Journal of Dr. NTR University of Health Sciences

: 2018  |  Volume : 7  |  Issue : 3  |  Page : 196--199

Tuberculosis: Cause or association in a young female with Takayasu arteritis with dilated cardiomyopathy

Kekathi Vidyasagar, Boya Chinna Maddiletigari Pullaiah, Penumadu Sudhakar, Sravan Kumar Korrapati 
 Department of General Medicine, Kurnool Medical College, Kurnool, Andhra Pradesh, India

Correspondence Address:
Dr. Kekathi Vidyasagar
Associate Professor of Medicine, Department of General Medicine, Kurnool Medical College, Kurnool, Andhra Pradesh


Takayasu arteritis (TA) is a rare, systemic, and inflammatory large-vessel vasculitis of unknown etiology. A possible relationship between TA and tuberculosis (TB) has been suggested. Both diseases have similar chronic inflammatory lesions and occasionally granulomas on the arterial walls. Although TA may present in many ways, its presentation as dilated cardiomyopathy (DCM) is rare. We hereby report a case of TA with DCM, associated with TB.

How to cite this article:
Vidyasagar K, Pullaiah BC, Sudhakar P, Korrapati SK. Tuberculosis: Cause or association in a young female with Takayasu arteritis with dilated cardiomyopathy.J NTR Univ Health Sci 2018;7:196-199

How to cite this URL:
Vidyasagar K, Pullaiah BC, Sudhakar P, Korrapati SK. Tuberculosis: Cause or association in a young female with Takayasu arteritis with dilated cardiomyopathy. J NTR Univ Health Sci [serial online] 2018 [cited 2023 Feb 8 ];7:196-199
Available from:

Full Text


Takayasu arteritis (TA) is a disease of unknown etiology that affects especially the aorta and its major branches. Its incidence varies between 1.2 and 2.3 cases per million per year, and it is more common in Asians than in other racial groups.[1] The etiology of TA is not clear. A number of features suggest an autoimmune base while others raise the question that the aortitis may be an expression of tuberculin sensitization.[2],[3],[4] TA being the commonest cause of renovascular hypertension in India,[5] also causes dilated cardiomyopathy (DCM) in 5% of affected patients.[6]

 Case Report

A 19-year-old female presented with history of low-grade fever for 3 months, headache for 2 months, breathlessness for 1 month, pedal edema for 1 week, with history of loss of weight and appetite. There was no past history of similar complaints and no history of similar complaints in the family. The patient appeared ill and underweight (body weight was 42 kg, height 162 cm, and BMI = 16). Pulse examination revealed feeble right lower limb femoral pulse while other pulses were felt normally in all other limbs. Carotid pulsations were felt equally on both sides. Blood pressure (BP) measurement was taken in the limbs and was recorded as the following: 200/150 mmHg in the right upper limb and 160/100 mmHg in the left upper limb. BP in right lower limb could not be ascertained properly. Cardiac examination showed normal heart sounds and a systolic bruit was heard at the left supraclavicular fossa. Respiratory examination revealed fine crepitations in both lung fields. Other system examinations were within normal limits. Fundus revealed arteriovenous crossing changes.

Hemoglobin level was 8.9 gm/dL, white blood cell (WBC) count 7,200/mm 3, platelet count 2.7 lakhs, erythrocyte sedimentation rate (ESR) = 20 mm in the first hour, C-reactive protein level was 20 mg/dL. The serological study for anti nuclear antibody (ANA), cytoplasmic anti-neutrophil cytoplasmic antibodies (c-ANCA), and perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA) were all negative; The patient's liver function test, renal function test, and thyroid function test were all within normal limits. Urine analysis showed albumin:2 plus and sugar: nil [Figure 1]. The Mantoux test was performed and it was strongly positive (28 mm), and tuberculosis was confirmed by Quantiferon-TB gold test, which was positive (7.23 IU/mL) [Figure 2].{Figure 1}{Figure 2}

Electrocardiogram (ECG) showed sinus tachycardia with left axis deviation and signs of left ventricle enlargement.

The chest x-ray showed cardiomegaly and abdominal ultrasound showed decreased size of right kidney with rest being normal. Echocardiography showed left atrium and left ventricular dilatation and ejection fraction was 20% with global hypokinesia and severe LV dysfunction with mild mitral and tricuspid regurgitation, suggestive of Dilated cardiomyopathy. Duplex vascular ultrasound of abdomen revealed decreased flow to right kidney with parvus tardus waveforms present. Left kidney normal size but irregular flow was noted suggestive of vasculitis. Carotid Doppler showed no abnormalities.

An aortogram revealed normal aortic arch, right subclavian artery, and left subclavian artery [Figure 3]. Abdominal aorta angiography showed long segment circumferential intimal thickening of the abdominal aorta extending into the celiac, superior mesenteric artery, inferior mesenteric artery, as well as bilateral renal arteries as a result of vasculitis/TA [Figure 4] and [Figure 5]. Computed tomography (CT) of chest showed branching and confluent alveolar opacities with cavitation in left upper lobe suggestive of tuberculosis. We planned for conventional angiography, cardiac catheterization vessel biopsy and renal angioplasty, but the patient's attendants refused these invasive procedures when risks associated with severe LV dysfunction were explained.{Figure 3}{Figure 4}{Figure 5}

With the available investigations, a diagnosis of TA type IV with DCM and pulmonary tuberculosis (TB) was made.

