The effects of a traditional drug, turmeric (Curcuma longa), and placebo on the healing of duodenal ulcer.

In a joint Vietnam-Sweden prospective double-blind two-center study, the herbal remedy of Curcuma longa (turmeric) - in a dosage of 6 g daily as suggested in the Vietnamese pharmacopoeia - was compared with an equal amount of placebo in 118 patients, suffering from duodenal ulcer. The patients in the two groups were well matched prior to treatment. Clinical assessments were carried out weekly, while laboratory investigations were carried out before beginning of the treatment and after four and eight weeks: Only patients, having one duodenal ulcer with a minimum diameter of 5 mm verified by endoscopy (Uong Bi General Hospital, UBGH) and/or radiography (UBGH and Viet Due University Hospital, VDUH) not more than 4 days prior the study were included in the study. No treatment with H(2)-receptor antagonists, anticholinergics or other drugs used in the treatment of ulcer disease during the preceding week were allowed. Follow-up endoscopy and/or radiography were performed after 28 ± 4 days and 56 ± 4 days. Turmeric was not superior to placebo in healing duodenal ulcer either after four or eight weeks of treatment. After eight weeks the ulcer-healing rate of turmeric was 27% while placebo had healed 29%. Both drugs were well tolerated.

Mitochondrial encephalomyopathy with corticosteroid dependence.

A 12-year-old boy with corticosteroid-responsive mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) is described. His mother proved to have an asymptomatic mitochondrial myopathy on examination of a muscle biopsy specimen. Three weeks after the onset of vomiting, headache, ataxia and visual and speech impairment, he presented with a background of somatic growth retardation, deafness and school failure. Examination revealed disorientation, dysphasia, dyspraxia, optic atrophy, hemianopia, hemiparesis and sensory inattention. A cranial computed tomographic scan disclosed a large, low-density area, which was consistent with infarction, in the left posterior hemisphere and marked calcification of the basal ganglia bilaterally. Within two weeks of the commencement of corticosteroid treatment, the neurological dysfunction resolved. Attempts to decrease the dosage of dexamethasone caused an exacerbation of symptoms repeatedly. Two weeks after ceasing corticosteroid therapy, the patient developed a serious neurological relapse and a new, large, low-density area, which resembled an infarction, in the right posterior hemisphere on a computed tomographic scan. The reintroduction of corticosteroid therapy again resulted in the rapid resolution of all symptoms. It became evident that the patient had an exquisitely sensitive corticosteroid dependency, whereby a reduction in the dexamethasone dosage of even 0.25 mg a day caused confusion, headaches and increasing lactic acidaemia. Although it is difficult to assess the impact of various therapies in MELAS because of the episodic natural course of the disease, this remarkable corticosteroid responsiveness also has been noted in four previously reported patients with MELAS syndrome; therefore, it would seem reasonable to suggest that corticosteroid therapy now should be considered as standard treatment for this condition. However, corticosteroid therapy in other forms of mitochondrial disorders still awaits careful evaluation.

Neuropathology of the cortical lesions of the Parkinsonian-dementia (PD) complex of Guam.

The Guam amyotrophic lateral sclerosis and Parkinsonian-dementia (ALS and PD) complex still presents a challenge to research. Previous papers have highlighted the lesions in the hippocampus and basal nuclei to explain the bizarre clinical syndrome. In our study of 20 to 62 cases of PD with or without ALS, significant widespread and often severe lesions were found throughout the entire cerebral cortex. These changes included variable degrees of nerve cell loss, spongy change, gliosis, increased lipofuscin content of nerve cells, the presence of granulovacuolar bodies and neurofibrillary tangles within neurones and, less frequently, Hirano bodies. The lesions show a characteristic topographical distribution. The global involvement of the cerebral cortex correlated well with the loss of higher mental function which was present in the patients.