Case Letters
Tuberculosis of palate Sir, A 13‑year‑ old girl presented to our Outpatient Department with a chief complaint of a painful ulcer on her palate for the last one‑and‑a‑half years, which had gradually increased to the present size. She had taken antibiotics from multiple local practitioners, but there had been no response. She did not have any systemic complaints, for example, cough fever or weight loss and had no history of any allergy. On examination, the ulcer was present in the midline of the hard palate, extending posteriorly to the soft palate [Figure 1a]. The ulcer was approximately 12 × 10 mm in size, with an erythematous surface. On examination of the neck region, no localized lesion was found and no lymph nodes were palpable. On further evaluation, she gave history of eating fish one‑and‑a‑half years back with a fish thorn prick on the palate. Following the prick, the ulcer had appeared on the palate that gradually increased in size over time. On presentation, she weighed 20 kg, blood pressure (BP) was 110/70, pulse rate (PR) 76/minute, respiratory rate RR 16/minute, and her routine blood investigation revealed a hemoglobin (Hb) of 9.8, total leukocyte count (TLC) of 9400, differential leukocyte count (DLC) of 66,29,4,1, platelet count of 3.31, and erythrocyte sedimentation rate (ESR) of 37 mm/first hour. The human immunodeficiency virus (HIV), hepatitis C virus (HCV), and hepatitis B surface antigen (HbsAg) were negative. She was a native of Bihar and presently residing in Punjab. Her father was an industrial worker, and her family resided in an overcrowded area of a low socioeconomic status neighborhood. Her chest x‑ray was done, which was normal, without any evidence of active lesions [Figure 2]. Her Mantoux test was 30 × 30 mm after 48 hours. On assuming a positive Mantoux, and a low socioeconomic status, residing in an overcrowded area, long history, and no response to antibiotics, a pathology of tuberculosis was suspected, and a biopsy of the ulcer was done. The biopsy revealed granulomatous inflammation with necrosis, consistent with a tuberculosis palate [Figure 3]. She was treated under Revised National Tuberculosis Control Program (RNTCP) category I regimen (thrice a week), with product code 13 + 14 containing Isoniazide 225 mg, Rifampicin 225 mg, pyrazinamide 750 mg, and Ethambutol 600 mg, for the first two months (intensive phase), followed
188
a
b
Figure 1: (a) Showing ulcer in the palate (b) Post-treatment photograph of the patient showing improvement
Figure 2: Chest x-ray PA view
a
b
c
d
Figure 3: Photomicrograph showing granulomatous inflammation with necrosis
Lung India • Vol 32 • Issue 2 • Mar - Apr 2015
Case Letters
by Isoniazide 225 mg, Rifampicin 225 mg for four months (continuation phase), and a dramatic response was observed within 20 – 25 days. Now she is well and the ulcer completely healed [Figure 1b]. In this case, the history of a fish‑thorn prick appears important, as this could have breached the mucosal surface of the palate, and given a chance to the Mycobacterium tuberculosis to cause the disease, and prompted us to report the case. Tuberculosis of the oral cavity may be either primary or secondary. The prevalence of the oral manifestation in pulmonary TB ranges from 0.8 – 3.5%.[1] The most common site of oral TB is the tongue. Other sites are the soft palate, hard palate, lip, cheek, tonsils, gingiva, floor of the mouth, uvula, and oral mucosa. [2] Oral TB is common in the 20 – 40 year age group.[3] In secondary tuberculosis, the bacilli may reach the oral mucosa either by the hematogenous route or by the lymphatic route. The pathogenesis of primary oral TB may be due to a direct gain of the bacilli into the oral mucosa through a break or loss of a natural barrier resulting from trauma, inflammatory condition, leukoplakia, tooth extraction, or poor oral hygiene.[4] The importance of an intact oral mucosal epithelium in resisting oral infection is shown by the observation of Abbott et al., who were able to isolate the tubercle bacilli from the mouth washings of 44.9% of the patients with active pulmonary lesions.[5] Other local predisposing factors are dental cysts, periapical granuloma, dental abscess, periodontitis, and jaw fractures.