Mario J. Mc Loughlin
Is Increased Hepatic Echogenicity A Sign of Hepatic Disease?
Authors: Mario Jorge Mc Loughlin, MD (1), Juan Esteban Vicente Fanti, MD (2), Diego Enrique Mc Loughlin, MD (1). (Note: The addresses are old. For any communication, please use Dr Mario Mc Loughlin e-mail: email@example.com )
(1) Instituto Medico Alberdi. Hipólito Yrigoyen No 696. (3200) Concordia - Entre Rios - República Argentina
(2) Servicio de Medicina Nuclear y Ecografia - Hospital Militar Central - L. M. Campos 765 - Capital Federal - República Argentina. Reprint Address: Mario Jorge Mc Loughlin - Hipólito Yrigoyen No 696 - 3200 Concordia - Entre Rios - República Argentina.
Paracelsus 1988; 1: 5-8. © 1988 by Instal
Ninety five patients with increased hepatic echogenicity were studied and it was found that 86 of them (90.5 %) presented one or more of the following abnormalities: Hypertrigliceridemia, Hypercholesterolemia, Obesity or Carbohydrate Metabolic Disorder.
Besides, there was a significant difference (P < 0.001) between the thickness of preabdominal fat of these patients in reference to a control group.
The conclusion of the study is that the increased hepatic echogenicity is, in most cases, a hepatic sign of systemic disease and when it is found, the attention should be lead more to the patient's metabolic state than to hepatic histology, except in cases in which there are other signs of hepatic disease or when the patient is under hepatotoxic treatment.
INDEX TERMS: Liver, diseases - Liver, Fatty - Liver, US studies.
Some authors have found that both the increase of liver echogenicity or the hepatic attenuation of the sound are histologically correlated with fatty liver and not with hepatic fibrosis (1, 2).
On the other hand, although the relation between fatty liver and metabolic disease is well known (3), the majority of the studies about increased hepatic echogenicity have related this finding with hepatic histology but they have done scarce reference to the possible causes of this abnormality in adults, although Renschke made this relation in children (4).
Based in previous studies in which we found that 35/56 patients with increased hepatic echogenicity had personal or familial antecedents of diabetes mellitus (5) and other in which wefound that 77% of patients with increased liver echogenicity presented hypertrigliceridemia (6), we decided to do a study in order to establish whether the increase of hepatic echogenicity is an isolated abnormality or if it goes with other alterations that show that is a hepatic sign of a systemic disorder.
So, we studied the metabolic state of patients with increased hepatic echogenicity and compared the thickness of the preabdominal fat of them with a control group.
Materials and Methods
When in the habitual ultrasonographic work a patient with increased hepatic echogenicity was found, his preabdominal fat was measured and we asked him about personal or familial antecedents of diabetes mellitus.
His weight, height, age, sex and alcoholic habits were written down. After informed consent was obtained, fast glycemia and seric cholesterol and triglycerides levels were measured and, when fast glycemia was normal, an oral glucose tolerance test was added. One hundred patient met this criteria and besides, we measured the thickness of preabdominal fat in 88 patients with normal hepatic echogenicity without evidences of liver disease (Control group).
The hepatic images of both groups were interchanged between the authors without identifying the cases for a blind comparison. There was agreement between the authors in reference to hepatic echogenicity in 88 controls and in 95 patients with increased liver echogenicity who had not any sign of liver disease and the other patients (Five patients with increased hepatic echogenicity) were discarded because there was not agreement between the authorsrespecting to their hepatic echogenicity.
INCREASED HEPATIC ECHOGENICITY: It was considered so when the hepatic echogenicity was more alike to perirenal fat than to the renal parenchymal echogenicity. All the images were obtained using commercially available real time ultrasonic scanners, using 3.5 Mhz transducers.
PREABDOMINAL FAT: It was measured using water path, from skin to linea alba at the thickest point between xifoides and umbilicus.
ALCOHOL: As it was difficult to obtain a reliable information about the quantity of alcohol that patients had been taking, it was considered positive the habit of daily drinking without considering the quantity. The abstinence from alcohol or drinking it on rare occasions was considered negative.
