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Background: Laryngeal tuberculosis is a rare form of extrapulmonary tuberculosis affecting the larynx, often misdiagnosed due to symptoms mimicking laryngeal cancer. It presents with hoarseness, dysphagia, and cough. Diagnosis involves laryngoscopy, biopsy, and microbiological testing. Early recognition and appropriate antitubercular therapy are essential for effective management and prevention of complications. Unilateral tubercular lung destruction is a rare but serious manifestation of pulmonary tuberculosis, characterized by extensive, often irreversible damage confined to one lung. This condition typically arises from chronic, untreated, or drug-resistant tuberculosis, leading to progressive cavitation, fibrosis, bronchiectasis, and eventual collapse of the affected lung. Clinically, patients may present with chronic cough, dyspnea, hemoptysis, weight loss, and signs of respiratory insufficiency. Radiological features include mediastinal shift, hyperinflation of the contralateral lung, volume loss, and extensive parenchymal distortion. Diagnostic confirmation relies on imaging modalities, sputum testing, bronchoscopy, and histopathology. Treatment involves standard anti-tubercular therapy (ATT), but outcomes are often suboptimal in cases with advanced destruction. Surgical intervention, such as pneumonectomy, may be required for symptom control or in cases complicated by massive hemoptysis or recurrent infections. The coexistence of laryngeal granuloma and UTLD reflects advanced disease and necessitates prompt diagnosis, antitubercular therapy, and sometimes surgical intervention for effective management and improved outcomes.
Tuberculosis (TB), is a chronic infectious disease caused by Mycobacterium tuberculosis, an acid-fast bacillus. It is a pulmonary and systemic disease and a leading cause of death worldwide.
According to the WHO Global Tuberculosis Report 2024, an estimated 10.8 million new tuberculosis cases were reported globally. Five countries accounted for 56% of the global burden, with India contributing the highest share at approximately 26% of the total cases.[1]
The incidence of TB is relatively higher in males and is more prevalent in low- and middle-income countries, with an immunocompromised (malnutrition, HIV, diabetes) state being a major predisposing factor.
Extrapulmonary TB may involve lymph nodes, pleura, upper airways (larynx, pharynx, epiglottis), genitourinary tract, bones, central nervous system, gastrointestinal tract, pericardium, and skin. Among these, laryngeal TB is a rare manifestation accounting for less than 1% of all TB cases globally. [2]
Laryngeal TB often arises as a secondary infection from pulmonary TB, spreading either via hematogenous routes or bronchial secretions. Although very rare, primary laryngeal TB cases have also been reported. This condition mainly affects the posterior part of the vocal cords, presenting clinically with symptoms like dysphonia, change in voice, and dyspnoea if the mass grows large enough to obstruct the airway. It is often confused with laryngeal carcinoma often leading to misdiagnosis or delayed treatment.[3]
There are many complications associated with TB, among whichunilateral tuberculouslung destruction (UTLD), is a serious and irreversible condition marked by extensive fibrosis and parenchymal damage. This impairs lung function and leads to respiratory symptoms, often as a result of an overprotective immune response. Finding both entities together is quite rare, so we report here a patient with laryngeal TB and unilateral tuberculous lung destruction who has a past history of pulmonary tuberculosis.
A 57 year old male presented to ENT OPD with change in voice and foreign body sensation in throat since 1 year .Voice change was insidious in onset, gradually progressive and increased over 1 year. The patient also complains of difficulty in breathing intermittently. Indirect laryngoscopy showed lesion in posterior vocal cords. There were no palpable lymph nodes. Symptoms were not associated with loss of weight or loss of appetite. Patient had no night sweats and no evening rise of temperature.
On VIDEOLARYNGOSCOPY lesion on posterior commissure was seen
Patient was advised for CECT scan of Neck. On Scan diffuse asymmetrical irregular mucosal thickening and enhancement of vocal cords and aryepiglottic folds (more on the right side) suggesting of inflammatory granulomatous process (possibility of Laryngeal tuberculosis)
After Preanaestheticcheck up, patient was planned for Microlaryngeal Excision Biopsy. Biopsy of the lesion was sent for HPE. Report stated granulomatous lesion confirming tubercular pathology
Patient had history of pulmonary TB 10 years back for which he didn’t take proper treatment. Hence patient was advised for Chest X Ray – PA View which showed white opacity of right lung (lung destruction post tuberculosis) (FIGURE 4). Patient gave history that his right lung collapse occurred 20 years back after he was diagnosed with pulmonary TB. There was compensatory hypertrophy of the left lung and patient was alive on one lung since then
Hence we are reporting a case of secondary laryngeal tuberculosis in an already diagnosed case of post tubercular lung destruction.