[1,4] The systemic factors that may favor the oral infection in TB are lowered host resistance[6] and increased virulence of the organisms.[1,4] Various factors that protect the oral cavity from tubercular invasion are the protective effect of saliva, presence of saprophytes, resistance of the striated muscles to bacterial invasion, and thickness of the protective epithelial covering. [2] Oral TB commonly presents as a non‑healing, [4] ulcerative lesion of the mucosa. The lesion may be preceded by an opalescent vesicle or nodule, which may break down as a result of caseation necrosis to form an ulcer.[1] The typical tuberculous ulcer is indurated, irregular, having an undermined margin, and a yellowish granular necrotic base.[1,4] Sometimes a tiny, single or multiple nodules are seen surrounding the ulcer. These are called ‘sentinel tubercles’.[1] Oral TB may also present as nodules, fissures, plaques, vesicles, tuberculomas, and granulomas.[4] The palatal lesions of TB may be seen as granulomas, ulcerations or perforations, [4] and are usually more common on the hard palate than on the soft palate.[1,3] According to Barauh et al., the secondary palatal TB may present as either lupus verrucosus (hypertrophic lesions) or lupus necrogenica (ulcerative lesions). [7] These lesions are usually seen in patients with strong immune responses and are considered to be due to hypersensitivity to acid fast bacilli (AFB), which further cause tissue destruction. [7] Even when evaluating a
chronic painful ulcer in the oral cavity, a clinician should consider both infectious processes such as syphilis and deep fungal disease, and non‑infectious processes such as chronic traumatic ulcer and squamous cell carcinoma. Other causes of palatal ulcer include leprosy, leishmaniasis, Wegener’s granulomatosis, sarcoidosis, major aphthous ulcer, ulcers in HIV patients, mucoepidermoid carcinoma, necrotizing sialometaplasia, drug abuse (cocaine), and midline lethal granuloma.[8] Mucoepidermoid carcinoma should be considered as a major differential diagnosis of a palatal ulcer among pediatric patients. The diagnosis may be difficult to establish because presentations of various conditions are similar and nonspecific.[7]A definitive diagnosis can be made by identifying or isolating the tubercle bacilli from the tissue obtained during biopsy or surgery.[7] Cultures of involved tissues are more often positive than are smears.[7] Many other methods are also available like polymerase chain reaction (PCR), Deoxyribonucleic acid (DNA) probes, and high performance liquid chromatography (HPLC). However, these are mainly used for species identification and to detect resistance to anti‑tubercular drugs. Their role is also limited by their cost, lack of availability, and lack of sensitivity.[7] Palatal TB patients should receive anti‑tubercular treatment promptly because oral lesions may prove to be a potential infectious hazard to the health personnel. Primary palatal tuberculosis is relatively rare, and may present as a chronic nonhealing ulcer or nodules, fissures, plaques, vesicles, and granulomas. When investigating such lesions with a nonhealing tendency, tuberculosis should be considered in the differential diagnosis.
Sanjay Solanki, Udham Chand Gadre, Manisha Solanki1, Rupinderjit Kaur2 Department of Pulmonary Medicine, Employees’ State Insurance Corporation Model Hospital, 1Department of Oral and Maxillofacial Surgery, Christian Dental College, 2Department of Health and Family Welfare, Employees’ State Insurance Dispensary, Ludhiana, Punjab, India E‑mail: [email protected]
REFERENCES 1. 2. 3. 4. 5.
Ebenezer J, Samuel R, Mathew GC, Koshy S, Chacko RK, Jesudason MV. Primary oral tuberculosis: Report of two cases.Indian J Dent Res2006;17:41‑4. Dixit R, Sharma S, Nuwal P. Tuberculosis of oral cavity.Indian J Tuberc2008;55:51‑3. Suhail Z, Khambaty Y, Ashrafi SK, Musani A. An unusual site of presentation of tuberculosis: Tuberculosis hard palate.Pak J Surg 2010;26:180‑1. Zaki SA, Bhongade S, Vartak SS. Perforation of the hard palate due to tuberculosis. Dent Res J (Isfahan) 2012;9:804‑6. Abbott JN, Briney AT, Denaro SA. Recovery of tubercle bacilli from mouth washings of tuberculous dental patients.J Am Dent
Lung India • Vol 32 • Issue 2 • Mar - Apr 2015 189
Case Letters
6. 7. 8.
