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International Journal of Human and Health Sciences Vol. 07 No. 01 January’23

Case Report

Lethal Complicationin a Newly Diagnosed Patient with Hypertension

Najwan Mustafa Alsulaimi
Abstract

Polyarteritis Nodosa (PAN) is a rare but lethal systemic vasculitis that affects the medium-
sized arteries. Although it is mostly idiopathic, few underlying etiologic agents have 
been identified and cause secondary PAN. Hepatitis B virus (HBV) is one of them. Early 
recognition of HBV-associated PAN is critical to improve the patient’s outcomes. We 
describe a case of 59-year-old gentleman who presented to multiple medical facilities 
over a few months with non-specific symptoms of unexplained abdominal pain and 
weight loss in addition to a new onset of hypertension. His clinical course deteriorated, 
and he was admitted to the intensive care unit with a hemorrhagic shock before he was 
diagnosed and treated for HBV-associated PAN resulted in renal arterial microaneurysms 
rupture. This case highlighted the importance of early management of PAN to prevent its 
fatal consequences. Therefore, we recommend screening for HBV or considering PAN – 
especially where HBV is endemic – in patients presenting with non-specific symptoms and 
unexplained weight loss with a new-onset diastolic hypertension.

Keywords:hepatitis B virus, polyarteritis nodosa, diastolic hypertension

Correspondence to: Dr. Najwan Mustafa Alsulaimi, Department of Internal Medicine, Faculty 
of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia. Email: nalsalaimi@kau.edu.sa

Introduction

Hepatitis B virus (HBV) is one of few infectious 
agents which causes secondary Polyarteritis 
Nodosa (PAN). PAN is a rare multi-organ 
necrotizing vasculitis and has a high mortality rate 
of 34 percent1. PAN can be categorized as primary 
or secondary. Secondary PAN needs prompt 
treatment of the underlying etiology for survival. 
We present a middle-aged man with a newly 
diagnosed HBV infection manifesting as life-
threatening PAN. We also discuss HBV-associated 
PAN with an emphasis of reviewing its clinical 
presentations for the purpose of improving early 
detection in the primary care settings.

Case Description 

A 59-year-old man presented to multiple clinics and 
Emergency Departments over a three-month period 
reporting intermittent abdominal pain, anorexia, and 
approximately sixteen Kilograms of unintentional 
weight loss. Initial Computed Tomography (CT) 
of the abdomen, esophagogastroduodenoscopy 
(EGD), and colonoscopy were grossly 
unremarkable. He was sent home from the 

Emergency Department (ED) with a new diagnosis 
of hypertension. He later returned to the ED with 
ongoing symptoms in addition to severe fatigue. 
On further assessment, he had a fever of 38.5 
degrees Celsius, tachycardia, and leukocytosis. 
He was started on broad-spectrum antibiotics and 
admitted with a presumed sepsis diagnosis with 
unknown source. Despite antibiotic therapy, he 
had persistent abdominal pain, leukocytosis and 
rising levels of inflammatory markers which led 
to consideration of connective tissue diseases and 
repeat CT of the abdomen. The new CT showed 
innumerable renal arterial aneurysms and wedge-
shaped infarcts in the kidneys bilaterally. High dose 
corticosteroids were initiated for the diagnosis of 
idiopathic PAN. The next day, he developed acute 
worsening of abdominal pain and was transferred 
to the intensive care unit for hemorrhagic shock. 
An emergent CT angiogram (CTA) showed left 
perinephric hemorrhage with an area of active 
arterial contrast extravasation suggestive of 
renal aneurysmal hemorrhage (Figure 1). The 
hemorrhage was successfully controlled with 
endovascular embolization (Figure 2). Additional 

International Journal of Human and Health Sciences Vol. 07 No. 01 January’23 Page : 95-98
DOI: http://dx.doi.org/10.31344/ijhhs.v7i1.505



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work-up revealed an active HBV infection with 
HBV DNA PCR of 28 million international unit/
ml. A Multi-disciplinary team of Rheumatologists, 
Nephrologists and Infectious Disease physicians 
were involved, and a combination treatment 
of corticosteroids, anti-viral regimen and 
plasmapheresis was initiated. A positive response 
in clinical symptoms, a decreased level of viremia, 
a stability of aneurysms on imaging and decreased 
level of inflammatory markers were achieved and 
maintained over a two-month outpatient follow-up.

