2. 37 Year old Mrs. Lakshmi was admitted
with
C/o Abdomen distension - 3 months
Abdomen Pain - 3 months
HOPI:
Patient was apparently normal till 3 months
ago after which she developed abdomen
distension insidious onset , increasing in
size , uniform abdomen distension
3. Abdomen distension not associated with
Oliguria , pedal edema , facial puffiness,
chest pain ,palpitation.
Dyspnoea – insidious onset ,
progressive , grade II was present.
Abdomen pain – right hypochondrium,
dull aching type pain, continuous,
aggravated by lying on right side & deep
inspiration .
4. H/O jaundice -3 months, yellow coloured
urine , no clay coloured stools , no pruritis
No LOW
LOA+
No fever, bleeding tendencies, altered
sleep
Past H/o
Hypothyroid – 8 months—on thyroxine -75
mcg
No other co morbid illness
5. Personal H/O
No Habituations
Menstrual and marital H/O
amennorhea-8 months
3 Children
Treatment H/o
No H/o chronic drug intake other than
thyroxine
6. General Examination
Conscoius
Oriented
obesity
Afebrile
Icteric
pale
Facial puffiness
Dry skin
Hoarse voice
BP:110/70 mmHg
PR:86/min
JVP not Raised
BMI 26.93kg/sq m
7. P/A
uniform distension
Skin normal
Hepatomegaly present
17 cm below right costal margin
tender , nodular surface, firm in
consistency , no bruit
No splenomegaly.
No Free fluid
Other systems normal
11. USG Abdomen:
Hepatomegaly with fatty infiltration.
Portal Vein 15 mm. normal flow
Splenomegaly 14 cm
12. CECT Abdomen
Liver enlarged – 24 cm. Diffusely
hypodense area of altered density seen
in segment 5/8
GB contracted
Spleen 15 cm enlarged
IMP: Fatty liver with hepatomegaly.
Areas of altered density noted in
segments 5/8 of right of liver
13. P.V Doppler
Liver increased in echoes ,enlarged.
portal vein 1 cm at the hilum .(Flow +)
Portal vein 1.4 cm at the confluence of splenic and
SM vein
Velocity 18.87 cm/s
Hepatopedal flow+
Hepatic veins flow +
Spleen 14.4 cm enlarged .
Splenic Vein 17 cm at the hilum
IMPRESSION
Hepatosplenomegaly with Fatty
liver
14. Blood for QBC – Negative
HBsAg -- Negative
Anti HCV – Negative
HIV I & II – Negative
AFP – not elevated
T. Cholesterol 174 mg/dl
HDL 32 mg/dl
LDL 120 mg/dl
VLDL 22 mg/dl
TGL 109 mg/dl
15. OGD: Lax OGJ . Otherwise normal
ECHO- Normal
16. NAFLD score
Age, BMI, hyperglycemia, AST/ALT ratio,
platelet count, and serum albumin level
Score =0.915
< -1.455: predictor of absence of significant fibrosis (F0-F2
fibrosis)(negative predictive value of 93%)
≤ -1.455 to ≤ 0.675: indeterminate score
> 0.675: predictor of presence of significant fibrosis (F3-F4
fibrosis)(positive predictive value of 90% )
Formula :
-1.675 + 0.037 × age (years) + 0.094 × BMI (kg/m2) + 1.13 ×
IFG/diabetes (yes = 1, no = 0) + 0.99 × AST/ALT ratio – 0.013 ×
platelet (×109/l) – 0.66 × albumin (g/dl)
17.
18. ANA -- Negative
S.Ceruloplasmin 20.5mg/dl(18-35mg/dl)
S . Iron 23.8 mcg/dl(50-150 mcg/dl)
TIBC 283 mcg/dl(300-360mcg/dl)
Ferritin 21.04 ng/dl (50-200mcg/dl)
19. Final diagnosis
Non alcoholic steatohepatitis
Pre -Obesity
Hypothyroidism
Nutritional anemia
20. Treatment given
Thyroxine dose increased to 125
mcg/day
T.vitamin E 400mg twice a day
FST 100 mg twice a day
21. At discharge
CBC
Hb 11.8 gm%
TC 8000
DC P80 L20
ESR 4/10
Platelet 2.5 lakh
TSH 39.98mIU/ml
Patient is now on thyroxine 150
mcg/day
22. DISCUSSION
NAFLD
a) There is evidence of hepatic steatosis ,
either by imaging or by histology.
b)There is no causes for secondary
hepatic fat accumulation such as alcohol
consumption , use of steatogenic drugs
or hereditary disorders.
