Monoclonal gammopathy (Waldenström's macroglobulinaemia) producing specific red cell antibody.

Two cases of Waldenström's macroglobulinaemia have been seen at University College Hospital, Ibadan in the last four years, Case 1 was a 30-year-old soldier who presented with splenomegaly and anaemia, was treated with chlorambucil, and had a complete remission sustained for over two years. Case 2 was a 58-year-old retired civil servant who presented with very severe anaemia and also splenomegaly, and died within three weeks of admission. Both patients had most of the typical features of Waldenström's disease, including retinal changes and serum IgM levels of 4200 and 5500 mg/dl respectively. In both cases an atypical cold antibody was detected in the course of blood cross-matching procedures. In case 1, the antibody agglutinated all adult and cord red cells tested, including the patient's own cells, to a titre of 8000 and above at 4 degrees C. Suprisingly enough, when the patient went into remission and the serum IgM level had fallen to 400 mg/dl, this antibody was no longer detectable and has not reappeared two years later. In case 2, the antibody agglutinated all adult red cells tested to a titre of 2000 at 20 degrees C but not the patient's own red cells. Since cord cells were agglutinated only to a titre of 4 to 20 degrees C it was concluded that the patient had an alloantibody with I-specificity. Therefore in both these patients the monoclonal immunoglobulin produced by the neoplastic lymphoid cell clone had specific activity against red cell antigens.

A clinicopathological study of human yellow fever.

During an epidemic of yellow fever in the Jos Plateau area of Nigeria, 9 adult males with clinically diagnosed yellow fever were studied by haematological, biochemical, virological, serological, and liver biopsy methods. The ages of the patients ranged from 20 to 55 years and the duration of illness was 3-62 days. No virus was isolated from any patient but all patients should biochemical evidence of severe hepatocellular damage. Leucopenia was a feature of the late acute stage of the disease. Five sera had antibodies to yellow fever at titres greater than 1: 32, 3 of them being monospecific for yellow fever. The classical histological features of yellow fever were present only in the acute or late acute stages, when complement-fixation tests may be negative. With convalescence and the production of complement-fixing antibodies in high titres, the histological features resembled those of a persisting nonspecific hepatitis. In an endemic area, the histological features of yellow fever will depend on the stage of the disease and a picture of nonspecific hepatitis would not exclude yellow fever in the absence of confirmation from serological tests.

Human alpha fetoprotein in body fluids.

Human alpha fetoprotein (AFP) has been detected by the agar double diffusion method in ascitic fluid, cerebrospinal fluid (CSF) and bile, from fetuses, neonates and patients with AFP seropositive hepatocellular carcinoma. AFP was detected in the meconium and faeces of fetuses and neonates respectively. The protein was not detected in the amniotic fluid nor the pericardial fluid. It was found in the urine in only two fetuses that had concomittant renal disease. It was not detected in breast milk of lactating females. When metastases occurred in the lung from a hepatocellular carcinoma producing AFP, the pleural effusions sometimes contained AFP. The concentrations of AFP in the serum and in the other body fluids were about the same. This indicates that other body fluids can be used for the diagnosis of hepatocellular carcinoma.

Immunofluorescent localisation of human alpha feto-protein in fetal and neonatal livers and cultured cells from hepatocellular carcinoma.

The indirect immunofluorescence technique demonstrated that human alpha fetoprotein (AFP) was present in a focal pattern in the cytoplasm of malignant liver cells of patients whose sera contained AFP. A few fibroblastlike cells in tissue culture of liver biopsies from patients with hepato-cellular carcinoma and AFP in their sera also had the protein. The intracellular localisation of human AFP was confirmed by centrifugation of washed, homogenised and ultra-sonically disrupted neonatal liver cells. Examination of livers of fetuses and neonates showed that AFP was present predominantly in the periportal parenchymal cells.

Genetically determined deficiency of glucose 6-phosphate dehydrogenase (type-A-) is expressed in the liver.

G6PD activity was determined in liver biopsy specimens from 31 patients (25 men and six women). The G6PD genotype of the patients was determined by carrying out on lysates of their red blood cells quantitative assays of the enzyme and starch-gel electrophoresis. In 21 subjects with normal G6PD activity in red cells, a relatively wide variation of G6PD activity was found in liver extracts. By contrast, in 10 subjects with G6PD deficiency, the activity of the enzyme in liver extracts was always low. The difference between the distribution of liver G6PD activity values of G6PD-normal and G6PD-deficient subjects was statistically significant (p less than 0.01). We conclude that G6PD deficiency of the African type is also expressed in the liver. These findings may have a bearing on hyperibilirubinemia, which cannot be entirely attributed to hemolysis, often encountered in G6PD-deficient patients.