The patient was started on an anti-tuberculous treatment according to her body weight along with anti-hypertensives, diuretics, and steroids. The patient's condition improved, and she was discharged and was on follow-up in the outpatient clinic.


Mikito Takayasu first described “Takayasu arteritis” or “pulseless disease,” in 1908. It is a chronic inflammatory disease mainly affecting aorta and its primary branches, leading to vessel stenosis, occlusion, or less frequently aneurysm formation. One century has passed since the first description of TA, but still we are not close to its etiology. Despite the association with TB and the similarity between granulomatous lesions in both diseases, the exact role of Mycobacterium tuberculosis in the pathogenesis of TA is still unknown.

Previous studies suggest that a crossreaction between Mycobacterium and human heat shock protein (HSP) might have a key role.[7],[8] This hypothesis is further supported by the increased expression of 65 KDa HSPs of the involved vessels as well as the activation of subpopulations of thymocytes (T) cells that may cross-react with the host HSP.[7],[8] It has also been speculated that M. tuberculosis can be the triggering factor, and through its production of super antigens, the suggested role of which is thought to be via the stimulation of auto-reactive T cells that induce vascular damage. The most accepted concept is that “pathogenesis of TA starts in genetically susceptible individual, with perhaps a specific humoral milieu, followed by exposure to a yet unidentified antigen, leading to immune response that targets the large vessels.”[9]

TA commonly affects the patients in their second and third decades of life. Females are affected more commonly than males, with a frequency varying in different geographical areas, in India the ratio being 2:1.[10] In India abdominal aorta is most commonly affected. The characteristic features of TA includes diminished or absent pulses (in 84-96% patients), vascular bruit (in 80-94% patients),[11] hypertension (in 33-83% patients),[11] generally due to renal artery stenosis, which is seen in 28-75% patients,[11] congestive heart failure (due to hypertension and DCM), and pulmonary artery involvement in 14-100% patients.

In active stage, TA is treated by steroids with a success rate of 20-100%, which has been reported in different studies. Cyclophosphamide and methotrexate are used as steroid sparing agents in resistant cases. Obstructive lesions need revascularization techniques such as angioplasty and surgery.

The present case had pyrexia of unknown origin, easy fatigability, and headache. These seem to reflect nonspecific and constitutional symptoms of TA. Hypertension in this case was due to renal artery stenosis. The cause of DCM here is difficult to define as both hypertension and TA could be responsible.

The purpose of reporting this case is to highlight the role of detailed physical examination including detailed vascular examination, aided by correct use of modern imaging to diagnose TA. Due to increased prevalence of the disease in Asian countries, tuberculosis can be considered as an etiological factor either triggering the autoimmune process or directly responsible for granulomatous lesions in TA. Further studies are required in ascertaining this hypothesis.

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.


We are grateful to the Department of Radiology, Department of Cardiology, Kurnool Medical College and Medall diagnostics, Government General Hospital, Kurnool.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Hall S, Buchbinder R. Takayasu's arteritis. Rheum Dis Clin North Am 1990;16:411-22.
2Kinare SG. Aortitis in early life in India and its association with tuberculosis. J Pathol 1970;100:69-76.
3Lupi-Herrera E, Sánchez-Torres G, Marcushamer J, Mispireta J, Horwitz S, Vela JE. Takayasu's arteritis: Clinical study of 107 cases. Am Heart J 1977;93:94-103.
4Schrire V, Asherson RA. Arteritis of the aorta and its major branches. Q J Med 1964;33:439-63.
5Arora P, Kher V, Singhal MK, Kumar P, Gulati S, Baijal SS, et al. Renal artery stenosis in nonspecific aortoarteritis: Spectrum of disease in children and adults. Kidney Blood Press Res 1997;20:285-9.
6Ghosh SK, Sinha DP, Ghosh S, Mitra D, Kar AK, Panja M. Dilated cardiomyopathy in non-specific aortoarteritis. Indian Heart J 1999;51:527-31.
7Aggarwal A, Chag M, Sinha N, Naik S. Takayasu's arteritis: Role of mycobacterium tuberculosis and its 65-kDA heat shock protein. Int J Cardiol 1996;55:49-55.
8Seko Y, Minota S, Kawasaki A, Shinkai Y, Maeda K, Yagita H, et al. Perforin-secreting killer cell infiltration and expression of a 65-kDa heat-shock protein in aortic tissue of patients with Takayasu's arteritis. J Clin Invest 1994;93:750-8.
9Bahl VK, Seth S. Takayasu's arteritis revisited. Indian Heart J 2002;54:147-51.
10Fraga A, Medina F. Takayasu arteritis. Curr Rheumatol Rep 2002;4:30-8.
11Kerr GS, Hallahan CW, Giordano J, Leavitt RY, Fauci AS, Rottem M, et al. Takayasu arteritis. Ann Inter Med 1994;120:919-29.