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American Journal of  Medical 
Science and Innovation (AJMSI) 

Morbid Obesity Associated with Non-Alcoholic Fatty Liver Disease and Complicated by 
Severe Non-Cirrhotic Portal Hypertension: A Case Report from Rural Kenya

Vonwicks C. Onyango1*, Kenneth H. Makokha2, Samuel M. Gachie3, Boniface Mutiso3

Nicholas M. Mutuma3, Paul M. Kamau3

Volume 2 Issue 2, Year 2023
ISSN: 2836-8509 (Online)

DOI: https://doi.org/10.54536/ajmsi.v2i2.1907
https://journals.e-palli.com/home/index.php/ajmsi

Article Information ABSTRACT

Received: July 17, 2023
Accepted: August 09, 2023
Published: August 14, 2023

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease and is closely 
linked with obesity and metabolic syndrome. Portal hypertension in NAFLD typically occurs 
in the cirrhotic phase of  the disease and may present with esophageal varices, splenomegaly 
with splenic sequestration syndrome, ascites, and features of  liver failure. However, recent 
experimental and clinical data show the occurrence of  portal hypertension in NAFLD in 
the absence of  fibrosis or cirrhosis. We present such a clinical case from rural Kenya in 
this study with the literature review that proposes novel mechanisms for such non-cirrhotic 
portal hypertension in NAFLD.

Keywords
Obesity, Non-Alcoholic Fatty 
Liver Disease, NAFLD, 
Portal Hypertension, Non-
Cirrhotic Portal Hypertension, 
Kenya

1 Department of  Medicine, St. Joseph Rift Valley Hospital, Gilgil, Nakuru County, Kenya
2 Department of  Endoscopy, St. Joseph Rift Valley Hospital, Gilgil, Nakuru County, Kenya
3 St. Joseph Rift Valley Hospital, Gilgil, Nakuru County, Kenya
* Corresponding author’s e-mail: drvonczelo@gmail.com

INTRODUCTION
The World Health Organization defines obesity as an 
excessive or abnormal accumulation of  body fat that 
presents a risk to health. A body mass index (BMI) of  
25-29.9 kg/m2 defines overweight individuals, while a 
BMI of  ≥30 is obesity. A BMI of  ≥40 kg/m2 (or ≥35 
kg/m2 in association with comorbidities) defines severe 
obesity, also called morbid obesity (Apovian, 2016). By 
2015, it was estimated that >600 million adults worldwide 
had obesity, with the number of  obese people having 
more than doubled since the 1980s in >70 countries. 
The prevalence was higher for females than males 
at all socioeconomic and age-group levels (Afshin et 
al., 2017). In this study, a high BMI accounted for >4 
million deaths globally, with 60% attributed to obesity, 
especially cardiovascular diseases. Obesity is associated 
with significant multisystemic dysfunction, including 
cardiovascular, metabolic, hepatobiliary, musculoskeletal, 
psychosocial, and neurological diseases, etc. Obesity 
(especially in the setting of  metabolic syndrome) is a 
major risk factor for non-alcoholic fatty liver disease 
(NAFLD), in which patients have hepatic steatosis with or 
without inflammation and fibrosis and in the absence of  
a secondary cause of  the steatosis (Younossi et al., 2011). 
NAFLD is the most common liver disease, with a global 
prevalence of  25% (Araújo et al., 2018). This prevalence 
was replicated in a Kenyan study by Mburu et al., in which 
the prevalence of  NAFLD was 26.2% among overweight 
and obese children in Nairobi (Mburu et al., 2023). 
However, most cases of  NAFLD are diagnosed in the 4th 
to 5th decades of  life (Cotter & Rinella, 2020). NAFLD 
encompasses a disease spectrum that includes steatosis 

with or without inflammation (non-alcoholic liver, i.e., 
NAFL), non-alcoholic steatohepatitis (NASH), which 
includes hepatic necroinflammation and fibrosis, and 
eventual liver cirrhosis. Patients with cirrhotic NAFLD 
should be screened for hepatocellular carcinoma and 
esophageal varices (Powell et al., 2021).