CONTROL GROUP: Preabdominal fat was measured in patients with normal hepatic echogenicity who had not evidence of hepatic disease. As our patients with increased hepatic echogenicity were adults, all controls were 30 years old or more.
OBESITY: It was considered so when the body weight of the patient was over 20% above mean ideal body weight (15).
ULTRASONOGRAPHIC EQUIPMENT USED: Ultrascan 500 (Pie Data Medical, Netherlands) 3,5 linear array transducer; Combison 111 (Kretz) 3,0 MHz mechanical sector transducer.
FIGURE: 1 - NORMAL HEPATIC ECHOGENICITY (Sagittal scan). The hepatic echogenicity is more similar to renal parenchyma than to the perirenal fat echogenicity. (L = liver; K = kidney; Arrowhead: perirenal fat).
FIGURE: 2 - INCREASED HEPATIC ECHOGENICITY (Sagittal scan). The hepatic echogenicity is more similar to perirenal fat than to the renal parenchymal echogenicity. (L = liver. K = kidney; Arrowhead: perirenal fat).
FIGURE: 3 - MEASUREMENT OF PREABDOMINAL FAT. (a: Sagittal scan; b: Transverse scan). The preabdominal fat is measured in the thickest point between skin and linea alba. (S = Skin; Arrowhead = linea alba; PAF = Preabdominal fat; RAM = Rectus abdominus muscle; Dashed line: Preabdominal fat measurement).
We have studied 95 patients with increased hepatic echogenicity (55 males and 40 females) with a mean age of 51.81 years (range: 26-75years) and 88 controls (50 males and 38 females) with a mean age of 51.04 years (range: 30-81 years).
There was found that 55/95 (57.8%) of patients with increased hepatic echogenicity were obese and 33/95 (34.7%) used to drink alcohol.
In 55/95 patients with abnormal liver echogenicity there was familial antecedents of diabetes mellitus, 20/95 (21%) had fast hyperglycemia and 37/75 (49.3%) presented an abnormal oralglucose tolerance test.
Hypertrigliceridemia was found in 69 patients (71.5%) and 47 (49.4%) had hypercholesterolemia.
The preabdominal fat in patients with increased hepatic echogenicity was 24.72 + 0.75 mm thick (range: 11-41 mm) and in control group was (17.34 + 0.70 mm (range: 5-39 mm) (P < 0.00 1 ).
On the whole, 90.5% (86/95) of patients with increased hepatic echogenicity presented one or more of the following abnormalities: Hypertrigliceridemia, Hypercholesterolemia, Obesity or Carbohydrate Metabolic Disorder.
Hepatic biopsy was not performed in our patients because no one of them had medical reasons that justified this procedure.
The first reports about increased hepatic echogenicity had related this finding with fatty liver, cirrhosis, chronic hepatitis, alcoholic hepatitis and other diffuse hepatic diseases (7-12), but new reports on the subject suggested that both hepatic echogenicity and attenuation of the sound by the liver are related with the amount of hepatic fat. Therefore, the increased hepatic echogenicity seems to be related with fatty liver and not with hepatic fibrosis (1,2).
One of the most important problems hepatic echogenicity presents is that there is not yet an objective method of measurement of hepatic brightness and the appreciation of it is still subjective, though the measure of attenuation of the sound seems to be a promising possibility (2,24).
Before this work we had intended to do a computed evaluation of the echo amplitude using histogram, but we discarded this method because the same operator with the same image obtained different results, which is in coincidence with other author's experience (13). For this reason, we have chosen to make the comparisonof hepatic echogenicity with renal and perirenal fat brightness, considering that the liver echogenicity is increased when it is more similar to the perirenal fat echogenicity than to the renal parenchymal echogenicity. To avoid subjectivity, we classified the patients in a blind way and those in which there was no agreement between the authors were discarded.
As radiological abnormalities of kidney have been described in diabetic patients (mainly increase of the size)( 14), we cannot be sure that the difference of echogenicity between kidney and liver that was observed in our patients was not increased by a diminution of renal echogenicity, but it seems not probable because the liver itself looked hyperechoic.
