Non-alcohol Fatty Liver Disease ( NAFLD )

Non-alcohol Fatty Liver Disease refers to a wider range of conditions caused by the increased accumulation of fat, especially triglycerides, in the liver cells. A healthy liver should contain little or no fat.

Although the early form of the disease, also known as simple fatty liver or steatosis, isn’t harmful to the liver, it still can be a serious condition. If the fat builds up and gets worse, it can cause inflammation in the liver called non-alcoholic steatohepatitis – NASH. NASH can lead to fibrosis, eventually cirrhosis.

NAFLD is associated with obesity and insulin resistance, it is now represents the most common cause of chronic liver disease in the world.

Case 1

Date: March 2012

Patient: Male, age 54 yrs old

Clinical history: On 10/03/2012, the patient had an Ultrasound examination, which revealed he had Non-alchohol-Fatty Liver Disease (stage 1 - stage 2). He started our TCM remedy therapy, three month later. On 30/06/2012 his Ultrasound Scan showed the liver is normal, no NAFLD was detected. The patient is well today, maintaining a more healthy life-style.

Case 2

Date: July 2012

Patient: A boy, 14 yrs old

Clinical history: The patient was hospitalised due to proteinuria and hematuria in Dec. 2011. Renal biopsy, light microscopy revealed: 1) the present of neutrophils within few of glomerular capillaries; 2) moderate to severe proliferation of mesangium and mesangial matrix; 3) focal mesangial interposition; 4) focal proliferation of few glomerular endothelial cell; mild proliferation of interstitial fibrous connective tissue; 5) mild tubular atrophy; 6) Albumin and red blood cell casts; 7) a thickening of a few renal arteries. Immunofluorescence microscopy marked the presence of granular deposits of IgM (+), IgA(+), C3 (2+), Fibrinogen (+) along the glomerular capillaries wall, linear deposits of IgG (+) along the glomerular capillaries wall. Pathological diagnosis: Mesangial proliferative glomerulonephritis accompanied with segmental glomerular endothelial cell proliferation. Not excluding the possibility of membranoproliferative glomerulonephritis.

In the hospital, the patient was treated with Mycophenolate mofetil and steroids. At the end of six months of treatment, his proteinuria (2+) and hematuria (3+) persisted. His laboratory tests showed :

ALT   94 IU/L        (9 - 50 IU/L)

AST   65 IU/L        (15 - 40 IU/L)

TP   77.8 g/L        (65 - 85 g/L)

Albumin   51.0 g/L        (40 - 55 g/L)

Triglyceride   2.4 mmol/L        (0.28 - 1.8 mmol/L )

Total bilirubin   2.7 umol/L        (3.4 - 30 umol/L)

Indirect bilirubin   5.5 umol/L        (6.8 - 12 umol/L)

GGT   215 IU/L             (10 - 60 IU/L)

Blood sugar   7.9 mmol/L        (3.9 - 5.8 mmol/L)

The Ultrasound examination revealed a larger and "brilliant liver", his gallbladder and pancreas were normal. The diagnosed was given as Non-alcoholic Steatohepatitis.

When the patient came to our clinic in July 2012, he was severely fatigued, had nausea with vomiting and hypochondrial pain. Two month after taking our remedy therapy, his haematuria became negative, proteinuria decreased from 2+ to +. His laboratory test showed that his ALT decreased to 62 IU/L, GGT decreased to 94 IU/L, blood sugar decreased to 7.0 mmol/L. He was able to go to school again. Six months after our remedial therapy, his proteinuria became negative, his laboratory tests showed his ALT decreased to 61 IU/L, AST decreased to 51 IU/L, GGT to 70 IU/L, Triglyceride to 1.81 mmol/L within the normal range, blood sugar to 5.3 mmol/L within the normal range.

Currently, this patient lives a normal life and goes to school every day. He is continuing with our remedial treatment. Although we require that all processed food and soda drink be excluded from his daily diet, sometime it proves not so easy with the teenagers.