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CASE SNIPPET
Year : 2013  |  Volume : 59  |  Issue : 1  |  Page : 66-68

Varied manifestations of vasculopathy in a HIV patient on antiretrovirals


1 Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
2 Department of Radiodiagnosis, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India

Date of Web Publication22-Mar-2013

Correspondence Address:
V Mukta
Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0022-3859.109504

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How to cite this article:
Mukta V, Ramesh A, Karthikeyan B, Deepanjali S, Das A K. Varied manifestations of vasculopathy in a HIV patient on antiretrovirals. J Postgrad Med 2013;59:66-8

How to cite this URL:
Mukta V, Ramesh A, Karthikeyan B, Deepanjali S, Das A K. Varied manifestations of vasculopathy in a HIV patient on antiretrovirals. J Postgrad Med [serial online] 2013 [cited 2020 Apr 6];59:66-8. Available from: http://www.jpgmonline.com/text.asp?2013/59/1/66/109504


Human immunodeficiency virus (HIV) infected patients present with a myriad of complications like vasculopathy, pulmonary hypertension, cardiomyopathy, coagulopathy and nephropathy. The term HIV-associated vasculopathy includes vascular diseases in HIV patients presenting as arterial aneurysms and occlusive disease. However, in the absence of a consensus definition, some authors include any abnormality of intracranial or extracranial blood vessels associated with HIV infection, as HIV-associated vasculopathy, except for vasculitis due to opportunistic infection or neoplastic involvement of blood vessels. [1]

A 34-year-old HIV positive woman, on three drug antiretroviral therapy (stavudine, lamivudine, nevirapine) for 3 years, presented to us with a history of pedal edema and progressive abdominal distension of 3 months duration and worsening breathlessness (NYHA IV) with reduced urine output for the past 1 month. There was no fever throughout this period. In the past, she had been treated for pulmonary tuberculosis and was to told to have been cured 5 years ago.

On physical examination, patient had bilateral pedal edema and an elevated Jugular Venous Pulse. All peripheral pulses, except right dorsalis pedis, were palpable and blood pressure was elevated (170/90 mmHg) in the right upper limb in supine position. Peripheral pulses in all four limbs were normal. On cardiovascular examination, there was a pansystolic murmur in the tricuspid area and a loud pulmonary component of second heart sound. Bilateral wheeze and occasional crepitations were present. Moderate ascites was present, there was no organomegaly or renal bruit. An initial diagnosis of congestive cardiac failure with HIV-associated pulmonary artery hypertension and tricuspid regurgitation was made, and intravenous diuretics for decongestion was started along with nasal oxygen. After decongestion, dyspnea improved but blood pressure was persistently elevated and renal artery stenosis was suspected to be the cause of hypertension in this young woman.

Initial serum creatinine was 1.5 mg/dl. Ultrasonography of abdomen revealed mild fusiform dilatation of abdominal aorta with thickened walls and a thrombosed saccular aneurysm just proximal to the bifurcation; contracted right kidney measuring 4.0 × 2.5 cm; normal sized left kidney; and mild ascites. Computed tomography (CT) angiogram of the abdomen showed mild fusiform dilatation of the entire abdominal aorta measuring up to 3.5 cm with tortuosity and irregularity of aortic contour. There was hypodense non-enhancing aortic wall thickening due to organized mural thrombi with intimal calcifications. Two saccular aneurysms were observed arising from the abdominal aorta: One near the origin of right renal artery and another fully thrombosed saccular aneurysm just proximal to the aortic bifurcation. There was a short segment moderate stenosis involving approximately 70% of the origin of celiac artery with intimal irregularity, post stenotic dilatation and minimal narrowing of the proximal superior mesenteric artery beyond its origin. Right renal and inferior mesentric arteries were blocked and not filled with contrast. Right kidney was contracted and did not show contrast enhancement. Left renal artery had a short bend in its proximal portion due to tortuosity of aorta with no significant stenosis. Left kidney was normal [Figure 1] and [Figure 2].
Figure 1: Computed tomography angiogram of abdomen with maximum intensity projection reconstructions showing diffuse irregular dilatation of the entire abdominal aorta with saccular aneurysm near the origin of right renal artery which is blocked

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Figure 2: Contrast enhanced computed tomography of abomen axial image showing dilated abdominal aorta and contracted right kidney showing no contrast enhance

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CT pulmonary angiography revealed dilated main pulmonary artery and central pulmonary arteries with pruning of the peripheral branches and main pulmonary artery measuring 4.3 cm. There was no evidence of wall thickening or thrombi in the pulmonary arteries. Doppler of the peripheral vessels was normal. Electrocardiogram (ECG) showed features of right ventricular hypertrophy. Echocardiography revealed a dilated right atrium and ventricle, severe tricuspid regurgitation and elevated right ventricular systolic pressure (78 mmHg), suggestive of pulmonary artery hypertension.