Case Presentation
Presenting Illness and Physical Examination
A 62-year-old married mother of  three from Naivasha, 
Kenya, a retired teacher, was referred to us for upper 
gastrointestinal endoscopy in the evaluation of  a 
2-week preceding history of  symptomatic microcytic 
hypochromic anemia with a hemoglobin of  8.4g/dl 
and a mean corpuscular hemoglobin (MCV) of  69 fl. 
Notably, she was morbidly obese with previous multiple 
comorbidities and complications including: obstructive 
sleep apnea syndrome, hypertension (well controlled 
on medications), previous mesenteric ischemia in 2013 
needing exploratory laparotomy with gangrenous bowel 
excision and primary anastomosis, proximal deep venous 
thrombosis of  the right leg in 2014 which was treated with 
6 months of  warfarin anticoagulation, left sided Bell’s 
palsy in 2016 treated with prednisone and acyclovir but 
having residual ipsilateral hemifacial weakness, bilateral 
lower limb varicose veins for which she was using bilateral 
external compression stockings, and severe bilateral knee 
osteoarthritis worse on the right knee for which she had 
undergone a total knee replacement in 2017. Six months 
earlier, she had an ultrasound diagnosis of  fatty liver 
disease with no complications during a routine medical 
evaluation at her local hospital. She was a lifetime non-



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smoker and non-ethanol user.
Her physical examination was remarkable for moderate 
conjunctival pallor, bilateral palmar erythema, and no 
obvious spider naevi, she was morbidly obese with a body 
mass index of  44.98 kg/m2 (weight of  121 kilograms, 
height of  1.64 meters), she had a blood pressure of  
114/69 mmHg, she was dyspneic at rest with a respiratory 
rate of  24 breaths per minute with a baseline oxygen 
saturation of  84% in room air; and a random blood sugar 
of  184mg/dl. Her abdomen was of  markedly increased 
girth with multiple striae distensiae and caput medusae, 
non-tender to palpation with bilateral flank dullness, and 
an obviously palpable splenomegaly about 6cm below 
the left costal margin in the mid-clavicular line. A digital 
rectal exam showed grade 2 hemorrhoids with melena 
stools. She had grade 2 bipedal pitting edema, distended 
external jugular veins with elevated jugular venous 
pressure to about 8 cm, a diffuse apex beat with loud P2, 
normal and regular S1 and S2 heart sounds, and a grade 
4/6 tricuspid regurgitation murmur. She had bi-basal lung 
crackles and a neurological examination remarkable for 
left hemifacial paresis (from prior Bell’s palsy) with no 
features of  hepatic encephalopathy.

Diagnostic Work Up
Her important work-up findings included a complete 
blood count showing anemia with a hemoglobin of  8 g/
dl with an MCV of  70 fl, leucopenia with total a white 
blood cells of  3.1 x 103/uL, and thrombocytopenia 
with platelets of  90 x 103/uL (the leucopenia and 
thrombocytopenia due to splenic sequestration from 
the portal hypertension). She had an elevated glycated 
hemoglobin (HbA1c) of  7.1% (insulin resistance), 
a normal creatinine of  0.9 mg/dl, normal aspartate 
transferase, bilirubin, and prothrombin time (INR). 
She had negative HIV and hepatitis B and C screening 
tests. An abdominal ultrasound showed a normal-sized 
liver with normal wall margins but with marked fatty 
infiltration and no other lesions, an enlarged spleen 
measuring 16.18cm with several prominent collateral 

