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Experimentally induced beriberi polyneuropathy in chickens.

W. Djoenaidi, S. L. H. Notermans, A.A.W.M. Gabreëls‐Festen, A. H. Lilisantoso, A. Sudanawidjaja

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Abstract

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.

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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.

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Available abstract

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.

Key concepts: Thiamine, Beriberi, Polyneuropathy, Medicine, Thiamine pyrophosphate, Thiamine deficiency, Internal medicine, Endocrinology

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