The patient's complete hemogram and erythrocyte sedimentation rate (ESR) were normal. Other serologies like hepatitis B, C, Venereal disease research laboratory (VDRL) test, Antinuclear antibody (ANA), and antitoxoplasma antibody were negative. Her lipid profile was normal. CD4 count was 356 cells/cu.mm. Viral load could not be estimated due to lack of this facility at our centre. Blood culture was sterile. The patient was treated with enoxaparin and warfarin and is on a regular follow-up. She is unwilling for surgery, presently.

Abdominal aortic aneurysms and occlusion of celiac, inferior mesenteric, and right renal artery are features of a possible HIV-associated vasculopathy in this patient. Thrombus within the aneurysm was probably related to stasis of blood. She also has pulmonary artery hypertension related to HIV.

Endothelial damage, direct infection of the arterial smooth muscle cell by HIV, accelerated atherosclerosis and immune-mediated leukocytoclastic vasculitis involving vasavasorum or periadventitial vessels are the proposed mechanisms of HIV-related vasculopathy. [2],[3] HIV-associated pulmonary hypertension is a serious complication with poor prognosis. Exact mechanism is unknown, and endothelial dysfunction due to HIV-nef has been suggested. [4]

For diagnosing HIV-associated vasculopathy, other causes of arterial occlusions and aneurysms have to be excluded. Mycotic aneurysms due to syphilis and tuberculosis, arterial occlusions due to Takayasu's arteritis, vasculitis, systemic lupus erythematosis (SLE), and Behcet's and antiphospholipid antibody syndrome-related aneurysms are close differentials. [5],[6] Our patient did not have any evidence of infective endocarditis, active tuberculosis, syphilis, and secondary bacterial or fungal infection. Her lipid profile was normal. Concentric contrast enhancing vessel wall enhancement with periadventitial inflammatory changes, classical of Takayasu arteritis, was absent. SLE was unlikely in the absence of ANA. Lupus anticoagulant could not be estimated. Arterial biopsy and histopathological examination of vessel wall and the thrombus could not be performed.

Our patient presented with right heart failure and was found to have vasculopathy in both its aneurysmal and occlusive form in addition to pulmonary artery hypertension. She did not have any abdominal lump due to the aneurysm or pain due to the arterial occlusions. Although it was not possible to establish an exact etiology of vasculopathy, we suggest that HIV infection may have lead to vasculopathy in the patient. We have reported this case because of its rare presentation and also to highlight the need for physicians to have a high degree of suspicion of vasculopathy in young HIV positive patients.

 
 :: References Top

1.Benjamin LA, Bryer A, Emsley HC, Khoo S, Solomon T, Connor MD. HIV infection and stroke: Current perspectives and future directions. Lancet Neurol 2012;11:878-90.  Back to cited text no. 1
[PUBMED]    
2.Eugenin EA, Morgello S, Klotman ME, Mosoian A, Lento PA, Berman JW, et al. Human immunodeficiency virus (HIV) infects human arterial smooth muscle cells in vivo and in vitro: Implications for the pathogenesis of HIV-mediated vascular disease. Am J Pathol 2008;172:1100-11.  Back to cited text no. 2
[PUBMED]    
3.Tilson MD 3 rd , Withers L. Arterial aneurysms in HIV patients: Molecular mimicry versus direct infection? Ann N Y Acad Sci 2006;1085:387-91.  Back to cited text no. 3
    
4.Duffy P, Wang X, Lin PH, Yao Q, Chen C. HIV Nef protein causes endothelial dysfunction in porcine pulmonary arteries and human pulmonary artery endothelial cells. J Surg Res 2009;156:257-64.  Back to cited text no. 4
[PUBMED]    
5.Marubayashi S, Sugi K, Ishiyama K, Fukuma K, Okada K, Hinoi T, et al. A case of abdominal aortic aneurysm associated with systemic lupus erythematosus. Hiroshima J Med Sci 1998;47:85-7.  Back to cited text no. 5
[PUBMED]    
6.Ehtuish EF, Mishra A. Multiple visceral aneurysms in antiphospholipid antibody syndrome - An unusual presentation. Br J Radiol 2008;81:e184-7.  Back to cited text no. 6
[PUBMED]    


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