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Year : 2022  |  Volume : 10  |  Issue : 2  |  Page : 100-104

Reversible hypertension and infective arteritis

1 Department of Obstetrics and Gynecology, Institute of Medical Science, BHU, Varanasi, Uttar Pradesh, India
2 Department of General Medicine, Institute of Medical Science, BHU, Varanasi, Uttar Pradesh, India
3 Centre of Experimental Medicine and Surgery, Institute of Medical Sciences, BHU, Varanasi, Uttar Pradesh, India

Date of Submission31-Mar-2022
Date of Decision22-Apr-2022
Date of Acceptance26-Apr-2022
Date of Web Publication12-Aug-2022

Correspondence Address:
Dr. Dhiraj Kishore
Department of General Medicine, Institute of Medical Science, BHU, Varanasi, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/heartindia.heartindia_24_22

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Background: Idiopathic vasculitides or arteritis have very few or none treatment options. Identification of infective arteritis based on high clinical suspicion opens a window for treatment of such cases . Although these are occasional clinical scenario.
Aims and Objectives: To identify the treatable cause of arteritis and starting initial treatment based on clinical suspicion.
Material and Methods: Based on high clinical suspicion we aim to identify chronic infective cause of arteritis among patients of SS Hospital from 2019 to 2020 coming in EOPD.
Results and Discussion: Three cases of reversible hypertension from different clinical setup relating to a common infective etiology, i.e., tuberculosis identified during the said duration, all cases presented with constitutional symptoms for 2–6 months with headache, loss of appetite, fever, and malaise. The first case presented as acute abdomen in EOPD having mesenteric ischemia and hypertension. The second case presented in antenatal care OPD with hypertension which was nonrelated to pregnancy. The third case presented in medicine OPD as a case of young hypertensive without mood changes. Partial renal artery stenosis relating to infective arteritis was a common finding in all cases. All cases responded well with the firstline antitubercular medication and became normotensive (without medication) in the follow up.
Conclusion: The cause of renal artery stenosis appeared to be related to tubercular arteritis of vessel with either a past history of pulmonary TB or TB contact. Renovascular tubercular arteritis has been defined in only a few literatures and only handful of cases being reported making worth presentation.

Keywords: Arteritis, hypertension, tuberculosis

How to cite this article:
Diwaker A, Kishore D, Singh SK, Singh S. Reversible hypertension and infective arteritis. Heart India 2022;10:100-4

How to cite this URL:
Diwaker A, Kishore D, Singh SK, Singh S. Reversible hypertension and infective arteritis. Heart India [serial online] 2022 [cited 2022 Sep 27];10:100-4. Available from: https://www.heartindia.net/text.asp?2022/10/2/100/353735

  Introduction Top

Infective arteritis correlated with several microbial pathogens. Identification of infectious agents and idiopathic vasculitis has an open the door to treat many of previously diagnosed idiopathic vasculitides.[1] Although the role of infection and inflammation in the pathogenesis of atherosclerotic disease is controversial conundrum, clinical high index of suspicion is needed since the clinical features are very non-specific. Confirmatory diagnosis need positive culture and serological evidence but in many occasions delay in the diagnosis could lead to adverse outcome, hence on the clinical suspicion initial, aggressive treatment may result in positive outcome.

Material and Methods

Based on high clinical suspicion we aim to identify chronic infective cause of arteritis among patients of SS Hospital from 2019 to 2020 coming in EOPD. A total of 3 such case were identified.

Result and Cases.