In spite of including patients with slight increase of hepatic echogenicity, in the daily ultrasonographic work we have seen patients with adult onset diabetes who had normal hepatic
ecogenicity and besides, four of our patients with increased liver echogenicity have normalized it after dietary treatment. This suggests that increased hepatic echogenicity may change andthis is correlative with the reversibility that some cases of fatty liver present(2).
In 86/95 of our patients there was one or more of the following abnormalities: Hypertrigliceridemia, Hypercholesterolemia, Obesity or Carbohydrate Metabolic Disorder and as there is a close relation between these abnormalities, we think it is reasonably to consider them all as a whole (Prof F. Puchulu, personal communication).
A significant difference was found between the thickness of the preabdominal fat of patients with increased hepatic echogenicity in reference to a control group (p<0.001) which also suggests a systemic disorder. However, there was not a direct relation between the thickness of preabdominal fat and the hepatic echogenicity because we had obese patients with normal hepatic echogenicity, including one patient whose preabdominal fat thickness was 39 mm. This can be explained because this patient had the "Lifelong obesity type" while patients with increased hepatic echogenicity had the "Adult onset obesity type".
Although obesity is a well established cause of fatty liver and peripheral resistance to insulin action (16), the distribution of body fat influences resistance to insulin and the risk of non insulin dependent diabetes mellitus (NIDDM)(17-20) and, as example, Mexican Americans compared with non Hispanic whites, have a higher prevalence of obesity (21,22), a more centralized distribution of fat and three to five times the prevalence of NIDDM(21,22). The excess of NIDDM persists even after their grater overall and more centralized adiposity are taken into account (18). Mexican Americans were found to have significant greater areas under the serum insulin curve than non Hispanic whites, which suggests that, like other populations. at high risk for NIDDM, Mexican Americans have more hyperinsulinemia than can be accounted by their adiposity(23).
So, the obesity itself doesn't seem to be a direct cause of increased hepatic echogenicity, and we think that increased hepatic echogenicity is produced by a metabolic disease which frequently causes obesity too.
1. The frequency with which increased hepatic echogenicity is found on routine ultrasonographic work (we have observed it in nearly 5% of the abdominal echographic studies).
2. The relation of this finding with systemic disorders.
3. The difference between the thickness of preabdominal fat of patients with increased hepatic echogenicity in reference to a control group.
4. The reports that have related increased hepatic echogenicity with fatty liver and not with hepatic fibrosis (1,2).
5. The change of hepatic echogenicity in some cases,
we think that increased hepatic echogenicity is, in most cases, a hepatic manifestation (Probably Fatty Liver) of a systemic disorder more than a sign of hepatic disease, except in cases in which there are other signs of hepatic disease or the patient is under hepatotoxic treatment.
As we have not made follow-up of patients (except some cases who return for echographic control), we don't know if increased hepatic echogenicity precedes or follow the other abnormalities or if periodic evaluation of hepatic echogenicity can be used for the evaluation of treatment success in patients with metabolic disorder as glycosided hemoglobin (Hb A1c) is used to follow-up diabetic patients (In the case of an objective way of measurement of hepatic echogenicity could be found).
1.- Sandford N, Walsh P, Mattis C, Beddeley H, Powell LW. Is Ultrasonography Useful in the assessment of Diffuse Parenchymal Liver Disease? Gastroenterology 1985; 89: 186-191.
Z.- Taylor KJW, Riely CA, Hmnmers L, et al: Quantitative U.S. attenuation in normal liver and in patients with diffuse liver disease. Importance of fat. Radiology 1986; 160: 65-71.
3.- Jeffries GH: Diseases of the liver. In Beeson PB, Mc Dermott W, Wyngaarden JB, ed: Cecil Textbook of Medicine. Vol 11, XVth ed. Philadelphia. WB Sanders Co. 1979; 1660-1661.
4.- Henschke CI, Golman H, Littlewood R: The hyperechogenic liver in children. Cause and sonographic appearance. AJR 1982; 138: 841-846.
