Alcohol is a most frequent cause of liver disease in western countries. Alcoholic hepatitis is observed in approximately 20% of heavy drinkers. Acute alcoholic hepatitis (AH) is associated with mortality as high as 50%.Up to 40% of patient with severe alcoholic hepatitis die within 6 months after the onset of the clinical syndrome. Identifying individuals with a high mortality risk is crucial in the management of acute alcoholic hepatitis. We observed a patients with acute alcoholic hepatitis tend to have an increased level of monocytes.
47-year-old male with a significant history of alcohol abuse for 30 years presented with confusion, generalized shaking, and tremors for 4 days was admitted to the hospital. The patient was hospitalized 6 months ago for acute alcoholic hepatitis. Physical examination: Bp 140/80mmHg, Ultrasound of Abdomen showed hepatomegaly with enlarged liver measuring 19.1 cm in the midclavicular line and hepatic steatosis and gallbladder sludge without evidence of wall thickening or pericystic fluid. CT of abdomen Suspected fatty infiltration of the liver. Patient had ammonia level of 56 -58. His MELD score was between 52 in which the alcoholic hepatitis was diagnosed. The patient was treated with Ativan, Chlordiazepoxide, Thiamine, folic acid, Mulativitamin, and lactulose. After patient was treated for 7 days, Symptoms had been well controlled, and all of tests went to back normal range. Table1 shows clinical data of current and previous admission.
Alcoholics develop acute hepatitis as an inflammatory reaction to the cells affected by fatty change. Diagnosis of alcoholic hepatitis based on clinical symptoms and laboratory finding alone including elevated AST/ALT (but may < 300 IU/mL), AST>ALT of 2, Total serum bilirubin > 5mg/deciliter, elevated INR, thrombocytopenia, and hypoalbuminimia, (cirrhosis). Leukocytosis with neutophilic predominance has been reported to correlates with degree of injury. As a feature of alcoholic liver disease, monocytosis was first reported on 1983, however, the mechanism mediates this clinical feature has been unclear. Recently data has been shown that activated monocytes have been postulated to play an important role in the pathogenesis of alcoholic liver disease (ALD), in which can produce Interleukin-1 (IL-1) induces interleukin-6 (IL-6) production during acute alcoholic liver injury phase reactant. The number of monocytes, one of the most important components of the inflammatory process in ALD maybe as an independent marker that can be utilized to determine the disease severity and predict outcome of the patients.
Our result suggests that monocytosis is associated with acute alcoholic hepatitis (Table 1). Further research may provide us with a better understanding of the clinical scenario and help elucidate the best prevention and treatment options of alcohol–related liver disease.
Monocytosis is associated with acute alcoholic hepatitis
| Clinical data . | Current Hospitalized . | Previous Hospitalized . | ||
|---|---|---|---|---|
| . | Admission . | Discharge . | Admission . | Discharge . |
| SCOT ( 0-37U/L) | 380 | 35 | 380 | 38 |
| SGPT (0-40U/L) | 150 | 42 | 150 | 40 |
| Plasma ammonia(10-39 Umol) | 60 | 20 | 65 | 18 |
| Serum Total Bilirubin (0-1.0mg/dl | 4 | 1.1 | 4 | 1.2 |
| Serum direct bilirubin (<0.2mg/dl) | 2.5 | 0.3 | 2.5 | 0.4 |
| Monocytes count (<13%) | 20% | 8% | 25% | 5% |
| Clinical data . | Current Hospitalized . | Previous Hospitalized . | ||
|---|---|---|---|---|
| . | Admission . | Discharge . | Admission . | Discharge . |
| SCOT ( 0-37U/L) | 380 | 35 | 380 | 38 |
| SGPT (0-40U/L) | 150 | 42 | 150 | 40 |
| Plasma ammonia(10-39 Umol) | 60 | 20 | 65 | 18 |
| Serum Total Bilirubin (0-1.0mg/dl | 4 | 1.1 | 4 | 1.2 |
| Serum direct bilirubin (<0.2mg/dl) | 2.5 | 0.3 | 2.5 | 0.4 |
| Monocytes count (<13%) | 20% | 8% | 25% | 5% |
No relevant conflicts of interest to declare.