Assoc1955;50:49‑52. Nunn P, Mungai M, Nyamwaya J, Gicheha C, Brindle RJ, Dunn DT, et al. The effect of human immunodeficiency virus type‑1 on the infectiousness of tuberculosis. Tuber Lung Dis1994;75:25‑32. Baruah B, Goyal A, Shunyu NB, Lynrah ZA, Raphael V. Tuberculosis of nose and palate with vanishing uvula. Indian J Med Microbiol2011;29:63‑5. Wood NK, Goaz PW. Solitary oral ulcers and fissures. In: Wood NK, Goaz PW, editors. Differential Diagnosis of Oral and Maxillofacial Lesions. 5th ed. USA: Mosby Publishers; 1997. p. 162‑81.
Access this article online Quick Response Code:
Website: www.lungindia.com DOI: 10.4103/0970-2113.152656
Advanced large cell lung tumor with neuroendocrine differentiation in an HIV positive patient Sir, Human immunodeficiency virus (HIV) infection is well known to be associated with several cancers and respiratory complications. Lung cancer is one of the most common cancers in HIV‑infected individuals. We report the case of a HIV‑positive smoker male who was admitted with fever, cough and right‑sided pleuritic chest pain. Imaging studies revealed the presence of right‑sided pleural effusion with multiple pleural based nodules and right lower lobe mass. Histopathologic examination of the tissue showed large cell lung tumor with neuroendocrine differentiation (LCNEC). LCNEC is an extremely rare lung cancer with this being the only case reported in an HIV‑positive patient. A 49‑year‑old HIV‑positive male smoker on antiretroviral therapy (tenofovir, emtricitabine and efavirenz) with good medication compliance presented with cough and progressively worsening right‑sided pleuritic chest pain for 2 weeks. He also stated having loss of appetite and 23 kg weight loss over the last 2 months. He denied having any hemoptysis, abdominal or neurologic symptoms at presentation. There was no history of preexisting lung disease, diabetes, illicit drug abuse or lung infections. Fifteen days ago his CD4 cell count was 750/µl with an undetectable viral load. Clinical examination showed stable vitals. Chest examination revealed decreased breath sounds on the right with decreased tactile vocal fremitus over the right middle and lower lung fields. Cardiovascular, abdominal, neurologic and skin examination failed to show any abnormality. Initial laboratory tests including complete blood counts and serum chemistries were within normal limits. Chest radiograph revealed a right‑sided effusion without any mediastinal shift. Chest computed tomography (CT) scan confirmed the presence of a large 190
right‑sided pleural effusion with multiple pleural based soft tissue densities and a right lower lobe mass [Figure 1]. Thoracocentesis showed an exudative hemorrhagic fluid with no malignant cells on cytologic examination. The patient underwent video‑assisted thoracoscopic examination (VATS) with biopsy of the pleural‑based soft tissue mass. Histopathologic examination of the tissue showed large cells with organoid growth pattern, high mitotic index and areas of necrosis [Figure 2]. The neuroendocrine phenotype was confirmed by the presence of positive staining for synaptophysin and chromogranin A. Due to pleural involvement, the patient was diagnosed with a stage IV large cell lung cancer with neuroendocrine differentiation. The patient agreed for a trial of chemotherapy with carboplatin and etoposide. Initial work‑up for metastatic spread of the disease failed to show any extra‑thoracic involvement. Over the course of next 9 months, the patient’s condition worsened with metastatic involvement of the liver and brain, ultimately leading to his death. Lung cancer, the leading cause of cancer‑related deaths in the general population is the third most common malignancy in HIV‑infected individuals, preceded only by Kaposi’s sarcoma and non‑Hodgkin’s lymphoma.[1‑3] The most common histologic variants of non‑small cell
Figure 1: CT chest showing right-sided effusion with pleural-based soft tissue (white arrow) density and a right lower lobe mass (red arrow) Lung India • Vol 32 • Issue 2 • Mar - Apr 2015
Attentions for Authors: If you wish to have the images printing in color, you needs to pay Rs. 4000/- (Rs. Four Thousand only). Otherwise those will be printed in black and white.
