Fructus Psoraleae (FP) is used by herbalists for the treatment of postmenopausal osteoporosis, vitiligo, and psoriasis. It is used alone, or in combination with other herbs, in some countries in the form of proprietary medicine. It is recognized as one of the emerging hepatotoxins and here we report three cases of acute hepatitis after exposed to FP and its related proprietary medicine. It seems possible that psoralen and its related chemicals may be responsible for the hepatotoxicity. Decoction with other herbs may result in higher concentration of toxic constituents and in more severe liver injury. In summary, FP is associated with hepatotoxicity in some individuals. Pharmacovigilance for the potential side effects of herbal products is necessary.

SummaryA 41-year-old woman presented with the clinical features of methaemoglobinaemia after drinking Chinese herbal medicine. A life threatening methaemoglobin level of 68% was measured. Both clinical and laboratory diagnostic difficulties were encountered. The pitfalls of pulse oximeter, blood gas analysis and co-oximeter interpretation during diagnosis and after methylene blue administration are discussed. Methaemoglobinaemia is an unusual and potentially fatal condition in which haemoglobin is oxidised to methaemoglobin and loses its ability to bind and transport oxygen. We present a case of accidental ingestion of sodium nitrite to illustrate the pitfalls of management. Case historyA 41-year-old woman with a history of hypertension presented to the Accident and Emergency Department with dizziness and a bluish skin colour. These symptoms occurred 5 min after taking some Chinese herbal medicine. Her treatment for hypertension included metoprolol (daily dose of 100 mg) and sustained release nifedipine (daily dose of 20 mg). The Chinese herbal medicine included 6 g Natrii Sulfa, which was prescribed by a herbalist for weight loss. On admission, she was disorientated as to time and place. Physical examination showed brownish blue cyanotic discoloration of the skin and tachycardia. The rest of the physical examination was unremarkable. Her blood pressure was 126 ⁄ 49 mmHg with a heart rate of 110 beats.min . The pulse oximeter showed an S p O 2 of 77-80% on 100% oxygen. An arterial blood sample was drawn which was chocolate brown and did not change in colour after agitation in air. The arterial blood gas analysis showed pH 7.398, P a CO 2 4.49 kPa, P a O 2 42 kPa and BE ) 4 mmol.l )1 . Chest X-ray was normal. With no identifiable cardiopulmonary pathology and normal alveolar-arterial oxygen gradient, methaemogloblinaemia was suspected. The patient was transferred to the intensive care unit (ICU). After ICU admission, the patient's conscious level improved. Arterial blood was sent for analysis by cooximetry and variable wavelength spectrophotometer; blood samples were also taken for full blood count, renal function and toxicology screening. These showed the methaemoglobin concentration was 68% and the haemoglobin concentration 12.5 g.dl )1 . The spectrophotometer found a small absorption peak at 628 nm, which disappeared after addition of potassium cynanide. The diagnosis of methaemoglobinaemia was confirmed. Methylene blue (100 mg) was given intravenously. The serial oxygen saturation changes in the pulse oximeter, arterial blood gases as well as the methaemoglobin concentrations are shown in Figs 1 and 2. The skin and arterial blood colour became pink 30 min after methylene blue injection. The S p O 2 increased from 88% to 98% and the P a O 2 25 kPa. The methaemoglobin concentration dropped to 10.8% after 30 min of methylene blue treatment. On the second day of admission, the patient remained well. The methaemoglobin concentration dropped to 0.6% and haemoglobin concentration to 11.4 g.dl )1

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A multidisciplinary approach using defined algorithms is a scientific approach in causality assessment for HILI. Further study is needed to assess its accuracy and applicability.

Numerous vitamin supplements are available over-the-counter to the general public. Some such supplements are available as candy-like chewable preparations to encourage consumption by children. We report 3 cases of overdose of such preparations. Each patient had taken an estimated 200,000 to 300,000 IU of vitamin A. Their circulating vitamin A (retinol and retinyl palmitate) concentrations were monitored over a 6-month period. There were no clinical or biochemical complications noted. However, there were marked increases in both retinol and retinyl palmitate concentrations above age-related reference ranges. In particular, it took 1 to 3 weeks for the serum retinol concentrations to peak and many months for them to normalize. Parents should be warned about the dangers of excessive vitamin consumption. Clinicians should be aware of the late peak in serum retinol concentrations, which may lead to late complications of vitamin A overdose.