A 24-year-old young female admitted to EOPD with a history of severe abdominal pain. Intensity of pain has increased for the past 2 days, with background history of moderate-grade fever for the past 15 days intermittent in nature. Fever was associated with intermittent abdominal pain of severe intensity, mainly present around umbilicus, charecter was squeezing type present for few minutes partially relieved on its own, reappear once again. This was associated with generalized weakness and easy fatigability, anorexia, and mild-grade fever, for the past 6 months associated with sharp chest pain mainly in the center sometimes radiating to the back responding partially to analgesics. The patient also had headache, dull aching in nature, present mainly in back of the head, without blurring or difficulty in vision and pain in the both lower limbs present for the past 3–4 months, crampy type, increases on walking and sometimes disabling her. There was no history of blood stained loose stools or discoloration of fingers or toes or hemoptysis. She had taken treatment for hypertension in the past. On examination, the patient was conscious and oriented. GCS was E4V5M6, pulse rate in right upper limb was 88/min regular rhythm and normal volume . In left upper limb pulse rate was 88/min and pulse volume was decreased in both brachial and radial arteries. In both lower limbs, pulse was felt and was equal. The left carotid pulses weekly palpable, blood pressure (BP)-right UL-210/120 mmHg, left UL-170/100 mmHg, lower limb 190/110 mmHg. General examination showed only moderate pallor, abdomen was scaphoid in shape, umbilicus central no scars or sinuses noticed, on palpation soft not distended non tender, no organomegaly or mass was palpable aortic pulses were felt on auscultation aortic bruit were heard over and above left to the umbilicus. On examination of chest normally moving with respiration, no palpable tenderness, breath sounds were normovesicular heard with b/l air entry equal, coarse crepitation were heard over left apical area. Central nervous system examination was normal. On investigations, her routine panel revealed anemia with hemoglobin being 8 g% and total leukocyte count was 3400/mm3, platelet count was 3.71 lac/mm3, erythrocyte sedimentation rate (ESR) was 48, bronchoalveolar lavage showed acid-fast bacilli (AFB), liver function tests showed raised enzymes, serum glutamic-oxaloacetic transaminase (SGOT)/serum glutamic pyruvic transaminase (SGPT)-141/109 IU, while kidney function test was normal, ultrasonography (USG) abdomen showed adrenal parenchymal disease, however, urine routine microscopy was normal, color Doppler of abdomen showed diffuse circumferential thickening of aortic wall with stenosis in distal half, changes in the waveforms noted in the b/l renal artery and superior mesenteric artery and celiac trunk (parvus-tardus pattern), echocardiography of heart showed only mild tricuspid regurgitation, contrast-enhanced computed tomography (CECT) [Figure 1] and angiography showed features of the left upper lobe collapse with traction bronchiectasis (post Koch's), with diffuse thickening involving left common carotid, subclavian, axillary artery, and mid abdominal aorta, superior mesenteric artery, and renal artery with significant subcentrimetric lymph node in the left apex of the lung, suggestive of tubercular aortoarteritis involving aorta and its branches. In hospital course, she was provisionally diagnosed with pulmonary tuberculosis, with aortoarteritis, with superior mesenteric artery ischemia [Figure 2]. Conservative management along with antitubercular therapy and amlodipine 10 mg was started, and regular monitoring of the patient was done. Patient's fever and abdominal pain improved becoming completely asymptomatic on day 16. The patient was discharged after 18 days along with antitubercular drugs. On follow-up, blood pressure was also under control with decreasing dose of antihypertensive medication.
Figure 1: (a) Consolidation of the left upper lobe of the lung abutting aorta causing aneurismal dilation and narrowing of descending aorta and stenosis of renal arteries. (b) Narrowed superior mesenteric artery with collaterals. (c) Bronchiectatic changes and consolidation of the left upper lobe abutting aorta with fusiform dilatation of ascending aorta. (d) Marked narrowing of descending aorta with lumen 9 mm

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Figure 2: Areas of caseous necrosis with epithelioid cell

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A 24-year-old female primigravida presented to ante natal checkup (ANC) clinic at 18th week of gestation with chief complaints of headache and generalized weakness for 2 weeks. Headache was insidious onset, gradually progressive, and global. Her weakness was generalized along with easy fatigability. These symptoms were not associated with vomiting, loss of consciousness, blurring of vision, fever, body swelling, and bleeding manifestations (perrectal or pervaginal). She had past history of antitubercular drug intake for pulmonary TB in 2010. On general examination, BP of 152 mmHg (systolic), and 106 mmHg (diastolic) were recorded. Although in previous antenatal records, she was normotensive. Thorough monitoring of BP was done after admission of patient, which showed elevated BP of >150/100 mmHg persistently. Routine workup showed hemoglobin ‒ 10.8 g/dl, TLC – 4506/mm3, platelets –1.8 lakh/mm3, SGOT/SGPT ‒ 56/40 IU, TP/Alb –6/3.2 mg/dl, creatinine ‒ 0.8, and urea ‒ 60 mg/dl. Routine urine microscopy examination did not show proteinuria or hematuria. Fundus examination showed normal arterial and venous ratio, no exudates observed and normal pulsations of vessels without macular edema noted. Lipid profile was within normal limits. On color Doppler USG of the abdomen showed increased peak systolic velocity in the right renal artery with increased turbulent flow in poststenotic area, suggestive of renal artery stenosis.

