Beriberi cardiomyopathy.

In Indonesia beriberi is still endemic, but subclinical cases are not uncommon. Three patients suffering from beriberi presented with different clinical manifestations. One had the classical features of Shoshin beriberi and the other two had the non-alcoholic cardiac beriberi (chronic type). The cardiac symptoms of all three patients responded dramatically to thiamine tetrahydrofurfuryl disulfide; there was also some improvement of their polyneuropathy, consistent with the neurophysiologic findings and somatosensory evoked potentials (SSEPs). We conclude that SSEPs provide additional clinical information on beriberi polyneuropathy. The mortality of untreated cardiovascular beriberi is high. In view of the harmless nature of the treatment, a good case could be made for routine administration of thiamine to all patients in whom heart failure is present without clear evidence of the cause.

Subclinical beriberi polyneuropathy in the low income group: an investigation with special tools on possible patients with suspected complaints.

OBJECTIVE: To determine the prevalence rate of subclinical beriberi polyneuropathy (PNP) in the low income group and to present new methods for early detection. DESIGN: We conducted a prospective, randomized observational study on all patients from family members of non-PNP patients presenting to the outpatient neurologic clinic of the Dr Soetomo Hospital in 1989 in Surabaya, Indonesia. MATERIAL AND METHODS: The 53 group I patients belonged to the low income series, whereas the 56 group II patients were from the mid- and high-income groups. We analyzed their diets and determined their blood thiamine levels. Neurologic, internal, psychiatric as well as neurophysiologic examinations were performed on all patients. RESULTS: The prevalence rate of subclinical beriberi PNP of the apparently healthy subjects of the low income group was 66% compared with 12.5% among the mid and high income groups. The exposure odds ratio was 13.6 (95% Cl, 2.78 to 8.04) indicating that the low income group ran a greater risk of developing beriberi PNP than the mid and high income groups. CONCLUSION: Most of our low income group patients had an inadequate diet, especially concerning deficient thiamine intake. Analysis of the diets revealed, that they were usually rich in carbohydrate especially steamed milled rice, whereas intake of fat and thiamine was low, protein was just sufficient. The calorie intake was marginal. Carbohydrate rich and non fat calories in the diet with low thiamine intake may provoke beriberi.

Electrophysiologic evaluation of beri-beri polyneuropathy.

The diagnostic utility of electroneuromyography including F-wave and H-reflex was studied in 68 patients with peripheral polyneuropathy due to nutritional deficiency of thiamine. Out of all the electrophysiologic evaluations assessed, denervation activity in electromyography, prolonged conduction velocity and reduced motor nerve action potentials and prolonged H-reflex latency were the most frequently found abnormal findings, followed by reduced sural nerve action potential and, much less frequently, prolonged F-wave latency. In experimental thiamine-deficiency evoked polyneuropathy in chickens, the prominent abnormal findings were found in the leg muscles such as F-wave pathology and reduction and prolongation of peroneal and sciatic motor nerve action potentials, and also a prolongation of the distal sensory peroneal nerve latency respectively.

Experimentally induced beriberi polyneuropathy in chickens.

Chickens fed with the same composition of diet as our low income beriberi polyneuropathic patients, developed clinical symptoms of thiamine deficiency in 22.3 +/- 6.3 days. There appeared to be a body store of thiamine which is utilized during a period of deficient intake. Haemoglobin content and serum albumin did not change appreciably during thiamine deficiency. The blood thiamine content was low and the thiamine pyrophosphate (TPP) effect increased to more than 25 percent during the development of the beriberi polyneuropathy, which resumed after one week on thiamine tetrahydrofurfuryl disulfide (TTFD) treatment. However, the clinical features gradually improved after about one month. Neurophysiological findings including somatosensory evoked potentials (SSEPs) and neuromorphological studies of the peroneal and sciatic nerves were compatible with a major degree of axonal degeneration and secondary minimal segmental demyelination. We may conclude that the experimentally induced beriberi polyneuropathy in chickens seems a good model for studying these forms of neuropathy in view of diagnosis and treatment.

Thiamine tetraphydrofurfuryl disulfide in nutritional polyneuropathy.

An open trial with thiamine tetrahydrofurfuryl disulphide (TTFD) was carried out on 44 patients with nutritional polyneuropathy who were admitted to the Neurological Department, Dr. Soetomo Hospital, Surabaya, Indonesia, Thirty-four patients showed improvement of their motor functions (P less than 0.01) with slight restoration of sensory function and reflexes (P less than 0.1). Of the 18 patients who were re-examined electrophysiologically 3 months later, 6 showed remarkable improvements. No side-effects were observed during TTFD treatment. It seemed that nutritional polyneuropathy in our low socio-economic patients was mostly caused by thiamine deficiency.