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CASE REPORT
Year : 2020  |  Volume : 18  |  Issue : 1  |  Page : 45-47

A case of tubercular lymphadenopathy and review of literature


1 Department of Internal Medicine and Rheumatology, VPS Lakeshore Hospital, Kochi, Kerala, India
2 Department of Radiology, VPS Lakeshore Hospital, Kochi, Kerala, India
3 Department of Pathology, VPS Lakeshore Hospital, Kochi, Kerala, India

Date of Submission02-Aug-2019
Date of Decision19-Aug-2019
Date of Acceptance30-Aug-2019
Date of Web Publication03-Feb-2020

Correspondence Address:
Dr. Muhammed Jasim Abdul Jalal
Department of Internal Medicine and Rheumatology, VPS Lakeshore Hospital, Nettoor P. O., Maradu, NH 47 – Byepass, Kochi - 682 040, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cmi.cmi_30_19

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  Abstract 


Tubercle bacilli infects approximately one-third of the world's population as per the World Health Organization. New cases of the active disease developing each year constitute eight million of which three million people die. Tubercular lymphadenopathy is often rare compared to pulmonary tuberculosis. We present a case of a 29-year-old Indian female, who was immunocompetent and HIV negative, with a 3-month history of recurring fever, loss of appetite, abdominal pain, vomiting, and loss of weight. On examination, she had disseminated lymphadenopathy including supraclavicular lymph nodes. Fine-needle aspiration cytology of the right supraclavicular node showed acid-fast bacilli along with caseation necrosis and was consistent with tubercular lymphadenopathy. Disseminated tubercular lymphadenopathy is extremely rare in immunocompetent individuals. The crux in the approach to disseminated lymphadenopathy lies in the diagnosis of tubercular lymphadenopathy, confirmed by histological and microbiological findings since it has a good prognosis with an active antituberculous treatment regime resulting in a favorable outcome.

Keywords: Caseation necrosis, disseminated lymphadenopathy, extrapulmonary tuberculosis, tubercular lymphadenopathy, tuberculosis


How to cite this article:
Mohammad Iqbal K M, Abdul Jalal MJ, Pratap T, Mathew IL. A case of tubercular lymphadenopathy and review of literature. Curr Med Issues 2020;18:45-7

How to cite this URL:
Mohammad Iqbal K M, Abdul Jalal MJ, Pratap T, Mathew IL. A case of tubercular lymphadenopathy and review of literature. Curr Med Issues [serial online] 2020 [cited 2020 Apr 3];18:45-7. Available from: http://www.cmijournal.org/text.asp?2020/18/1/45/277518




  Introduction Top


Tubercular lymphadenopathy comprises only <5% of all cases of tuberculosis. It is more common among children, women as well as in immunosuppressed patients.[1] The cervical lymph nodes are most frequently involved, followed by the mediastinal lymph nodes and the axillary lymph nodes.[2] Disseminated tubercular lymphadenopathy is extremely rare in immunocompetent individuals. We present a case of a 29-year-old Indian female, who was immunocompetent and HIV negative, with a 3-month history of recurring fever, loss of appetite, abdominal pain, vomiting, and loss of weight.


  Case Report Top


A 29-year-old Indian female presented with a 3-month history of recurring fever, loose stools, abdominal pain, and vomiting. She had associated loss of appetite. She gave a history of significant weight loss of 6 kg in 1 month. There was no history of cough, chest pain, and dysuria. She denied a history of any skin lesions and oral or genital ulcers.

General examination showed mild pallor. There was no icterus, cyanosis, clubbing, or edema. She was found to have bilateral supraclavicular, cervical, axillary, and inguinal lymphadenopathy. Her lymph nodes were firm and tender. She was febrile with axillary temperature of 38°C. She was hemodynamically stable with a blood pressure of 100/70 mmHg, respiratory rate of 20 breaths/min, and a heart rate of 100 beats/min.

Systemic examination revealed a clear chest with air entry bilaterally equal. Heart sounds were regular without any murmurs. The abdomen was soft, nontender without any hepatosplenomegaly. Bowel sounds were present. There was no renal bruit. She did not have any focal neurological deficits.

Laboratory investigations showed hemoglobin: 10 g/dl, white blood cell count: 6450 cells/mm3 (48% neutrophils, 43% lymphocytes, 4% transformed lymphocytes, and 5% eosinophils), and platelet count: 220,000 cells/mm3. Erythrocyte sedimentation rate was 54 mm/h. The international normalized ratio was 1, and activated partial thromboplastin time was 32 s. Total bilirubin was 0.5 mg/dl, serum glutamic oxaloacetic transaminase was 16 IU/l, serum glutamic pyruvic transaminase was 8 IU/l, total protein was 7.7 mg/dl, and creatine phosphokinase was 170 IU/l. Serum albumin was 3.9 mg/dl. C-reactive protein was positive (>113 mg/L). Renal function tests were within the normal ranges. The Mantoux test was positive (20 mm). Hepatitis A, B, and C serology and HIV were negative. Serum cortisol was also normal.

Chest X-ray did not show any infiltrative lesions or hilar prominences. There was no evidence of cardiomegaly. Computed tomography (CT) of the thorax was normal apart from few reactive mediastinal lymphadenopathies.