Laryngeal tuberculosis (LTB) is the most common granulomatous lesion of the larynx, typically secondary to pulmonary TB, though primary laryngeal involvement is rare (<1% of extrapulmonary TB).[4,5] It usually affects adults aged 40–60, with a recent shift toward older males; immunocompromised individuals, including those with HIV or on steroids, are at higher risk . Hoarseness is the most reported symptom (80–100%), often accompanied by odynophagia, dysphagia, cough, and throat pain; fever and weight loss are less frequent, especially in primary LTB.[5] Endoscopically, lesions range from ulcerative and granulomatous to polypoid, often mimicking carcinoma. ).[4] Spread is usually via direct extension from pulmonary sites, though hematogenous and lymphatic paths can occur.[5] Histologically, LTB mirrors pulmonary TB, with acid-fast bacilli within granulomas, often within macrophages.[6]
In the present case, the patient had a history of pulmonary TB many years ago. The reemergence of the disease in form of a laryngeal mass brings out an important question on its resurfacing after a long latency.
One likely explanation is that it persisted in bronchial secretions and upon reactivation it infected the larynx during the immunosuppression.
Another important aspect in this case is development of Unilateral Tuberculous Lung Destruction (UTLD) which results from body’s immune response aiming at containing the infection. The main response is the host’s cell mediated response, when TB bacilli enter lungs they are engulfed by alveolar macrophages. The infected macrophages then present antigens to CD4+ T-helper (Th1) cells, which then release interferon-gamma (IFN-γ)—a key cytokine that activates macrophages to enhance their killing capacity. Once activated, macrophages aggregate around the infected site, and with the help of other immune cells, form granulomas or tubercles, which aim to wall off the infection and prevent its spread.[7]
However, in individuals with risk factors(like malnutrition, immunosuppression, chronic diseases)the macrophage activation is insufficient or delayed, and bacilli continues to multiply to which the host immune system compensates with an exaggerated delayed-type hypersensitivity (DTH) response, dominated by excessive T-cell mediated inflammation. This leads to caseous necrosis, cavitary formation in lung tissue. The prolonged inflammatory state leads to the release of, fibrogenic cytokines (like TGF-β), and enzymes like Matrix metalloproteinases (MMP) resulting in extensive fibrosis, parenchymal damage, and resulting in lung destruction which causes substantial loss of lung function.[8]
Laryngeal tuberculosis (LTB) is the most common granulomatous lesion of the larynx, typically secondary to pulmonary TB, though primary laryngeal involvement is rare (<1% of extrapulmonary TB).[6,7] It usually affects adults aged 40–60, with a recent shift toward older males; immunocompromised individuals, including those with HIV or on steroids, are at higher risk . Hoarseness is the most reported symptom (80–100%), often accompanied by odynophagia, dysphagia, cough, and throat pain; fever and weight loss are less frequent, especially in primary LTB.[7] Endoscopically, lesions range from ulcerative and granulomatous to polypoid, often mimicking carcinoma. ).[6] Spread is usually via direct extension from pulmonary sites, though hematogenous and lymphatic paths can occur.[7] Histologically, LTB mirrors pulmonary TB, with acid-fast bacilli within granulomas, often within macrophages.[8]
Several studies have highlighted that unilateral pulmonary TB is often associated with specific forms such as tubercular pleuritis, post-primary cavitary TB, or endobronchial TB, which may result in lobar collapse, obstructive hyperinflation, or fibrosis confined to one side.[9] Radiographically, unilateral TB can mimic malignancy or fungal infections, making radiologic differentiation crucial. CT imaging is particularly beneficial in identifying features such as cavitation, centrilobular nodules, and tree-in-bud patterns, which are more suggestive of TB.[10]
In our case, this destructive process progressed to the point where the entire right lung was non-functional. Certain factors likely contributed to unilateral lung involvement, like the anatomical factors: the right main bronchus is anatomically wider, shorter, and more vertically oriented than the left, facilitating easier entry of bacilli into the right lung. The lymphatic drainage of right lung also varies from that of left lung causing delay in clearance of infection and leading to prolonged inflammatory exposure. Variations in blood supply and other host specific factors including pre-existing structural lung weakness or uneven immune response, may further predispose one lung over the other.[11]
Another important clinical aspect to this case is confusion between laryngeal TB and laryngeal carcinoma. Both can present with similar symptoms like persistent hoarseness, dysphonia, odynophagia, cough, and in severe cases, airway obstruction. Laryngoscopic findings may not distinguish between the two which leads to misdiagnosis or delay in treatment. [12]
Diagnosis can only be confirmed with biopsy where in case of TB on Histopathological examination, granuloma with casseous necrosis is found and in case of cancer atypical malignant epithelial cells are found. Therefore, in TB-endemic regions or in patients with a prior history of TB, laryngeal TB should always be considered as a differential diagnosis. [13]
The coexistence of laryngeal TB and UTLD in a previously treated TB patient is extremely rare. This case highlights the importance of timely diagnosis, prompt treatment to prevent such complications, and public health awareness, ensuring TB control measures are being taken and there is adherence to treatment protocols.
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