Duodenal ulcer in the Sudan. Clinical features and treatment with H2 blockers.

In a prospective study, 168 Sudanese patients with endoscopically proven duodenal ulcer were studied. The mean age was 36 (SD 3) years and the male:female ratio was 3:1. Most of the patients belonged to the lower social class (class 3) and the chief presenting features were long standing epigastric pain (72.6%), heartburn (66.4%) and upper gastrointestinal bleeding (45.5%). The endoscopic appearance of the ulcers was severe in 40% of patients; this, together with the genetic and distinct dietary factors, may have contributed to the low healing rates following treatment with H2 receptor blockers.

Diagnosis of pathologically confirmed Symmers' periportal fibrosis by ultrasonography: a prospective blinded study.

Symmers' periportal fibrosis of the liver is the major cause of morbidity and mortality in Schistosoma mansoni infection. The diagnosis is best established definitively by a wedge biopsy of the liver. The ability of abdominal ultrasonography to diagnose this condition was prospectively compared with two independent pathological examinations of wedge biopsies of the liver. Both pathologists and the ultrasonographer were unaware of the clinical diagnosis and each other's findings. Twenty-eight of 41 patients had Symmers' fibrosis by pathological examination and all were diagnosed correctly by ultrasonography prior to surgery. Symmers' fibrosis was not diagnosed by ultrasound in any of 10 patients without Symmers' fibrosis on biopsy. In 3 patients the diagnosis of Symmers' fibrosis was uncertain because the pathologists disagreed as to its presence. These results confirm the findings of previous studies and establish that ultrasonography is at least as sensitive as wedge biopsy in diagnosing Symmers' fibrosis.

Propranolol disposition in patients with hepatosplenic schistosomiasis.

Eight Sudanese patients with hepatosplenic schistosomiasis and seven Sudanese controls were administered a single oral dose of long acting (LA), propranolol 160 mg; blood propranolol levels were measured at regular intervals for 12 h using g.l.c. In patients with hepatosplenic schistosomiasis, propranolol blood concentrations were greater (P less than 0.05) at all time intervals, Cmax 63.5 (29-143) ng ml-1 (median and range) than controls Cmax 23 (12-37) ng ml-1. Median AUC0-12 was also greater (P less than 0.05) (533 and 218 ng ml-1 h respectively), tmax were not significantly different. In patients and controls prior to treatment, standing heart rate (77.5 (60-110), 72 (68-74) beats min-1) systolic (120 (105-150), 110 (100-120) mm Hg) and diastolic blood pressure (75 (60-90), 70 (60-80) mm Hg) were not significantly different. However following propranolol administration a reduction (P less than 0.05) occurred in both systolic (median 20 mm Hg) and diastolic (median 12.5 mm Hg) blood pressure in the patients compared with controls. Heart rate was reduced by a median of 10 beats min-1 in both groups. These observations indicate that propranolol bioavailability in patients with hepatosplenic schistosomiasis is increased possibly due to reduced presystemic extraction.

Assessment of oxidative metabolism in adults with hepatocellular carcinoma in the Sudan.

The hypothesis that an increased rate of oxidative metabolism may be an initiator or promoter of hepatocellular carcinoma was tested in vivo. Elimination of antipyrine (phenazone) was used as an index of the activity of microsomal mixed function oxidative enzymes. Plasma antipyrine kinetics were examined in 10 patients with hepatocellular carcinoma and in 10 normal Sudanese adults. The half life, volume of distribution and clearance of antipyrine in patients were 18.8 +/- 7.9 hours (mean +/- SD), 33.8 +/- 7.7 litres and 23.7 +/- 10.1 ml/min, respectively; and in normal adults were 20.3 +/- 8.8 hours, 40.1 +/- 10.4 litres and 25.7 +/- 12.0 ml/min, respectively. These differences were not significant. Antipyrine plasma clearance when corrected for weight was similar in the two groups. This study suggests that in a population at risk for hepatocellular carcinoma, the overall activity of mixed function oxidative enzymes is not an important determinant in selectively increasing this risk.