Focal Liver Lesions that can be safely managed and monitored at the primary care setting (Part 3)
Focal nodular hyperplasia (FNH)
FNH is a rather common (0.3-3%), usually asymptomatic liver lesion.(9) It was postulated to be caused by injury to the portal tract resulting in arterial to venous shunts, which in turn causes hyperperfusion and oxidative stress, triggering a response from hepatic stellate cells that produce the typical central scar.
On CT examination a typical finding is a ‘spoke- wheel” central scar; it should be homogeneously hyperdense during arterial phase and hypo- or isodense during portovenous phase. (3) If the diagnosis could not firmly established after a CT scan, especially if it could not be differentiated from hepatocellular adenoma, referral to a specialist is recommended for further opinion. MRI would usually provide more information but rarely, biopsy alone could differentiate the two conditions.
Since FNH are mostly asymptomatic and stable, surgical treatment is seldom indicated. Malignant transformation and rupture are extremely rare (those could be adenomas mistaken as FNH to begin with). Females taking OC pills with no intention to stop treatment are advised to undergo annual USG for 2-3 years, other patients with a firm diagnosis of FNH do not need regular imaging as follow up.
Hepatic haemangioma is the most common benign liver tumour, with prevalence of 0.4-20% reported. (4) It is a benign vascular liver lesion of unknown etiology. Females (5:1) are much more commonly affected though a direct causal relationship with female hormone could not be established. Most are asymptomatic unless large in size but rarely, a giant haemangioma could cause consumptive coagulopathy and disseminated intravascular coagulation.
USG by an experienced ultrasonographer with the finding of a hyperechoic liver mass with well-defined rim and intranodular vessels is considered diagnostic and reliable; CT examination is only indicated if the USG findings are ambiguous—classical features was peripheral nodular enhancement and progressive centripetal fill-in. Owing to its vascular nature, biopsy is contraindicated.
Surgical treatment for haemangioma is rarely necessary, but specialist referral should be made if the lesion was large and asymptomatic or growing in size. Small haemangioma with classical features do not need regular imaging for monitoring.
- Smith-Bindman R, Miglioretto DI, Johnson E et al. Use of diagnostic imaging studies and associated radiation exposure for patients enrolled in large integrated health care systems. 1996-2010. JAMA 2012;307:2004-9.
- Lee KH, O'Malley ME, Haider MA, Hanbidge A.AJR Am J Roentgenol. 2004 Mar;182(3):643-9. Triple-phase MDCT of hepatocellular carcinoma.
- Marrero JA, Ahn J, Rajender Reddy K. ACG clinical guideline: the diagnosis and management of focal liver lesions. Am J Gastroenterol. 2014; 109(9): 1328-47
- Shaked O, Siegelman ES, Olthoff K et al. Biologic and clinical features of benign solid and cystic lesions of the liver. Clini Gastroenterol Hepatol 2011;9:547-62
- Hernandez- Nieto L, Brugeuera M, Bombi J et al. Benign liver-cell adenoma associated with long-term administration of an androgenic- anabolic steroid(methandienone). Cnacer 1977;40:1761-4
- Labrune P, Trioche P, Duvaltier I et al. Hepatocellular adenomas in glycogen storage disease type I and III: a series of 43 patients and review of the literature. J Paediatr Gastroenterol Nutr 1997;24:276-9
- Bunchorntavakul C, Bahirwani R, Drazek D et al. Clinical features and natural history of hepatocellular adenomas: the impact of obesity. Aliment Pharmacol Ther 2011;34:664-74
- Bioulac-Sage P, Taouji S, Possenti L et al. Hepatocellular adenoma subtypes:the impact of overweight and obesity. Liver Int 2012;32:1217-21
- Karhunen PJ. Benign hepatic tumours and tumour like condition in men. C Clin Pathol 1986;39:183-9
- Oto A, Tamm EP, Szklaruk J. Multidetector row CT of the liver. Radiol Clin North Am 2005;43:827-48
The above information is provided by Dr Chik Hsia Ying, Barbara