OBJECTIVE: To determine the incidence, clinical features and risk factors of cADRs among hospitalized patients.
METHODS: A prospective study was conducted among medical inpatients from July to December 2014.
RESULTS: A total of 43 cADRs were seen among 11 017 inpatients, yielding an incidence rate of 0.4%. cADR accounted for hospitalization in 26 patients. Previous history of cADR was present in 14 patients, with 50% exposed to the same drug taken previously. Potentially lifethreatening severe cutaneous adverse reactions (SCAR), namely drug reaction with eosinophilia and systemic symptoms (DRESS: 14 cases) and Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (SJS/TEN: 6 cases) comprise almost 50% of cADRs. The commonest culprit drug group was antibiotics (37.2%), followed by anticonvulsants (18.6%). Cotrimoxazole, phenytoin and rifampicin were the main causative drugs for DRESS. Anticonvulsants were most frequently implicated in SJS/TEN (66.7%). Most cases had "probable" causality relationship with suspected drug (69.8%). The majority of cases were of moderate severity (65.1%), while 18.6% had severe reaction with 1 death recorded. Most cases were not preventable (76.7%). Older age (> 60 years) and mucosal involvement were significantly associated with a more severe reaction.
CONCLUSION: The incidence of cADRs was 0.4%, with most cases classified as moderate severity and not preventable. The commonest reaction pattern was DRESS, while the main culprit drug group was antibiotics. Older age and mucosal membrane involvement predicts a severe drug reaction.
METHODS: A case-control study to examine serum 25- hydroxyvitamin D [25(OH)D] levels in children with and without AD was done. Serum 25-hydroxyvitamin D [25(OH)D] level was measured by immunoassay. AD severity was evaluated using the SCORing Atopic Dermatitis (SCORAD) index.
RESULTS: The serum levels of 25(OH)D, measured in 135 children with AD was not statistically different from 65 children without AD [median (IQR): 25.2ng/mL (15.45) vs 25.9ng/mL (15.87), p=0.616]. However, serum vitamin D levels were significantly lower in children with severe AD compared to those with mild-to-moderate AD [median (IQR): 16.0ng/mL (19.32) vs 26.3ng/mL (15.56), p=0.021]. The odds of having vitamin D deficiency in children with severe AD was 3.82 times that of children with non-severe AD (95% confidence level: 1.13, 12.87).
CONCLUSION: This study suggests that there is an inverse association between vitamin D level and the severity of AD in Malaysian children.
OBJECTIVE: To determine the clinical characteristics, culprit drugs and outcome of patients with AGEP.
METHODS: A retrospective note review of all AGEP patients seen from 2001-2015.
RESULTS: Among 21 AGEP patients, 76% were Malays, 9.5% Chinese, 9.5% Indians, and 5% Iban. Sixteen were females and 5 were males. Median age of patients was 40 years (IQR: 26). The main culprit drug was amoxicillin (10 cases), followed by cloxacillin (three cases), phenytoin (two cases) and one case each of carbamazepine, sulphasalazine, allopurinol, cephalexin, ceftriaxone, celecoxib and herbal product. The median time from drug initiation to onset of AGEP was 3 days (IQR: 5.5). Fever was documented in 52.4 %, mucosal involvement 9.5%, purpura 4.7% and blisters 4.7%. Neutrophilia was observed in 63.6% of patients and eosinophilia in 28.5%. While most patients required admission (67%), all achieved complete recovery within 15 days without any sequela.
CONCLUSIONS: AGEP predominantly affects Malay females in this study. The most common culprit drug was amoxicillin. Our patients exhibited the classic clinical manifestations of AGEP and confirmed the generally benign nature of this reaction upon drug withdrawal. Although the overall prognosis is good, prompt diagnosis of AGEP is important because drug withdrawal is the mainstay therapy.
SUBJECTS/METHODS: We used a cross-over designed feeding trial in 53 healthy Asian men and women (20-50 years) to test this hypothesis by exchanging 20% energy of palm olein (PO; control) with randomly interesterified PO (IPO) or high oleic acid sunflower oil (HOS). After a 2-week run-in period on PO, participants were fed PO, IPO and HOS for 6 week consecutively in randomly allocated sequences. Fasting (midpoint and endpoint) and postprandial blood at the endpoint following a test meal (3.54 MJ, 14 g protein, 85 g carbohydrate and 50 g fat as PO) were collected for the measurement of C-peptide, insulin, glucose, plasma glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1, lipids and apolipoproteins; pre-specified primary and secondary outcomes were postprandial changes in C-peptide and plasma glucose.
RESULTS: Low density lipoprotein cholesterol was 0.3 mmol/l (95% confidence interval (95% CI)) 0.1, 0.5; P<0.001) lower on HOS than on PO or IPO as predicted, indicating good compliance to the dietary intervention. There were no significant differences (P=0.58) between diets among the 10 male and 31 female completers in the incremental area under the curve (0-2 h) for C-peptide in nmol.120 min/l: GM (95% CI) were PO 220 (196, 245), IPO 212 (190, 235) and HOS 224 (204, 244). Plasma glucose was 8% lower at 2 h on IPO vs PO and HOS (both P<0.05).
CONCLUSION: Palmitic acid in the sn-2 position does not adversely impair insulin secretion and glucose homeostasis.