Liver resection for non-cirrhotic hepatocellular carcinoma in South African patients.

BACKGROUND: We describe the clinicopathologic features and outcome of South African patients who have undergone hepatic resection for hepatocellular carcinoma (HCC) arising in a non-cirrhotic liver. METHODS: We utilised the prospective liver resection database in the Surgical Gastroenterology Unit at Groote Schuur Hospital, Cape Town, to identify all patients who underwent surgery for HCC with non-cirrhotic liver parenchyma between 1990 and 2008. RESULTS: Twenty-two patients (10 men, 12 women, 3 black, 19 white, median age 47 years, range 21-79 years) underwent surgery for non-cirrhotic HCC. Sixteen patients had non-fibrolamellar HCC (Group 1); 6 patients had fibrolamellar HCC (Group 2). Group 1 had a median age of 55 years, and 6 (38%) were men; group 2 had a median age of 21 years, and 5 (83%) were men. Most patients had a solitary tumour at diagnosis; median largest tumour diameters in Groups 1 and 2 were 10 cm (range 4-21) and 12 cm (range 4-17), respectively. Patients in Group 1 underwent extended right hepatectomy (N=3), right hepatectomy (N=3), left hepatectomy (N=3), partial hepatectomy (N=7), cholecystectomy (N=6), and appendicectomy (N=1). Patients in Group 2 underwent extended right hepatectomy (N=1), right hepatectomy (N=1), left hepatectomy (N=2), segmentectomy (N=2), and portal lymphadenectomy (N=3). Recurrence rates in Groups 1, 2, and overall were 81%, 100% and 86%, respectively. Median overall survival was 46 months, with 1-, 3-, and 5-year survival rates of 95%, 59% and 45%, respectively. In Group 1, median survival was 39 months, with 1-, 3-, and 5-year survival rates of 100%, 56% and 38% respectively. In Group 2, median survival was 61 months, with 1-, 3-, and 5-year survival rates of 83%, 67% and 67%, respectively. CONCLUSION: Despite aggressive surgical resection, HCC arising in normal liver parenchyma has a high recurrence rate and an ultimately poor outcome. This finding is similar to both the recent international experience of non-cirrhotic HCC and local experience of fibrolamellar HCC.

Warfarin-induced skin necrosis in HIV-1-infected patients with tuberculosis and venous thrombosis.

BACKGROUND: At the turn of the century, only 300 cases of warfarin-induced skin necrosis (WISN) had been reported. WISN is a rare but potentially fatal complication of warfarin therapy. There are no published reports of WISN occurring in patients with HIV-1 infection or tuberculosis (TB). METHODS: We retrospectively reviewed cases of WISN presenting from April 2005 to July 2008 at a referral hospital in Cape Town, South Africa. RESULTS: Six cases of WISN occurred in 973 patients receiving warfarin therapy for venous thrombosis (0.62%, 95% CI 0.25 - 1.37%). All 6 cases occurred in HIV-1-infected women (median age 30 years, range 27 - 42) with microbiologically confirmed TB and venous thrombosis. All were profoundly immunosuppressed (median CD4+ count at TB diagnosis 49 cells/microl, interquartile range 23 - 170). Of the 3 patients receiving combination antiretroviral therapy, 2 had TB-IRIS (immune reconstitution inflammatory syndrome). The median interval from initiation of antituberculosis treatment to venous thrombosis was 37 days (range 0 - 150). The median duration of parallel heparin and warfarin therapy was 2 days (range 1 - 6). WISN manifested 6 days (range 4 - 8) after initiation of warfarin therapy. The international normalised ratio (INR) at WISN onset was supra-therapeutic, median 6.2 (range 3.8 - 6.6). Sites of WISN included breasts, buttocks and thighs. Four of 6 WISN sites were secondarily infected with drug-resistant nosocomial bacteria (methicillin-resistant Staphylococcus aureus (MRSA), Acinetobacter, extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli and Klebsiella pneumoniae) 17 - 37 days after WISN onset. In 4 patients, the median interval from WISN onset to death was 43 days (range 25 - 45). One of the 2 patients who survived underwent bilateral mastectomies and extensive skin grafting at a specialist centre. CONCLUSION: This is one of the largest case series of WISN. We report a novel clinical entity: WISN in HIV-1 infected patients with TB and venous thrombosis. The occurrence of 6 WISN cases in a 40-month period may be attributed to (i) hypercoagulability, secondary to HIV-1 and TB: (ii) short concurrent heparin and warfarin therapy; and (iii) high loading doses of warfarin. Active prevention and appropriate management of WISN are likely to improve the dire morbidity and mortality of this unusual condition.