We used Bayes' theorem to calculate the probability of enteric fever in 260 patients presenting with undiagnosed fever, without recourse to blood or stool culture results. These individuals were divided into 110 patients with enteric fever (63 culture positive, 47 culture negative) and 150 patients with other causes of fever. Comparison of the frequencies of occurrence of 19 clinical and laboratory events, said to be helpful in the diagnosis of enteric fever, in the two groups revealed that only 8 events were significantly more frequent in enteric fever. These were: a positive Widal test at a screening dilution of 1:40; a peak temperature greater than = 39 degrees C; previous treatment for the fever; a white blood cell count less than 9 X 10(6)/litre; a polymorphonuclear leucocyte count less than 3.5 X 10(6)/litre; splenomegaly; fever duration greater than 7 d; and hepatomegaly. When the probability of enteric fever was determined prospectively in 110 patients, using only 6 of these discriminating events, the probability of patients with a positive prediction having enteric fever (diagnostic specificity) was 0.80 (95% confidence interval: 0.68 to 0.91) and the probability of those with a negative prediction not having enteric fever (diagnostic sensitivity) was 0.92 (0.85 to 0.99). Using all 19 events did not alter the diagnostic specificity or diagnostic sensitivity. This study shows that a small number of clinical and laboratory features can objectively discriminate enteric fever from other causes of fever in the majority of patients. Calculating the probability of enteric fever can aid in diagnosis, when culturing for salmonella is either unavailable or is negative.
We analysed clinical and histological diagnoses in patients admitted with liver-related illnesses in order to determine the spectrum ofliver disease in our community. In a total of 380 such patients, liver disease was sixfold more frequent in males than in females. Admissions for cirrhosis were more common amongst the Indian ethnic group. Indians constituted 39% of the admissions (expected 11. 7%), Chinese 37% (expected 51%) and Malays 21% (expected 36%) (~2 = 293, p = H 0.001). Liver histology from 179 of the patients was reviewed blind by one pathologist. Based on the histological findings, the pre-biopsy diagnosis was 'wrongin 75%of cases. The age standardized incidence rate of hepatocellular carcinoma was 22/100,000/year in males 225 and 5/100,000/year in females. However, the peak age of onset was in the seventh decade and the age specific incidence in males aged 60 years or older was 93/100,000/year. The ethnic group representation of patients with hepatocellular carcinoma did notshow a racial preponderance. This study highlights a public health problem related to acute viral hepatitis and alcohol abuse. It also confirms a high incidence of hepatocellular carcinoma
We determined the prevalence of cholelithiasis, by ultrasound in 728 Asian subjects and calculated the annual incidence of disease amongst the gallstone carriers. The prevalence of asymptomatic cholelithiasis in the age group> 29 years, was 11.8% (95% confidence interval: 7.2-16.4%) in males and 13.7% (8.4-19.0%) in females. The median diameter of the stones 10mm (range 4-17) did not differ from that of symptomatic stones - 12.5mm (3·21). The odds of having cholelithiasis increased by 5% each year of life (p 29 years) developing symptoms leading to a hospltal-based investigation was estimated as only 1/1000, whilst the annual cholecystectomy rate was 6/100,000. The chance of a carrier having a cholecystectomy in Malaysia was approximately 5 times less than the chance in the United Kingdom. We conclude that asymptomatic gallstones are common In Malaysians, but the risk of disease is low. The low cholecystectomy rate may be the result of a conservative approach to cholelithiasis due to limited surgical resources.
The results of 2449 investigations of the upper gastrointestinal tract were analysed to determine the incidence of disease. Abnormalities were detected in 53% of patients who had endoscopy, but were found in only 24% of patients who had barium studies (p <= 0.001). Altogether 916 patients had abnormal findings. Duodenal ulcer accounted for 42% of cases, gastric ulcer 16% and gastric cancer 9%. The prevalence of perforated ulcer was 13%. The annual incidence/1000 in males and females (>14 years) were respectively, for duodenal ulcer 1.66 and 0.42, for gastric ulcer 0.57 and 0.25, for perforated ulcer 0.36 and 0.05, and for gastric cancer 0.29 and 0.14. Most types of gastro-duodenal disease were less common in Malays than expected (p = <0.001). However oesophageal cancer and varices were more common in Indians compared to Malays and Chinese (p = <0.001). This study showed that the pallern of perforating ulcers was not the same as that of non-peforating ulcers, suggesting a differing pathogenesis. Identification of the factors causing a different prevalence of disease between the three ethnic groups would help in the understanding of the causes of upper gastrointestinal disease.
Serological markers were used to determine the infective agents causing acute viral hepatitis in 246 patients. The frequencies of the five viral infections investigated were: non-A, non-B hepatitis - 99 patients (40.2%); hepatitis A - 98 patients (39.8%); hepatitis B - 43 patients (17.5%); cytomegalovirus - 4 patients (1.6%); and Epstein-Barr virus - 2 patients (0.8%). The log mean ages of presentation for the three predominant infections were: hepatitis A - 18 years; hepatitis B - 25 years; and non-A, non-B hepatitis - 30 years (F = 18.8, p =< 0.001). 52% of all cases were Malays (expected 32. 7%); 32% Chinese (expected 54.6%); and 16% Indians (expected 1l.5%) (X2 = 53, p = < 0.001). Hepatitis A virus infection was more common amongst Malays whilst non-A, non-B hepatitis was more frequent amongst Chinese and Indians. 28% of children <16 years) and 50% of adults had serological markers of previous hepatitis B infection. The variation in frequency for the different forms of hepatitis amongst the three main ethnic groups would suggest that socioeconomic and/or cultural factors are important in the propagation of acute viral hepatitis in Malaysia. HBsAg-negative chronic liver disease in our community may be a product of the high incidence of non-A, non-B hepatitis.