Copyright of Lung India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Tuberculosis of palate Sir, A 13‑year‑ old girl presented to our Outpatient Department with a chief complaint of a painful ulcer on her palate for the last one‑and‑a‑half years, which had gradually increased to the present size. She had taken antibiotics from multiple local practitioners, but there had been no response. She did not have any systemic complaints, for example, cough fever or weight loss and had no history of any allergy. On examination, the ulcer was present in the midline of the hard palate, extending posteriorly to the soft palate [Figure 1a]. The ulcer was approximately 12 × 10 mm in size, with an erythematous surface. On examination of the neck region, no localized lesion was found and no lymph nodes were palpable. On further evaluation, she gave history of eating fish one‑and‑a‑half years back with a fish thorn prick on the palate. Following the prick, the ulcer had appeared on the palate that gradually increased in size over time. On presentation, she weighed 20 kg, blood pressure (BP) was 110/70, pulse rate (PR) 76/minute, respiratory rate RR 16/minute, and her routine blood investigation revealed a hemoglobin (Hb) of 9.8, total leukocyte count (TLC) of 9400, differential leukocyte count (DLC) of 66,29,4,1, platelet count of 3.31, and erythrocyte sedimentation rate (ESR) of 37 mm/first hour. The human immunodeficiency virus (HIV), hepatitis C virus (HCV), and hepatitis B surface antigen (HbsAg) were negative. She was a native of Bihar and presently residing in Punjab. Her father was an industrial worker, and her family resided in an overcrowded area of a low socioeconomic status neighborhood. Her chest x‑ray was done, which was normal, without any evidence of active lesions [Figure 2]. Her Mantoux test was 30 × 30 mm after 48 hours. On assuming a positive Mantoux, and a low socioeconomic status, residing in an overcrowded area, long history, and no response to antibiotics, a pathology of tuberculosis was suspected, and a biopsy of the ulcer was done. The biopsy revealed granulomatous inflammation with necrosis, consistent with a tuberculosis palate [Figure 3]. She was treated under Revised National Tuberculosis Control Program (RNTCP) category I regimen (thrice a week), with product code 13 + 14 containing Isoniazide 225 mg, Rifampicin 225 mg, pyrazinamide 750 mg, and Ethambutol 600 mg, for the first two months (intensive phase), followed
188
a
b
Figure 1: (a) Showing ulcer in the palate (b) Post-treatment photograph of the patient showing improvement
Figure 2: Chest x-ray PA view
a
b
c
d
Figure 3: Photomicrograph showing granulomatous inflammation with necrosis
Lung India • Vol 32 • Issue 2 • Mar - Apr 2015
Case Letters
by Isoniazide 225 mg, Rifampicin 225 mg for four months (continuation phase), and a dramatic response was observed within 20 – 25 days. Now she is well and the ulcer completely healed [Figure 1b]. In this case, the history of a fish‑thorn prick appears important, as this could have breached the mucosal surface of the palate, and given a chance to the Mycobacterium tuberculosis to cause the disease, and prompted us to report the case. Tuberculosis of the oral cavity may be either primary or secondary. The prevalence of the oral manifestation in pulmonary TB ranges from 0.8 – 3.5%.[1] The most common site of oral TB is the tongue. Other sites are the soft palate, hard palate, lip, cheek, tonsils, gingiva, floor of the mouth, uvula, and oral mucosa. [2] Oral TB is common in the 20 – 40 year age group.[3] In secondary tuberculosis, the bacilli may reach the oral mucosa either by the hematogenous route or by the lymphatic route. The pathogenesis of primary oral TB may be due to a direct gain of the bacilli into the oral mucosa through a break or loss of a natural barrier resulting from trauma, inflammatory condition, leukoplakia, tooth extraction, or poor oral hygiene.[4] The importance of an intact oral mucosal epithelium in resisting oral infection is shown by the observation of Abbott et al., who were able to isolate the tubercle bacilli from the mouth washings of 44.9% of the patients with active pulmonary lesions.[5] Other local predisposing factors are dental cysts, periapical granuloma, dental abscess, periodontitis, and jaw fractures.