A prospective study of Chinese patients with megaloblastic anaemia was conducted at the Pamela Youde Nethersole Eastern Hospital from 1 May 1994 to 31 August 1997. Megaloblastic anaemia was diagnosed in 57 patients, 52 of whom were eligible for further evaluation. The median age of these 52 patients was 73.5 years and the male to female ratio was 1.08:1. The serum cobalamin level (median, 56 ng/L) was low in 46 (86.5%) patients. In five (9.6%) patients, both serum cobalamin and red blood cell folate concentrations were low. Isolated low red blood cell folate level was demonstrated in one (1.9%) patient. Serum antibodies against intrinsic factor and gastric parietal cells were detected in 32 (61.5%) and 26 (50.0%) patients, respectively; 19 (36.5%) patients had both types of antibody. The aetiology of megaloblastic anaemia included pernicious anaemia in 39 (75%) patients, postgastrectomy vitamin B12 deficiency in five (9.6%) patients, and nutritional deficiency in two (3.8%) patients; the cause was undetermined in six (11.5%) patients.

This study investigated the use of anti-ribosomal P antibodies in the diagnosis of cerebral complications of systemic lupus erythematosus using two different methods-western blotting and enzyme-linked immunosorbent assay. Anti-ribosomal P antibodies in patient serum were detected in both methods using a purified ribosomal P antigen substrate. Western blotting detected anti-ribosomal P antibodies with a 90% specificity for systemic lupus erythematosus in 56% of patients with the disease. The detection of anti-ribosomal P antibodies by western blotting in patients with systemic lupus erythematosus was significantly associated with psychosis and/or seizures; detection was positive in 90% of patients with these cerebral complications and in 41% of those without. Elevation of the level of anti-ribosomal P antibody, as measured by enzyme-linked immunosorbent assay, was 99% specific for systemic lupus erythematosus in 44% of patients with systemic lupus erythematosus that was not associated with cerebral involvement. We conclude that the measurement of anti-ribosomal P antibodies by western blotting is helpful in the diagnosis of cerebral lupus in selected patients.

This is a descriptive study of 168 patients with nasopharyngeal carcinoma who were referred to public oncology departments for primary treatment between July and September 1996. The mean duration from the onset of the symptoms to histological diagnosis was 5.0 months; the duration ranged from 6.1 months (for patients presenting with nasal symptoms) to 1.8 months (for those with cranial nerve dysfunction). The mean period between the onset of symptoms and the seeking of medical advice was 2.9months. For 54% of the patients, there was a further delay of up to 2.4 months between the initial medical consultation and referral to the appropriate specialist. The majority (84%) of patients attended public institutions for histological confirmation. The mean total time taken from the onset of symptoms to the commencement of radiotherapy was 6.5 months (range, 1.3-74.0 months)--45% of the delay was attributed to the patient, 20% to initial consultations, 14% to diagnostic arrangement, and 21% to preparation for radiotherapy. Concerted efforts are needed to minimise further the time between the onset of symptoms and treatment. A substantial reduction in this delay can be achieved if both public and primary care doctors were made more aware of the significance of relevant symptoms.

Thalassaemia major is a classic example of a disease that is preventable by prenatal diagnosis. Although the technology was introduced to Hong Kong more than a decade ago, new patients are continuously seen in the Hong Kong Administrative Region. This retrospective review concerns children who were diagnosed to have severe beta-thalassaemic syndromes at the Tuen Mun Hospital from 1990 to 1996. Seventeen children (including a pair of identical twins) with homozygous beta-thalassaemia and five children with double heterozygous beta-E thalassaemia were identified. All except three children were transfusion-dependent. Thirty-six parents were available for the thalassaemic study. Thirty-one of them had beta-thalassaemic traits and the other five were carriers of haemoglobin E. Two of the parents with beta-thalassaemic traits and all five haemoglobin E carriers had a mean corpuscular volume above the cut-off for screening in antenatal diagnosis (>75 fL). Of the 21 at-risk pregnancies, seven were managed by public hospitals, 11 by maternal and child health centres, and two by private practitioners. Thalassaemia had not been diagnosed prenatally because of the lack of maternal screening (n=9), lack of paternal screening (n=3), late antenatal visit (n=7), and parental refusal (n=1). Thus, many of our patients are not benefiting from the availability of prenatal screening.

We compared the effectiveness of calcium acetate as a phosphate binder with that of calcium carbonate by substituting one for the other in patients undergoing continuous ambulatory peritoneal dialysis. Twenty patients who had been receiving calcium carbonate as a phosphate binder were instead given calcium acetate, initially with two thirds of the previous dose of elemental calcium. The calcium acetate dose was adjusted to achieve adequate calcium-phosphate balance; 65.6% of the previous dose of elemental calcium in calcium carbonate was required. Eighteen of the 20 patients completed the 3-month study. There were no significant differences in the pre-study and study levels of serum phosphate (1.81±0.04 [SEM] versus 1.89±0.06 mmol/L), corrected serum calcium (2.54±0.04 versus 2.57±0.03 mmol/L), calcium phosphate product (4.60±0.15 versus 4.87±0.18), serum alkaline phosphatase (64.75±4.17 versus 69.94±3.77 U/L), and serum parathyroid hormone (122±31 versus 124±27 ng/L). Three patients developed a total of five episodes of hypercalcaemia (corrected calcium level ≥2.85 mmol/L) and four other patients developed gastrointestinal upset. Calcium acetate can thus achieve similar phosphate control to calcium carbonate, using 65.6% of the dose of elemental calcium in calcium carbonate; how- ever, its clinical superiority was not demonstrated in this study.