An ultrasonography of the abdomen was normal. Upper gastrointestinal endoscopy was normal apart from antral gastritis. CT of the abdomen was normal apart from a right ovarian cyst. There were no evidences of para-aortic or pelvic lymphadenopathy. An ultrasonography of the neck showed multiple level III and level IV lymph nodes on the right side, which was predominantly necrotic, the largest measuring 1.4 cm [Figure 1]a. Level II and level III cervical lymph nodes with mild heterogeneous parenchyma were noted on the left side, the largest measuring 5.0 mm × 0.3 mm [Figure 1]b.
Figure 1: (a) Ultrasonography of the right side of the neck showing the largest (1.4 cm) level III cervical lymph node. (b) Ultrasonography of the left side of the neck showing the largest (5.0 mm × 0.3 mm) level II cervical lymph node with mild heterogeneous parenchyma

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Fine-needle aspiration cytology (FNAC) from the right supraclavicular node was done. Smears showed abundant caseous necrotic material with occasional aggregates of lymphoid cells [Figure 2] and [Figure 3]. Acid-fast bacilli was also seen [Figure 4]. This was consistent with tubercular lymphadenopathy.
Figure 2: Tuberculosis necrosis (×10 views)

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Figure 3: Tuberculosis necrosis (×40 views)

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Figure 4: Ziehl-Neelsen staining showing acid-fast bacilli

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Standard four-drug regimen, antituberculous treatment, consisting of rifampin, pyrazinamide, ethambutol, and isoniazid (INH) was started. She was asymptomatic after 2 months of treatment with a prominent reduction in most lymph node swelling. A two-drug regimen of INH and rifampin was continued for 7 months. At the end of the intensive phase therapy after 2 months, the patient had residual lymph nodes in the neck, which was subsequently cleared at the end of 9 months after the completion of the continuation phase therapy.


  Discussion Top


Tubercular lymphadenopathy can occur.

  1. Along with pulmonary infection
  2. Due to dormant foci reactivation
  3. Directly from a contiguous focus.


History of contact with tuberculosis is seen in 21.8% of tubercular lymphadenopathy.[1],[2] Systemic symptoms in tubercular lymphadenopathy include low-grade fever, weight loss, and fatigue. Cough is not a prominent feature unlike pulmonary tuberculosis. Tubercular lymphadenopathy is clinically diagnosed depending on the multiplicity, matting, and caseation of the lymph nodes.

Tubercular lymphadenopathy is classified into 5 stages.[3] Stage 1 constitutes enlarged, firm, mobile, and discrete nodes showing nonspecific reactive hyperplasia. Stage 2 includes large rubbery nodes fixed to the surrounding tissue owing to periadenitis. Stage 3 lymph nodes have central softening due to abscess formation. Stage 4 results in collar-stud abscess formation. Stage 5 is characterized by sinus tract formation.

The lymph nodes are usually not tender. Tuberculous lymph nodes become tender in the presence of secondary bacterial infection and when co-existing with HIV infection.

Viral, bacterial, or fungal infections can present with lymphadenopathy. Lymphomas and metastatic carcinomas too have enlarged lymph nodes. Sarcoidosis and connective tissue diseases also manifest with lymphadenopathy. Hence, tubercular lymphadenopathy requires a high index of clinical suspicion.

Ziehl-Neelsen staining is specific for tuberculosis. FNAC is a sensitive (84%), specific (91%), and cost-effective way to diagnose tubercular lymphadenopathy.[4] Histopathology is diagnostic of tubercular lymphadenopathy.[5]

Tubercular lymphadenopathy is treated by the antituberculosis treatment regime. DOTS guidelines categorize tubercular lymphadenopathy under Category III.[6] First-line antituberculous drugs are INH, rifampin, ethambutol, pyrazinamide, and streptomycin. Second-line drugs include capreomycin, kanamycin, ethionamide, thiacetazone, para-aminosalicylic acid, and cycloserine. Treatment should not be deferred during pregnancy.[6] Corticosteroid in the treatment of tubercular lymphadenopathy is not well established and remains controversial.[7]


  Conclusion Top


Lymphadenitis is the most common extrapulmonary manifestation of tuberculosis. A high index of suspicion is required for their diagnosis and distinction. The approach to diagnosis should be individualized depending on the location of the disease and the clinical evaluation.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Geldmacher H, Taube C, Kroeger C, Magnussen H, Kirsten DK. Assessment of lymph node tuberculosis in Northern Germany: A clinical review. Chest 2002;121:1177-82.  Back to cited text no. 1
    
2.
Nwagbara VI, Asuquo ME, Akpan S, Nwachukwu IE, Nnoli M, Ugbem T. Tuberculous axillary lymphadenopathy: A case report. J Trop Dis 2013;1:113-4.  Back to cited text no. 2
    
3.
Jones PG, Campbell PE. Tuberculous lymphadenitis in childhood: The significance of anonymous mycobacteria. Br J Surg 1962;50:302-14.  Back to cited text no. 3
    
4.
Lau SK, Wei WI, Hsu C, Engzell UC. Fine needle aspiration biopsy of tuberculous cervical lymphadenopathy. Aust N Z J Surg 1988;58:947-50.  Back to cited text no. 4
    
5.
Chao SS, Loh KS, Tan KK, Chong SM. Tuberculous and nontuberculous cervical lymphadenitis: A clinical review. Otolaryngol Head Neck Surg 2002;126:176-9.  Back to cited text no. 5
    
6.
American Thoracic Society, CDC, Infectious Diseases Society of America. Treatment of tuberculosis. MMWR Recomm Rep 2003;52:1-77.  Back to cited text no. 6
    
7.
Dooley DP, Carpenter JL, Rademacher S. Adjunctive corticosteroid therapy for tuberculosis: A critical reappraisal of the literature. Clin Infect Dis 1997;25:872-87.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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