The patient was diagnosed to have hypertension (as per the ADA guidelines 2020) and management was started with tablet labetalol (100 mg bd). On follow-up, her BP was still in the range of 150/100 mmHg. Consequently, she was started with calcium-channel blocker nifedipine. Regular fetal monitoring was done. The patient delivered at full term through normal vaginal delivery. However, on three instances during term, her BP raised to 180/120 mmHg for which labetalol (i.v.) was given. Postdelivery, her BP was still raised on amlodipine 10 mg and telmisartan 80 mg daily. Computed tomography (CT) angiography of the renal vessels showed normal-sized kidneys with narrowing of the right renal artery measuring 5 mm in length and 2 mm in diameter. The poststenotic segment was 6 mm in diameter with 40% stenosis. Antinuclear antibodies were negative, and ESR was 78 mm/h in 1st h with a positive Mantoux test. On clinical suspicion, a trial of ATT was started. On 3-month follow-up, the patient's requirement decreased to single oral antihypertensive. Repeat color Doppler of the renal vessels showed poststenotic segment was 4 mm in diameter with 25% stenosis.

Case– 3

A 32-year-old male presented with headache for1 month which was generalized, mild, dull aching, and global not associated with vomiting, seizures, loss of consciousness, and fever. There was no family history of hypertension and diabetes mellitus but an antitubercular intake history was present in the family. On examination, he was found to have BP of 148/98 mmHg in the right arm sitting position, which was again recorded 152/100 mmHg after rest. BP in the left arm was 148/98 mmHg, and both lower limbs was150/100 mmHg. His pulse rate was 80/min with all peripheral pulses palpable. A lymph node was palpable in the left axilla of size approximately 1.3 cm × 3 cm, nontender, smooth, and mobile with no overlying skin changes. Cardiovascular examination showed normal s1, s2 with no signs of the left ventricular hypertrophy. In addition, other systemic examination was within normal limits. Routine laboratory reports revealed TLC ‒ 7040/mm3, hemoglobin ‒ 11 gm/dl, platelet count ‒ 1.76 lakh/mm3, hematocrit ‒ 33%, red blood cell count ‒ 5.2 million/mm3, SGOT/SGPT - 60/62 IU, total protein ‒ 7.2 g/dl, albumin ‒ 3.1 g/dl, creatinine ‒ 0.6 mg/dl, urea ‒ 40 mg/dl, sodium – 139 mmol/L, potassium – 3.5 mmol/L, and fasting plasma glucose – 102 mg/dl with a HbA1c ‒ 5.8%. Thyroid profile with a free T3 ‒ 5.02 pmol/L, free T4 ‒ 14.08 pmol/L, and TSH ‒ 4 microIU/ml. Abdominal USG depicted right adrenal mass along with the right renal artery stenosis seen on color Doppler of the renal vessels. Abdominal CT scan further revealed right adrenal mass which was homogenous 29 mm × 22 mm in size, and well encapsulated with no calcification; left adrenal gland showed no abnormal finding; right renal artery showed narrowing with 60% stenosis. Serum cholesterol ‒ 180 mg/dl, triglyceride ‒ 108 mg/dl, HDL ‒ 48 mg/dl, and LDL ‒ 140 mg/dl. Morning (8 a.m.) serum cortisol ‒ 10 μg/dl, ESR – 58 mm/h, and CRP- 0.2 mg/dl; ANA was negative. Mantoux test was positive. Chest X-ray showed bilateral hilar lymphadenopathy without calcifications. Treatment was started with telmisartan and amlodipine combination (as per the AHA guidelines). On 1-month follow-up, his BP was still in range of 150/100 mmHg. Chlorothiazide (diuretic) was added to his previous medication. Further, after 1 month, his BP was 148/96 mmHg. Then after, total right adrenalectomy was planned and performed through laparoscopy. The mass isolated was 32 mm × 14 mm × 24 mm in size. Histology showed areas of caseous necrosis with epithelioid cell [Figure 2] but AFB was negative. Postadrenalectomy patient still required three antihypertensive for BP control. On the basis of histopathology of the adrenal gland with raised ESR and history of tubercular contact, antitubercular therapy was started. On 4-month follow-up, after starting ATT, the patient required no antihypertensive medication. A repeat color Doppler of renal vessels depicted decreased peak systolic velocity in the right renal artery and stenosis of around 38% on CT angiography of the renal vessels. This patient which was diagnosed as a case of unilateral adrenal tuberculosis which showed improvement in narrowing of the right renal artery and need for antihypertensive after antitubercular therapy suspecting it to be renovascular arteritis of tubercular etiology. Already tubercular arteritis of the renal vessel being a rare presentation, finding of an adrenal tuberculosis with it makes it a further rare presentation of extrapulmonary TB.

