Chronic splenomegaly in Nairobi, Kenya. II. Portal hypertension.

Eighty-five patients with chronic splenomegaly and proven oesophageal varices were studied at Kenyatta National Hospital, Nairobi. The major defined groups were hepatosplenic schistosomiasis (24%), cirrhosis (20%) and portal vein occlusion (11%). Hyper-reactive malarial splenomegaly (tropical splenomegaly syndrome) was considered as the cause of oesophageal varices in only one patient. In 26% of cases liver biopsy was non-diagnostic and the extrahepatic portal vein was demonstrated radiologically to be patent. Such patients were thought to be suffering from idiopathic portal hypertension, not previously described elsewhere in Africa. Hepatitis B surface antigen was detected in 12% of controls and in 58% of patients with cirrhosis (p less than 0.001). Some serological marker of previous hepatitis B virus infection was present in 92% of patients with cirrhosis and in 79% of controls. Kamba patients from Machakos and Kitui Districts were significantly more prevalent than expected among these 85 cases of portal hypertension.

Hepatitis delta virus infection in Kenya. Its geographic and tribal distribution.

In 1982-1984, an epidemiologic survey of the prevalence of hepatitis B virus surface antigen (HBsAg) in circulating blood (HBs-antigenemia) and of hepatitis delta virus infection was performed in Kenya. The distributions of hepatitis B virus and the delta virus were shown to be very variable. In southern Kenya, only two of 202 sera from HBsAg-positive individuals with no known liver disease and none from 123 HBsAg-positive patients with hepatitis B-related liver disease were positive for delta antibody. In contrast, in northern Kenya, there was an overall prevalence of delta antibody in healthy individuals of 31%. The distribution of delta infection is discussed in relation to lifestyle, ethnic group, and geographic area.

Integration of HBV-DNA may not be a prerequisite for the maintenance of the state of malignant transformation. An analysis of 110 liver biopsies.

Hundred and ten liver biopsy specimens from various parts of the world were examined for episomal and integrated HBV-DNA sequences. In 54 patients with HBsAg chronic liver disease episomal HBV-DNA was found in 83% of HBeAg-positive patients, compared to only 22% of patients with anti-HBe. Furthermore episomal HBV-DNA in the latter predominated among the Asians. Integrated HBV-DNA was found only in 5.5% of HBeAg-positive patients but in 16.5% of patients with anti-HBe. In 28 HBsAg-positive patients with hepatoma, episomal HBV-DNA was found in 50% of HBeAg-positive patients but in only 11% of anti-HBe patients. Conversely integrated sequences were less common (25%) in HBe-Ag-positive patients than in anti-HBe patients (50%), giving an overall incidence of integration in this group of 45%. No episomal, and only one case of integrated sequences of HBV-DNA, could be detected among 10 patients with HBsAg-negative hepatoma. In addition neither episomal nor integrated HBV-DNA could be detected in 18 patients with non-HBV-related liver disease. Our data suggests that stable integration of HBV-DNA into the host's genome is not necessarily a prerequisite for the maintenance of the state of malignant transformation but may be necessary for its initiation. Alternatively, the detection of integrated HBV-DNA may represent a 'snap shot' of a random integration event amplified by clonal expansion promoted by other factors.

Aetiology of acute sporadic hepatitis in adults in Kenya.

Markers for acute hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis non-A, non-B (HNANB) infections were examined in the sera of 94 patients presenting with acute hepatitis in Kenya. Hepatitis B virus was responsible for 70% of cases, HNANB for 18%, and HAV for only 12%. The use of an IgM anti-HBc assay increased the rate of diagnosis of acute HBV infection, thereby reducing the proportion of cases designated as NANB.

Portal hypertension in Nairobi, Kenya.

Previous reports have suggested that idiopathic portal hypertension, a condition quite distinct from tropical splenomegaly syndrome, occurs in Kenya. In the present study patients with oesophageal varices were allocated to diagnostic groups on the basis of liver histology and results of splenoportovenography , and these groups were then compared for prevalence of hepatitis B markers, immunoglobulin levels and results of enzyme-linked immunosorbant assay (ELISA) for S. mansoni infection. 85 patients with oesophageal varices were studied. 29.4% had histological evidence of Schistosoma mansoni infection, 20% had cirrhosis and in 25.9% liver histology was non-diagnostic and the portal vein was radiologically shown to be patent. A comparison of clinical findings, serological data and parasitological investigations suggested that this latter group was a distinct one, and did no result from failure of histological diagnosis of cirrhosis or schistosomiasis. It is likely that these patients had idiopathic portal hypertension. In 82 normal controls, the carrier rate of hepatitis B surface antigen (HBsAg) was 12.2%, 59.8% had antibody to HBsAg (anti-HBs) and 7.3% showed antibody to core antigen (anti-HBc) as the only viral marker. 58.3% of the cirrhotics and 26.7% of patients with probable idiopathic portal hypertension were HbsAg positive. The implications of these results, and limited data on hepatitis Be antigen and antibody are discussed.

Esophageal varices in Nairobi, Kenya: a study of 68 cases.

Sixty-eight patients with proven esophageal varices wer studied at Kenyatta National Hospital, Nairobi, Kenya. Of these patients, 29.4% had schistosomal portal hypertension, 22.1% cirrhosis and only 8.8% extrahepatic portal vein occlusion. One quarter of the patients had a normal liver biopsy and extrahepatic portal vein that was demonstrated to be patent. Problems relating to liver biopsy sampling resulting in underdiagnosis of specific causes of esophageal varices such as schistosomiasis are discussed. We argue that many of these patients were likely to be suffering from idiopathic portal hypertension, a condition apparently not previously recognized in Africa. Of this last group, 70.6% had suffered gastrointestinal bleeding, as had 50% of the patients with schistosomiasis. Together these two groups accounted for three-quarters of all patients who had bled. The detection of eggs of Schistosoma mansoni in stool and/or rectal snip correlated well with liver biopsy findings in both a positive and negative sense. Only 18% of patients with negative stools and snips had evidence of schistosomiasis in the liver, and positive stools or snips were found in only 14.6% of patients without schistosomal liver involvement. Of the patients in the study, 50% were of the Kamba tribe, although only 12.9% of all medical admissions to the hospital were Kamba (P less than 0.01). Luo patients were significantly more frequent within the group with schistosomiasis (P less than 0.02). Esophageal varices were attributed to tropical splenomegaly syndrome in only one patient. The implications of our results are discussed and our findings are compared with previous work from East Africa.