5.- Mc Loughlin MJ, Fanti JEV. Higado ecogenico y Diabetes tipo II. Boletin del Instituto Alberdi 1984; 2: 12-16.
6.- Mc Loughlin MJ, Fanti JEV. Incremento sutil de la ecogenicidad hepatica como signo de enfermedad metabólica. Boletin del Instituto Alberdi 1985; 4: 17-22.
7.- Mountford RA, Wells PINT. Ultrasonic Liver Scanning: The A scan in the Normal and Cirrhosis. Phys Med Biol 1972; 17: 14-25.
8.- Taylor KJW Carpenter DA, Hill CR, Mc Cready NR: Gray Scale Ultrasound Image. The anatomy and pathology of the liver. Radiology 1976; 119: 415-423.
9.- Birnholz JC: Ultrasound evaluation of diffuse liver disease In Taylor KJW, ed: Diagnostic ultrasound in gastrointestinal disease. London. Churchill and Livingstone. 1979; 23-33.
10.- Needleman L, Kurtz AB, Rifkin MD, Cooper HS, Pasto ME, Goldberg BB : Sonography of Benign Diffuse Liver Disease. Accuracy of pattern recognition and grading. AJR 1986; 146: 1011-1015.
11.- Joseph AEA, Dewbury KC, Mc Guire PE: Ultrasound in the detection of chronic liver disease (The bright liver). Br J Radiol 1979; 52: 184-188.
12.- Gosink BB, Lemon SK, Scheible W, Leopold GR: Accuracy of ultrasonography in diagnosis of hepatocellular disease. AJR 1979; 133: 19-23
13.- Rosenfield AT Taylor KJW, Jaffe CC: Clinical applications of ultrasound tissue characterization. Radiol Clin N Am 1980; 18: 31-58.
14.- Segel MC, Lecky JW, Slasky BS : Diabetes Mellitus: The predominant cause of bilateral renal enlargement. Radiology 1984; 153: 341-342.
15.- Harrison A, Wintrobe M, Thorn, Admns R : Medicina Interna. Ed IV (Spanish). Prensa Medica Mexicana, Mexico D.F 1983, Cuadro 48.1. pag. 302.
16.- Olefsky JM. Kulterman OG: Mechanism of insulin resistance in obesity and non insulin dependent (type II) diabetes. Am J Med 1981: 70: 151-158.
17 - Feldman R, Sender AJ, Sigelaub AB; Difference in diabetic and non diabetic fat distribution and patterns by skinfolds measurements. Diabetes 1969: 18: 478-486.
18.- Haffner SM, Stern MP, Hazuda HP, et al: Role of obesity and fat distribution in NIDMM in Mexican Americans and non Hispanic whites. Diabetes Care 1986: 9: 153-161.
19.- Krotkiewski M, Bjontorp P Sjostrom L, Smith V. Impact of obesity on metabolic in men and women: Importance of regional adipose tissue distribution. J Clin Investigation 1983: 72: 1150-1152.
20.- Kissebah AH, Vydelingum N, Murray R, et al: Relation of body fat distribution to metabolic complications of obesity. J Clin Endocrinol Metab 1982: 54: 254-260.
21.- Stern MP Gaskin SP, Hazuda HP, et al: Does Obesity explain excess prevalence of diabetes among Mexicans Americans? Results of the San Antonio Heart Study. Diabetologia 1983: 24: 272-277
22.- Gardner LI Jr, Stern MP, Haffner SM, et al: Prevalence of diabetes in Mexican Americans: Relationship to percent gene pool derived from native American source. Diabetes 1984: 33: 86-92.
23.- Haffner SM, Stern MP, Hazuda HP, et al: Hyperinsulinemia in a population at high risk for NIDDM. N Engl J Med 1986: 315: 220-224.
24.- Garra BS, Isana MF Shawker TH, Russel MA : Quantitative estimation of liver attenuation and echogenicity: Normal state versus diffuse liver disease. Radiology 1987: 162: 61-67
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