodes or new nodes during treatment seen in 23 30% Among HIV negative patients: Baseline peripheral monocytosis is a significant predictor for PR but NOT age, sex, node size, low Vitamin D, AFB smear/culture positive, ANC or ALC.

Paradoxical Response:

Paradoxical Response Among HIV positive patients: PRs noted in 7% not on HAART Vs 36% on HAART. Steroid use did not change duration of PRs Aspiration, I&D and excision were associated with a shorter duration of PR but not significantly so ( p=0.1)

Outcomes:

Outcomes Cure rates vary from 81% - 95% with surgery + Anti TB regimen for 12 - 18 months Relapse rates noted to be 8.1 per 1000 person yrs of follow up Residual palpable adenopathy in 5 - 30% of cases Spontaneous drainage in 17%

Chronic granulomatous disease:

Chronic granulomatous disease Results from enzymatic defect of granulocytes and monocytes These cells ingest microorganisms but are unable to destroy them Due to defects in NADPH oxidases Pattern of inheritance is Y- linked in majority of patients Autosomal recessive Nitro blue tetrazolium test is the technique for its detection

Clinical features:

Clinical features lymphadenitis, hepatosplenomegaly, Skin rash, anaemia,leucocytosis,hypergammaglobulinemia pulmonary infiltrates

Microscopic features:

Microscopic features Granulomas with necrotic purulent centres Histiocytes are common

Acute non-specific lymphadenitis:

Acute non-specific lymphadenitis Typical case is rarely biopsied Microscopically: -sinus dilatation -accumulation of neutrophils -Vascular dilatation -capsular edema two forms:1.suppurative 2.necrotizing lymphadenitis

Chronic non-specific lymphadenitis:

Chronic non-specific lymphadenitis General features: -follicular hyperplasia - pominence of postcapillary venules -increase in immunoblast,plasma cells and histiocytes -fibrosis other features: -capsular inflammation and or fibrosis -presence of eosinophils and mast cells

Histoplasmosis :

Histoplasmosis Presents as: 1.chronic suppurative lesions 2.granulomatous lesions May results in widespread nodal necrosis and diffuse hyperplasia of sinus histiocytes Histologic diagnosis:1.Gomori methanamine silver stain 2.PAS stain

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Other diagnostic modalities: -culture -molecular testing - immunohistochemistry

Toxoplasmosis:

Toxoplasmosis One of the commonest parasitic diseases of man Caused by T.gondii Posterior cervical nodes in young women Nodes are firm and moderately enlarged Microscopically: -marked follicular hyperplasia -small granulomas of composed of entirely epithelioid cells

:

Distension of marginal and cortical sinuses There may be immunoblast and plasma cells in the medullary cords Other techniques: -PCR - IgM immunoflorescent antibody test

HIV /AIDS –related lymphadenitis:

HIV /AIDS –related lymphadenitis There four types: 1.Florid reactive hyperplasia 2.Mycobacteria 3.Opportunistic infection 4.Malignacy Microscopically: -collection of monocytoid B cells in the sinusoids

:

Reactive germinal centres show follicle lysis Evagination of mantle zone B-cells into germinal centres HIV may be found in follicular dendritic cells by immunohistochemistry { fascin stain} HIV protein p24 may be found in germinal cetres Other features: -lymphocyte depletion -Prominent interfollicular vascular proliferation

Recommendations:

Recommendations Detailed clinical information by clinicians Procurement and utilization of modern diagnostic methods by the pathologist Proper record keeping of histopathological results Political will to improve the efficiency of our Laboratories Clinico -pathological collaboration A careful approach at sample collection, processing, and utilization of ancillary techniques optimizes diagnostic yield

Conclusion:

Conclusion TB is the commonest cause of lymphadenitis in our environment Expansion of DOTS TB treatment progammes Not every lymphadenitis is tuberculous Need for exploration of modern diagnostic technique Increasing need for utilization of commonly used staining methods Lymph nodes provide invaluable information in the diagnostic evaluation of several diseases

References:

References Surgical pathology(ninth edition) by Juan Rosai pages 1893-1917 Robins Pathological basis of diseases , sixth edition page 645-650 E-medicine 2012 NPMCN update course ,faculty of pathology

THANK YOU :

THANK YOU

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