[1,4] The systemic factors that may favor the oral infection in TB are lowered host resistance[6] and increased virulence of the organisms.[1,4] Various factors that protect the oral cavity from tubercular invasion are the protective effect of saliva, presence of saprophytes, resistance of the striated muscles to bacterial invasion, and thickness of the protective epithelial covering. [2] Oral TB commonly presents as a non‑healing, [4] ulcerative lesion of the mucosa. The lesion may be preceded by an opalescent vesicle or nodule, which may break down as a result of caseation necrosis to form an ulcer.[1] The typical tuberculous ulcer is indurated, irregular, having an undermined margin, and a yellowish granular necrotic base.[1,4] Sometimes a tiny, single or multiple nodules are seen surrounding the ulcer. These are called ‘sentinel tubercles’.[1] Oral TB may also present as nodules, fissures, plaques, vesicles, tuberculomas, and granulomas.[4] The palatal lesions of TB may be seen as granulomas, ulcerations or perforations, [4] and are usually more common on the hard palate than on the soft palate.[1,3] According to Barauh et al., the secondary palatal TB may present as either lupus verrucosus (hypertrophic lesions) or lupus necrogenica (ulcerative lesions). [7] These lesions are usually seen in patients with strong immune responses and are considered to be due to hypersensitivity to acid fast bacilli (AFB), which further cause tissue destruction. [7] Even when evaluating a
chronic painful ulcer in the oral cavity, a clinician should consider both infectious processes such as syphilis and deep fungal disease, and non‑infectious processes such as chronic traumatic ulcer and squamous cell carcinoma. Other causes of palatal ulcer include leprosy, leishmaniasis, Wegener’s granulomatosis, sarcoidosis, major aphthous ulcer, ulcers in HIV patients, mucoepidermoid carcinoma, necrotizing sialometaplasia, drug abuse (cocaine), and midline lethal granuloma.[8] Mucoepidermoid carcinoma should be considered as a major differential diagnosis of a palatal ulcer among pediatric patients. The diagnosis may be difficult to establish because presentations of various conditions are similar and nonspecific.[7]A definitive diagnosis can be made by identifying or isolating the tubercle bacilli from the tissue obtained during biopsy or surgery.[7] Cultures of involved tissues are more often positive than are smears.[7] Many other methods are also available like polymerase chain reaction (PCR), Deoxyribonucleic acid (DNA) probes, and high performance liquid chromatography (HPLC). However, these are mainly used for species identification and to detect resistance to anti‑tubercular drugs. Their role is also limited by their cost, lack of availability, and lack of sensitivity.[7] Palatal TB patients should receive anti‑tubercular treatment promptly because oral lesions may prove to be a potential infectious hazard to the health personnel. Primary palatal tuberculosis is relatively rare, and may present as a chronic nonhealing ulcer or nodules, fissures, plaques, vesicles, and granulomas. When investigating such lesions with a nonhealing tendency, tuberculosis should be considered in the differential diagnosis.
Sanjay Solanki, Udham Chand Gadre, Manisha Solanki1, Rupinderjit Kaur2 Department of Pulmonary Medicine, Employees’ State Insurance Corporation Model Hospital, 1Department of Oral and Maxillofacial Surgery, Christian Dental College, 2Department of Health and Family Welfare, Employees’ State Insurance Dispensary, Ludhiana, Punjab, India E‑mail: [email protected]
REFERENCES 1. 2. 3. 4. 5.
Ebenezer J, Samuel R, Mathew GC, Koshy S, Chacko RK, Jesudason MV. Primary oral tuberculosis: Report of two cases.Indian J Dent Res2006;17:41‑4. Dixit R, Sharma S, Nuwal P. Tuberculosis of oral cavity.Indian J Tuberc2008;55:51‑3. Suhail Z, Khambaty Y, Ashrafi SK, Musani A. An unusual site of presentation of tuberculosis: Tuberculosis hard palate.Pak J Surg 2010;26:180‑1. Zaki SA, Bhongade S, Vartak SS. Perforation of the hard palate due to tuberculosis. Dent Res J (Isfahan) 2012;9:804‑6. Abbott JN, Briney AT, Denaro SA. Recovery of tubercle bacilli from mouth washings of tuberculous dental patients.J Am Dent
Lung India • Vol 32 • Issue 2 • Mar - Apr 2015 189
Case Letters
6. 7. 8.