veins, and moderate ascites (in keeping with portal 
hypertension). Upper gastrointestinal endoscopy showed 
grade 3 esophageal varices with hyperemic gastric fundus 
but no obvious ulcers or active bleeding (see Figure 1 
Series of  the esophageal varices on endoscopy). A chest 
x-ray showed cardiomegaly with pulmonary edema and 
prominent pulmonary vessels. An electrocardiogram 
showed a normal sinus rhythm, right axis deviation, 
and p-pulmonale (right atrial enlargement); an interval 
echocardiogram showed a normal left ventricular 
ejection fraction of  70% with concentric left ventricular 
hypertrophy, both atria and right ventricular outflow 
tract markedly enlarged, moderate-to-severe tricuspid 
regurgitation with an estimated right ventricular systolic 
pressure elevated at 55 mmHg (features of  pulmonary 
hypertension), and no obvious intracardiac thrombi.

Management and Follow-Up
The patient was clinically diagnosed with morbid obesity 
associated with non-alcoholic fatty liver disease (NAFLD) 
and complicated with features of  non-cirrhotic portal 
hypertension (splenomegaly with splenic sequestration, 
ascites, esophageal varices, and hemorrhoids). This was 
against a background of  other multiple target organ 
damages. She underwent a multidisciplinary team 
review, with specific management including: endoscopic 
esophageal variceal banding with initial 6-to-12-week 
surveillance endoscopies and repeat banding when 
needed as per our institutional protocol. She has since 
undergone three banding events (See Figure 2 series 
taken post endoscopic esophageal variceal banding).
She was also put on propranolol to prevent re-
bleeding of  the esophageal varices, omeprazole and 
metoclopramide for the gastritis, hematinic drugs for 
the anemia, the heart failure (which was predominantly 
due to cor pulmonale) was managed with furosemide, 
spironolactone, losartan, and sildenafil (the latter to 

Figure 1: Grade 2-3 esophageal varices (red arrows) 
for the patient seen on endoscopy. There was no active 
bleeding observed during endoscopy.

Figure 2: Esophageal variceal banding done for the 
patient on the initial, and subsequent serial follow-up 
endoscopy. Notice the bands in place (black arrows).



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reduce pulmonary hypertension). Nocturnal continuous 
positive airway pressure (CPAP) for the obstructive sleep 
apnea syndrome was recommended following a formal 
polysomnogram, but the patient could not afford it and 
currently uses nocturnal nasal-prong oxygen delivered  
by an oxygen concentrator. She is also receiving multiple 
supportive therapies within a multidisciplinary team. She 
was enrolled in the nutritional program to help with diet 
and weight management and has been active to date (she 
has since lost 12 kg). She developed a second episode of  
unprovoked proximal deep venous thrombosis on the left 
leg 3 months later, which was treated with rivaroxaban for 
6 months, and was subsequently put on life-long warfarin 
(the cheaper option) with careful monitoring of  the INR 
and surveillance for bleeding disorders. The leucopenia 
and thrombocytopenia have persisted during follow-up, 
but the anemia has since resolved.