Figure 1: Left perinephric hemorrhage with an 
area of active arterial contrast extravasation best 
visualized on CTA coronal image and likely from 
renal aneurysm rupture

Figure 2A: Left renal arteriogram image 
demonstrates small extravasation emanating from 
a microaneurysm within the left upper renal pole

Figure 2B: Left renal arteriogram post 
embolization image demonstrates no further signs 
of bleeding with coils in place

Discussion

HBV has been identified as the underlying 
etiology in 7 to 36 percent of PAN cases 2. 
Based on the prevalence of HBV infection in a 
population, the annual incidence of PAN has been 
reported to be between 2 and 77 per million2. The 
lower prevalence has been seen in the countries 
with effective HBV immunization and blood 
products screening programs2. HBV-associated 
PAN commonly complicates the picture early in 
the course of HBV infection and is infrequently 
co-occurred with jaundice or the typical hepatitis 
manifestations and laboratory findings2. Since 
PAN is a systemic disease, it may affect almost 
any organ with the exception of the lungs3. Early 
presenting symptoms are usually non-specific such 
as polyarthralgia, fatigue, fever, and abdominal 
pain which have broad differential diagnoses. 
In this phase, the findings of elevated blood 
pressure specifically new diastolic hypertension, 
and unintentional weight loss can be important 
clues. Eventually, the focal symptoms developed 
due to involvement of the vasculatures of specific 
organ systems such as the kidneys, the skin and 
the nervous system4. The American College of 
Rheumatology (ACR) has established ten criteria 
to help the clinical diagnosis in a suspected PAN 
case. The presence of three criteria or more, has 
been associated with the sensitivity and specificity 
of 82.2 precent and 86.6 precent respectively in a 
cohort of patients with vasculitis5. In our patient, 



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International Journal of Human and Health Sciences Vol. 07 No. 01 January’23

four of these criteria were met; unexplained weight 
loss of four or more kilograms, new onset elevated 
diastolic blood pressure of greater than 90 mmHg, 
evidence of HBV infection, and the characteristic 
arteriographic abnormalities of microaneurysms 
in the renal arteries. 

Conclusion

HBV immunization has made secondary PAN rare, 
making it lower on the differential of diagnosis 

for the frontline healthcare providers such as 
Internal Medicine, Emergency Medicine and 
Family Medicine physicians. The early diagnosis 
and treatment of PAN is crucial given the high 
morbidity and mortality associated with delayed 
management. A new diagnosis of hypertension in 
a patient with weight loss, fatigue, or unexplained 
abdominal pain may warrant screening for HBV or 
consideration of PAN. 

References
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Le Guern V, et al. Clinical features and outcomes in 
348 patients with polyarteritis nodosa: A systematic 
retrospective study of patients diagnosed between 
1963 and 2005 and entered into the French vasculitis 
study group database. Arthritis & Rheumatism. 
2010;62(2):616–26.

2. Sharma A, Sharma K. Hepatotropic Viral Infection 
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Associated Polyarteritis Nodosa and Hepatitis C Virus 
Associated Cryoglobulinemic Vasculitis. Journal of 
Clinical and Experimental Hepatology. 2013;3(3): 
204-12.

3. Guillevin L, Mahr A, Callard P, GodmerP, Pagnoux 

C, Leray E, et al. Hepatitis B Virus-Associated 

Polyarteritis Nodosa: Clinical Characteristics, 

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Patients. Medicine. 2005;84(5):313-22.

4. Han SH. Extrahepatic manifestations of chronic 

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5. Lightfoot RW Jr, Michel BA, Bloch DA, Hunder GG, 

Zvaifler NJ, McShane DJ, et al. The American college 

of rheumatology 1990 criteria for the classification 

of polyarteritis nodosa. Arthritis and Rheumatism. 

1990;33(8):1088-93.



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