  Discussion Top

Aortitis is described as inflammation of the aorta. The most common causes of aortitis are the large-vessel vasculitides giant cell arteritis and Takayasu arteritis, although it also is associated with several other rheumatologic diseases. Infectious aortitis is a rare but potentially life-threatening disorder. A number of organisms are known to infect the aorta include  Neisseria More Details (e.g., gonorrhea), tuberculosis, Rickettsia, spirochetes (syphilis), fungi (mucormycosis), and viruses (e.g., hepatitis B and C) these have been associated with infectious aortitis, most commonly the  Salmonella More Details and Staphylococcal species, along with Streptococcus pneumoniae. In most cases of bacterial aortitis, usually infecting area with preexisting pathology such as an atherosclerotic plaque or aneurysm sac are seeded by bacteria through the vasa vasorum.[2] Tuberculous aortitis, an uncommon problem in the developed world, but since tuberculosis is the most common infectious disease in India may occur as a result of direct spread of the thoracic aorta from infected tissues adjacent to these important structures such as infected lymph nodes or lung lesions or by miliary spread. Tuberculous aortitis is invariably indicative of disseminated tuberculosis and represents a rare manifestation of tuberculosis leading to the formation of a mycotic aneurysm in about half the cases. Tubercular Arteritis (TA), a rare disease entity involving the aorta, resulting in a stenosis and is indicative of extensive disseminated tuberculosis. Aneurysm with fever and clinical suspicion of tuberculosis should raise the suspicion of TA.[3] More commonly, TA is associated with aneurysm formation in about half of cases with possible complication of perforation of aorta. It involves abdominal and thoracic aorta with equal frequency. Fatal outcomes are frequently reported even after antituberculosis chemotherapy and surgical intervention,[4] the presentation of tubercular aortitis can be with constitutional symptoms along with hypertension and is usually a consequence of renal artery stenosis or aortic coarctation. Mycotic aneurysm secondary to tuberculous infection of the aorta is another kind of TA, featuring presentation of pain, palpable mass, or hypovolemia secondary to aneurysmal leak. Pulmonary tuberculosis usually is localized to the apical and posterior segments of the upper lobes and superior segments of the lower lobe, and the latter is usually close to the descending thoracic aorta. The close spatial relationship between the enlarged arch and thoracic aortic, and the previously infected segment of pulmonary tuberculosis was clearly demonstrated in the present case series. It is suggested that direct extension was the most likely mechanism of disease progression of TA in this case, suggesting a unique presentation along with possible inflammation resulting in the arteritis of superior mesenteric ischemia, especially when the initial infected foci are close to vital organs. We have presented this case also to remind physicians that TA as in literature, <50 cases of tuberculous aortic aneurysm were reported between 1945 and 2003.,[5] The patient was started on antitubercular therapy and was followed up in the outpatient basis once her symptoms improved after 2–3 weeks of inpatient care; surgical repair of the aneurysm was suggested to the patient but patient denied, so was followed up, after 2 months of care, patient general condition improved. However, many authors as in various papers suggested, we should consider lifelong suppression therapy with isoniazid after completing the treatment course, the goal is to prevent further bacillary growth.[6]

  Conclusion Top

Although rare, a reversible cause of hypertension should be looked upon. A poor responsive hypertension should raise the possibility of secondary hypertension. Infective arteritis has been infrequently reported, but the prevalence could be much more in third world country and it can present in the wide range of clinical setup.

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 initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

Ethical approval


Authors' contributions

All the authors have contributed equally in every aspect of study.

  References Top

Foote EA, Postier RG, Greenfield RA, Bronze MS. Infectious aortitis. Curr Treat Options Cardiovasc Med 2005;7:89-97.  Back to cited text no. 1
Bojar RM, Turner MT, Valdez S, Haskal R, McGowan K, Khabbaz KR. Homograft repair of a tuberculous pseudoaneurysm of the ascending aorta. Chest 1998;114:1774-6.  Back to cited text no. 2
Gajaraj A, Victor S. Tuberculous aortoarteritis. Clin Radiol 1981;32:461-6.  Back to cited text no. 3
Gornik HL, Creager MA. Aortitis. Circulation 2008;117:3039-51.  Back to cited text no. 4
Aebert H, Birnbaum DE. Tuberculous pseudoaneurysms of the aortic arch. J Thorac Cardiovasc Surg 2003;125:411-2.  Back to cited text no. 5
Bukhary ZA, Alrajhi AA. Tuberculous aortitis. Ann Saudi Med 2006;26:56-8.  Back to cited text no. 6
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