ONE OF THE CAUSE OF DVT

1. 98 Medical Journal of Dr. D.Y. Patil University | January-February 2016 | Vol 9 | Issue 1
Introduction
Human immunodeficiency virus (HIV) infection is one of
the recognized risk factors for deep vein thrombosis (DVT).
Venous thrombo embolism (VTE) has been reported 2-10
times more common in HIV-infected individuals than non
HIV-infected individuals.[1]
DVT in HIV-infected patients
often occur in the absence of thrombogenic factors like
advanced age, prolonged immobility, pelvic trauma or
surgery, pregnancy, smoking and oral contraceptive therapy,
and family history of DVT.[1-3]
The mechanisms of HIV-associated VTE include protein
C and S deficiency, elevated factor VIII levels, low
antithrombin levels, and increased homocysteine level, all
induced by the viral antigen.[3]
Case Report
A 35-year-old male patient was diagnosed as having
HIV Infection for 4 years. Since then he has been on
antiretroviral therapy (ART) (zidovudine, lamivudine,
efavirenz). He was admitted with complaints of painful
progressive swelling of right lower limb for last 7 days.
This swelling started from leg and progressed up to thigh.
Human immunodeficiency virus-associated
deep vein thrombosis
Akhilesh Kumar Singh, Duraikannan Premnath, Keshri Singh Yadav
Department of Medicine, SN Medical College, Agra, Uttar Pradesh, India
ABSTRACT
Deep vein thrombosis (DVT) has been reported to occur 2-10
times more common in human immunodeficiency virus-infected
individuals than in the general population. We are reporting
a case of DVT of right lower limb who was on highly active
antiretroviral therapy. The patient did not have any acquired risk
factors of DVT. The patient responded well to anticoagulation
therapy.
Keywords: Deep vein thrombosis, human immunodeficiency
viral infection, venous thrombo embolism
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DOI:
10.4103/0975-2870.167967
Case Report
The pain was moderately severe that was aggravated by
exertion and relieved on rest. There was no history of
trauma to limbs, prolonged immobilization, recent surgery,
and smoking. He was not known case of hypertension and
diabetes.
Physical examination revealed pulse rate of 90/minute
and blood pressure of 130/86 mmHg. The right lower limb
shows edema from foot to thigh and differential warmth as
compared to left lower limb. There was no tenderness. The
peripheral pulses of right lower limb were weaker than the
contralateral pulses. Other systemic examination revealed
normal findings.
Doppler of the lower limb showed-DVT involving right
posterior tibial vein, popliteal vein, femoral vein, external
iliac vein, and common iliac vein [Figures 1 and 2].
His blood counts, (Hb = 10.4 mg/dl, total leukocytic
count = 7800/mm3
, differential leukocytic count = P78,
L22
M2
,
platelet count = 1.8 lac/mm3
), fasting blood sugar
(108 mg/dl), lipidprofile (total cholesterol = 168 mg/
dl, triglyceride = 130 mg/dl, low-density lipoprotein
[LDL] = 80 mg/dl, very LDL = 48 mg/dl, high-density
lipoprotein = 42 mg/dl) liver function test (serum bilirubin)
(total = 1.2 mg/dl, direct = 0.8 mg/dl, indirect = 0.4 mg/dl),
serum glutamic oxaloacetic transaminase = 23 IU/L serum
glutamic-pyruvic transaminase = 39 IU/L, serum protein
Address for correspondence:
Keshri Singh Yadav, 27/80/3F Ashok Nagar, Near Home Guard Office, Agra 282002, Uttar Pradesh, India.
E-mail: keshri2005gsvm@gmail.com
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2. Singh, et al.: Human immune difficiency virus associated deep vein thrombosis
Medical Journal of Dr. D.Y. Patil University | January-February 2016 | Vol 9 | Issue 1 99
(total = 5.8 g/dl, serum albumin = 3.1 g/dl, serum globulin
= 2.7 g/dl) kidney function test (serum creatinine = 0.9 mg/
dl, blood urea nitrogen = 32 mg/dl), urine (albumin = nil,
sugar = nil, microscopic examination-pus cells 1-3/hpf,
epithelial cells 2-4/hpf) were all within normal limits. His
clotting profile was normal with INR = 1.1. His CD4+
count
was 106/µl.
He was treated with subcutaneous injection of enoxaparin 40
mg twice daily, tablet* warfarin 5 mg daily. His right lower
limb was elevated. The enoxaparin injection was given for
7 days, and anticoagulation therapy was continued with
warfarin tablet 5 mg daily and aspirin tablet 75 mg daily. He
remained admitted for 15 days. At the times of discharge,
his right lower limb swelling reduced significantly, and the
patient was discharged on warfarin and aspirin.
Discussion
Deep vein thrombosis is approximately 10 times more
common in HIV/AIDS patients than in the general
population.[4]
ART has prolonged the life expectancy of
HIV patients. Increased survival has been associated with
increased prevalence of non-AIDS-related conditions like
cardiovascular diseases which is now a major cause of
mortality and morbidity in HIV patients.[4]
HIV infection
has been known as prothrombotic state, and that association
has been proven by many studies.[1-4]
There are several
factors that are associated with DVT in patients with HIV
infection. These factors can be divided into three categories;
a hypercoagulable state, endothelial dysfunction and due to
therapy.[4]
In our patient, the last two categories may apply.
The incidence of VTE is more in patients with low CD4+
counts,[5]
this might have been the causative factor in our
patient. Another study concluded that higher viral load and
low CD4+
count had been associated with higher frequency
of thrombosis.[6]
The presence of opportunistic infection
such as Mycobacterium intracellulare, Cytomegalovirus, and
Pneumocystis jiroveci pneumonia appears to be additional
risk factor for thrombosis,[6]
although our reported case did
not appear to have any above-mentioned infections.
Highly active ART and particularly the use of protease
inhibitor (PI) have been associated with thrombosis.[7]
Current data show association of PI with lipodystrophy,
and HIV patients with fat redistribution might be having
altered coagulation profile such as increased fibrinogen,
D-dimer, plasminogen activator inhibitor-1, and protein S
deficiency.[7-10]
The management of VTE in HIV-infected individuals is
same as in non-HIV-infected individuals.
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Figure 1: Colour doppler of common femoral vein
Figure 2: Colour doppler of right popliteall artery
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3. Singh, et al.: Human immune difficiency virus associated deep vein thrombosis
100 Medical Journal of Dr. D.Y. Patil University | January-February 2016 | Vol 9 | Issue 1
How to cite this article: Singh AK, Premnath D, Yadav KS. Human
immunodeficiency virus-associated deep vein thrombosis. Med J DY
Patil Univ 2016;9:98-100.
Source of Support: Nil. Conflicts of Interest: None declared.
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Absolute risk of venous and arterial thrombosis in HIV-infected
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