Clinical Cases

A 45-year-old man goes to his general practitioner due to reduced appetite and weight loss

A 45-year-old man goes to his general practitioner due to reduced appetite and weight loss 1 Medicine Made Easy Clinical Cases
A man of 45 consults his general practitioner (GP) with a 6-month history of reduced appetite and weight loss, from 78 to 71 kg. During the last 3 months, he has had intermittent nausea, especially in the mornings, and in the last 3 months, the morning nausea has been accompanied by vomiting on several occasions. For 1 month he has noted swelling of his ankles.

Despite his weight loss, he has recently noticed his trousers getting tighter. He has had no abdominal pain. He has no relevant past history and knows no family history as he was adopted. He takes no medication. From the age of 18 he has smoked 5–6 cigarettes daily and drunk 15–20 units of alcohol per week. He has been a chef all his working life, without exception in fashionable restaurants. He now lives alone as his wife left him 1 year ago.


He has plethoric features. There is pitting edema of his ankles. He appears to have lost weight from his limbs, but not his trunk. He has nine spider naevi on his upper trunk. His pulse is normal and the rate is 92/min. His jugular venous pressure (JVP) is not raised and his blood pressure is 146/84 mmHg. The cardiovascular and respiratory systems are normal. The abdomen is distended. He has no palpable masses but there is shifting dullness and a fluid thrill.

  • Haemoglobin – 12.6 g/dL (13.3–17.7 g/dL)
  • Mean corpuscular volume (MCV) – 107 fL (80–99 fL)
  • White cell count – 10.2 x 10^9/L (3.9–10.6 x 10^9/L)
  • Platelets – 321 x 10^9/L (150–440 x 10^9/L)
  • Sodium – 131 mmol/L (135–145 mmol/L)
  • Potassium – 4.2 mmol/L (3.5–5.0 mmol/L)
  • Urea – 2.2 mmol/L (2.5–6.7 mmol/L)
  • Creatinine – 101 μmol/L (70–120 μmol/L)
  • Calcium – 2.44 mmol/L (2.12–2.65 mmol/L)
  • Phosphate – 1.2 mmol/L (0.8–1.45 mmol/L)
  • Total protein – 48 g/L (60–80 g/L)
  • Albumin – 26 g/L (35–50 g/L)
  • Bilirubin – 25 mmol/L (3–17 mmol/L)
  • Alanine transaminase – 276 IU/L (5–35 IU/L)
  • Gamma-glutamyl transaminase – 873 IU/L (11–51 IU/L)
  • Alkaline phosphatase – 351 IU/L (30–300 IU/L)
  • Urinalysis: no protein and no blood


  • What is the diagnosis?
  • How would you manage this patient?


This man has abnormal liver function tests which indicate hepatic failure; the hypoproteinaemia has caused the ascites and ankle swelling. The number of spider naevi is more than the accepted normal of three. The cause is likely to be alcohol as it is a common cause of this problem, he is at increased risk through his work in the catering business. His symptoms of morning nausea and vomiting are typical, and this would account for his cushingoid appearance (alcohol increases adrenocorticotrophic hormone (ACTH) secretion) and the macrocytosis on the blood film (due to dietary folate deficiency and direct toxic action on the bone marrow by alcohol). However, his alcohol intake is too low to be consistent with the diagnosis of alcoholic liver disease. When the provisional diagnosis is discussed with him though, he eventually admits that his alcohol intake has been at least 40–50 units per week for the last 20 years and has increased further during the last year after his marriage had ended, the reason for this being his drinking.

The slight reductions in the sodium and urea reflect a chronic reduced intake of salt and protein; the rise in bilirubin is insufficient to cause jaundice.

Further investigations are the measurement of hepatitis viral serology, which was negative, and an ultrasound of the abdomen. This showed a slight reduction in liver size, and an increase in splenic length of 2–3 cm. There was no evidence of a hepatoma. These findings indicate that portal hypertension has developed. A liver biopsy, performed to confirm the diagnosis, assess the degree of histological damage and exclude other pathology, showed changes of cirrhosis.

The crucial aim in management is to impress upon the patient the necessity to stop drinking alcohol, in view of the degree of liver damage, the presumed portal hypertension and the risk of esophageal varices and bleeding, and to effect this by his attending an alcohol addiction unit. In the short term, he should also improve his diet to increase his protein intake. Diuretics could be used to reduce his edema, but it should be remembered that they could cause postural hypotension more easily against this background.

His attendance at the addiction unit was fitful, he continued to drink heavily and he died 3 years later as a result of a second bleed from esophageal varices.

Key points

  • Patients who drink excessive amounts of alcohol will often disguise this fact in their history.
  • Alcoholic liver disease has a poor prognosis if the alcohol intake is not terminated.

Source: 100 Cases in Clinical Medicine

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