DISCUSSION
Portal hypertension develops when there is increased 
pressure in the portal venous system and is associated with 
increasing portal collateral blood flow (porto-systemic 
anastomosis). This leads to ascites, esophageal varices, 
caput medusae, hemorrhoids, liver failure manifestations 
(including hepatic encephalopathy, coagulopathy, etc.), 
and hepatorenal syndrome (Simonetto et al., 2019). The 
two most common causes of  portal hypertension globally 
are cirrhosis and non-cirrhotic periportal fibrosis from 
hepatic schistosomiasis, or portal vein thrombosis (Mauro 
& Gadano, 2020). Our patient has splenomegaly with 
features of  splenic sequestration (thrombocytopenia and 
leucopenia, both of  which have persisted in her follow-
up tests), esophageal varices needing repeat bandings, 
ascites, caput medusae, and hemorrhoids. The etiology of  
the anemia is multifactorial, with the most prevalent cause 
being iron deficiency anemia from multiple etiologies, 
including portal hypertensive gastropathy.
Portal hypertension in NAFLD usually occurs in the 
cirrhotic phase of  the disease. It is unusual to find 
manifestations of  portal hypertension in NAFLD 
without associated liver cirrhosis. However, recent 
clinical and experimental data shows the occurrence of  
portal hypertension in the absence of  significant fibrosis 
or cirrhosis. There is growing evidence that portal 
venous pressure may begin to rise early in the NAFLD 
pathogenetic process when fibrosis is either absent or 
insignifican. In an observational study of  100 patients 
with NAFLD associated with clinically significant portal 
hypertension (encephalopathy, esophageal varices, ascites, 
and splenomegaly) undergoing staging liver biopsy, 88 
of  them had cirrhosis. However, in 12 of  the patients 
(12% of  cases), fibrosis was mild or absent (Mendes et 
al., 2012). These patients had a greater degree of  hepatic 
steatosis compared to those without portal hypertension. 
Our patient has not had any features of  liver cirrhosis 
in multiple follow-up ultrasound scans of  the liver over 
the last 2 years. There was a marginal increase in fatty 
infiltration of  the liver initially, but this has plateaued 

and remained static since the onset of  her weight loss 
journey. Admittedly, the utility of  ultrasonography in 
general medical diagnosis is limited by user-dependent 
variabilities.
One of  the proposed mechanisms for this non-cirrhotic 
portal hypertension in NAFLD is a combination of  
impaired hepatic sinusoidal hemostasis and hepatocellular 
ballooning leading to increasing intrahepatic vascular 
resistance and thus portal hypertension before the 
development of  cirrhosis. Both of  these processes 
are initiated by progressive lipid accumulation in the 
hepatocytes (steatosis), which causes a mechanical 
barrier to sinusoidal flow and eventual hepatotoxicity 
from the lipidosis-induced hepatocyte ballooning 
(Baffy, 2018). Other proposed intrahepatic factors 
include steatosis-induced endothelial cell dysfunction 
and splanchnic vasodilatation, both of  which increase 
intrahepatic vascular resistance early in NAFLD. Insulin 
resistance is associated with NAFLD non-cirrhotic portal 
hypertension through increased hepatocyte burden of  
adipose tissue lipolysis with resultant hepatotoxicity, 
endothelial dysfunction, and increased portal pressures 
(Nababan & Lesmana, 2022). Our patient also has insulin 
resistance, with a HbA1c of  7.1%.
The first-line therapy for NAFLD is lifestyle changes, 
especially diet and physical exercise, to reduce body weight 
to a more normal BMI. Non-selective beta blockers, e.g., 
propranolol and carvedilol, help to reduce portal and 
splanchnic pressures, thus reducing the incidence of  
primary and repeat variceal bleeding. Other medications 
include statins, renin-angiotensin-aldosterone system 
(RAAS) blockade, and sodium-glucose transport protein 
2 (SGLT2) inhibitors given in a judicious and rational 
manner (Nababan & Lesmana, 2022). Our patient is 
already on most of  these strategies, which have been 
individualized based on her practical realities.

CONCLUSION
The occurrence of  portal hypertension in NAFLD is 
usually encountered during the cirrhotic phase of  the 
disease. However, novel pathophysiological mechanisms 
have recently been proposed to explain the experimental 
and clinical observations of  non-cirrhotic portal 
hypertension in NAFLD, as presented in this case report. 
Admittedly, more advanced non-invasive (e.g., transient 
elastography, computerized tomography, magnetic 
resonance imaging scans, etc.) and invasive diagnostic 
tests and procedures (e.g., liver biopsy) need to be carried 
out to further evaluate and characterize the hepato-portal 
dysfunction in our patient, preferably in a specialized 
center. These ideal interventions are unfortunately limited 
by financial and other constraints that define the reality 
of  rural medicine.
REFERENCES
Afshin, A., Forouzanfar, M. H., Reitsma, M. B., Sur, 