Assoc1955;50:49‑52. Nunn P, Mungai M, Nyamwaya J, Gicheha C, Brindle RJ, Dunn DT, et al. The effect of human immunodeficiency virus type‑1 on the infectiousness of tuberculosis. Tuber Lung Dis1994;75:25‑32. Baruah B, Goyal A, Shunyu NB, Lynrah ZA, Raphael V. Tuberculosis of nose and palate with vanishing uvula. Indian J Med Microbiol2011;29:63‑5. Wood NK, Goaz PW. Solitary oral ulcers and fissures. In: Wood NK, Goaz PW, editors. Differential Diagnosis of Oral and Maxillofacial Lesions. 5th ed. USA: Mosby Publishers; 1997. p. 162‑81.
Access this article online Quick Response Code:
Website: www.lungindia.com DOI: 10.4103/0970-2113.152656
Advanced large cell lung tumor with neuroendocrine differentiation in an HIV positive patient Sir, Human immunodeficiency virus (HIV) infection is well known to be associated with several cancers and respiratory complications. Lung cancer is one of the most common cancers in HIV‑infected individuals. We report the case of a HIV‑positive smoker male who was admitted with fever, cough and right‑sided pleuritic chest pain. Imaging studies revealed the presence of right‑sided pleural effusion with multiple pleural based nodules and right lower lobe mass. Histopathologic examination of the tissue showed large cell lung tumor with neuroendocrine differentiation (LCNEC). LCNEC is an extremely rare lung cancer with this being the only case reported in an HIV‑positive patient. A 49‑year‑old HIV‑positive male smoker on antiretroviral therapy (tenofovir, emtricitabine and efavirenz) with good medication compliance presented with cough and progressively worsening right‑sided pleuritic chest pain for 2 weeks. He also stated having loss of appetite and 23 kg weight loss over the last 2 months. He denied having any hemoptysis, abdominal or neurologic symptoms at presentation. There was no history of preexisting lung disease, diabetes, illicit drug abuse or lung infections. Fifteen days ago his CD4 cell count was 750/µl with an undetectable viral load. Clinical examination showed stable vitals. Chest examination revealed decreased breath sounds on the right with decreased tactile vocal fremitus over the right middle and lower lung fields. Cardiovascular, abdominal, neurologic and skin examination failed to show any abnormality. Initial laboratory tests including complete blood counts and serum chemistries were within normal limits. Chest radiograph revealed a right‑sided effusion without any mediastinal shift. Chest computed tomography (CT) scan confirmed the presence of a large 190
right‑sided pleural effusion with multiple pleural based soft tissue densities and a right lower lobe mass [Figure 1]. Thoracocentesis showed an exudative hemorrhagic fluid with no malignant cells on cytologic examination. The patient underwent video‑assisted thoracoscopic examination (VATS) with biopsy of the pleural‑based soft tissue mass. Histopathologic examination of the tissue showed large cells with organoid growth pattern, high mitotic index and areas of necrosis [Figure 2]. The neuroendocrine phenotype was confirmed by the presence of positive staining for synaptophysin and chromogranin A. Due to pleural involvement, the patient was diagnosed with a stage IV large cell lung cancer with neuroendocrine differentiation. The patient agreed for a trial of chemotherapy with carboplatin and etoposide. Initial work‑up for metastatic spread of the disease failed to show any extra‑thoracic involvement. Over the course of next 9 months, the patient’s condition worsened with metastatic involvement of the liver and brain, ultimately leading to his death. Lung cancer, the leading cause of cancer‑related deaths in the general population is the third most common malignancy in HIV‑infected individuals, preceded only by Kaposi’s sarcoma and non‑Hodgkin’s lymphoma.[1‑3] The most common histologic variants of non‑small cell
Figure 1: CT chest showing right-sided effusion with pleural-based soft tissue (white arrow) density and a right lower lobe mass (red arrow) Lung India • Vol 32 • Issue 2 • Mar - Apr 2015
Attentions for Authors: If you wish to have the images printing in color, you needs to pay Rs. 4000/- (Rs. Four Thousand only). Otherwise those will be printed in black and white.
Copyright of Lung India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