23. NAFL
The presence of hepatic steatosis with
no evidence of hepatocellular injury in
the form of ballooning of the
hepatocytes
NASH
The presence of hepatic steatosis and
inflammation with hepatocyte
injury(ballooning) with or without fibrosis
24. Prevalence :
NAFLD 6.3 to 33%(median -20%)
NASH 3 to 5 %
High risk groups
Type 2 Diabetes Mellitus
Obesity
Dyslipedemia
Metabolic syndrome
26. What is significant alcohol consumption
for eligibility for NASH in clinical practice
>21 drinks per week in men
>14 drinks per week in women
over a period of 2 years before baseline
histology
27. When to evaluate incidentally
discovered hepatic steatosis
Unsuspected hepatic steatosis detected
on imaging have symptoms or signs
attributable to liver disease or have
abnormal liver biochemistries – should
be evaluated as for NAFLD
29. Non invasive methods to
assess steatohepatitis
S.Aminotransferase, USG ,CT,MR donot
reliably assess steatohepatitis and
fibrosis in patients with NAFLD.
Liver biopsy is the most reliable
approach
Non invaisve approaches include
a) NAFLD fibrosis score
b)Enhanced fibrosis score
c)Transient elastography
30. When to do biposy ?
Those who are increased risk to have
steatohepaitis and advanced fibrosis.
( NAFLD score , metabolic syndrome
can be used to predict risk)
Competing etiologies for hepatic
steatosis and co existing chronic liver
disease cannot be excluded without a
liver biopsy
31. Management
Loss of 3 to 5 % weight loss improves
steatosis ,loss of 5 to 10 % improves
necroinflammtion
Metformin is not recommended as a
specific treatment for liver disease in
adults with NASH
32. Vitamin E 800IU/day improves liver
histology in biopsy proven NASH.
Considered as first line therapy in this
population
Statins should not be used specifically
to treat NASH. Can be used in
dyslipedemia.
UDCA is not recommended
33. Hypothyroidism and NASH
Journal of Clinical Gastroenterology:
October 2003 - Volume 37 - Issue 4 - pp 340-343
Liver, Pancreas, and Biliary Tract: Clinical Research
Is Hypothyroidism a Risk Factor for Non-Alcoholic
Steatohepatitis?
Liangpunsakul, Suthat MD; Chalasani, Naga MD
Abstract
Purpose: Thyroid hormones play an important role in the regulation of lipid and
carbohydrate metabolism, both of which are affected in patients with non-
alcoholic steatohepatitis (NASH). Anecdotally, we have observed that a number
of patients with NASH carried a diagnosis of hypothyroidism. However, it is
unknown if thyroid dysfunction plays any role in the pathogenesis of NASH. To
further investigate this observation, we conducted a case-control study to
determine the association between hypothyroidism and NASH
Conclusion: These data suggest that hypothyroidism
is associated with human NASH. Further research is
needed to confirm this finding and to understand its
implications.
34. Dig Dis Sci. 2012 Feb;57(2):528-34. doi: 10.1007/s10620-011-2006-2. Epub 2011 Dec 20.
Prevalence of hypothyroidism in nonalcoholic
fatty liver disease.
Pagadala MR, Zein CO, Dasarathy S, Yerian LM, Lopez R, McCullough AJ.
Source
Department of Gastroenterology and Hepatology, Cleveland Clinic Foundation, Cleveland, OH, USA.
Abstract
BACKGROUND:
A possible association between nonalcoholic fatty liver disease (NAFLD) and
hypothyroidism has been suggested. The recognized link between hypothyroidism
and elements of the metabolic syndrome may explain this association.
AIM:
The purpose of this study was to determine the prevalence of hypothyroidism in a
cohort of patients with NAFLD and analyze the potential factors associated with
hypothyroidism in this patient population.
CONCLUSIONS:
A higher prevalence of hypothyroidism was demonstrated in patients
with NAFLD compared to controls. Among subjects with NALFD, female
gender, increased BMI and history of abstinence from alcohol were
associated with hypothyroidism. Patients with hypothyroidism were also
more likely to have NASH
Hypothyroidism and NASH
35. Hypothyroidism and
anaemia
Anaemia is seen in 1/3 to ½ patients with
hypothyroidism
Usually mild to moderate , lower levels do
occur
Anaemia can be microcytic , normocytic ,
macrocytic. Aneamia of chronic disease is the
most common(normocytc normochromic) .
Microcytosis occurs in the setting of
mennorhagia
Macrocytosis can be seen even without
anaemia . Overt macrocytosis suggest
perinicious anaemia or folate deficiency