P., Estep, K., Lee, A., Marczak, L., Mokdad, A. H., 
Moradi-Lakeh, M., Naghavi, M., Salama, J. S., Vos, 
T., Abate, K. H., Abbafati, C., Ahmed, M. B., Al-Aly, 



Pa
ge

 
60

https://journals.e-palli.com/home/index.php/ajmsi

Am. J. Med. Sci. Innov. 2(2) 57-60, 2023

Z., Alkerwi, A., Al-Raddadi, R., Amare, A. T., . . . 
Murray, C. J. L. (2017). Health Effects of  Overweight 
and Obesity in 195 Countries over 25 Years. N Engl 
J Med, 377(1), 13-27. https://doi.org/10.1056/
NEJMoa1614362 

Apovian, C. M. (2016). Obesity: definition, comorbidities, 
causes, and burden. Am J Manag Care, 22(7 Suppl), 
s176-185. 

Araújo, A. R., Rosso, N., Bedogni, G., Tiribelli, C., 
& Bellentani, S. (2018). Global epidemiology of  
non-alcoholic fatty liver disease/non-alcoholic 
steatohepatitis: What we need in the future. Liver Int, 
38 Suppl 1, 47-51. https://doi.org/10.1111/liv.13643 

Baffy, G. (2018). Origins of  Portal Hypertension in 
Nonalcoholic Fatty Liver Disease. Dig Dis Sci, 63(3), 
563-576. https://doi.org/10.1007/s10620-017-4903-5 

Cotter, T. G., & Rinella, M. (2020). Nonalcoholic Fatty 
Liver Disease 2020: The State of  the Disease. 
Gastroenterology, 158(7), 1851-1864. https://doi.
org/10.1053/j.gastro.2020.01.052 

Mauro, E., & Gadano, A. (2020). What’s new in portal 
hypertension? Liver Int, 40 Suppl 1, 122-127. https://
doi.org/10.1111/liv.14366 

Mburu, A. N., Laving, A., Macharia, W. M., & Sande, 
J. (2023). Prevalence of  non-alcoholic fatty liver 
disease in overweight and obese children seeking 
ambulatory healthcare in Nairobi, Kenya. BMJ 

Open Gastroenterol, 10(1). https://doi.org/10.1136/
bmjgast-2022-001044 

Mendes, F. D., Suzuki, A., Sanderson, S. O., Lindor, K. 
D., & Angulo, P. (2012). Prevalence and indicators of  
portal hypertension in patients with nonalcoholic fatty 
liver disease. Clin Gastroenterol Hepatol, 10(9), 1028-1033.
e1022. https://doi.org/10.1016/j.cgh.2012.05.008 

Nababan, S. H. H., & Lesmana, C. R. A. (2022). Portal 
Hypertension in Nonalcoholic Fatty Liver Disease: 
From Pathogenesis to Clinical Practice. J Clin Transl 
Hepatol, 10(5), 979-985. https://doi.org/10.14218/
jcth.2021.00593 

Powell, E. E., Wong, V. W., & Rinella, M. (2021). Non-
alcoholic fatty liver disease. Lancet, 397(10290), 2212-
2224. https://doi.org/10.1016/s0140-6736(20)32511-
3 

Simonetto, D. A., Liu, M., & Kamath, P. S. (2019). Portal 
Hypertension and Related Complications: Diagnosis 
and Management. Mayo Clin Proc, 94(4), 714-726. 
https://doi.org/10.1016/j.mayocp.2018.12.020 

Younossi, Z. M., Stepanova, M., Afendy, M., Fang, 
Y., Younossi, Y., Mir, H., & Srishord, M. (2011). 
Changes in the prevalence of  the most common 
causes of  chronic liver diseases in the United States 
from 1988 to 2008. Clin Gastroenterol Hepatol, 9(6), 
524-530.e521; quiz e560. https://doi.org/10.1016/j.
cgh.2011.03.020


