Generalised peripheral nerve dysfunction in acromegaly: a study by conventional and novel neurophysiological techniques.

G A Jamal; D J Kerr; A R McLellan; A I Weir; D L Davies

doi:10.1136/jnnp.50.7.886

Home/Archive/PubMed

PubMed · 3040913

Generalised peripheral nerve dysfunction in acromegaly: a study by conventional and novel neurophysiological techniques.

G A Jamal·D J Kerr·A R McLellan·A I Weir·D L Davies

View original source ↗Export metadata ↓

Abstract

Twenty four patients with clinical, radiological and biochemical evidence of acromegaly were investigated by a number of independent neurophysiological tests. Two-thirds of the patients showed evidence of generalised peripheral nerve dysfunction. A significant correlation was found between total exchangeable body sodium, an indicator of disease activity, and the severity of the neuropathy. The generalised peripheral nerve abnormality was found to occur independently of the associated carbohydrate intolerance human growth hormone levels and other endocrinological dysfunction in this disorder.

Explore related subjects

Acromegaly Adult Aged Carpal Tunnel Syndrome Female Hot Temperature Humans Male Middle Aged Motor Neurons Neural Conduction Peripheral Nervous System Diseases Reaction Time Sensory Thresholds Vibration Journal Article Research Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

G A Jamal, D J Kerr, A R McLellan, A I Weir, D L Davies. 1987. Generalised peripheral nerve dysfunction in acromegaly: a study by conventional and novel neurophysiological techniques.. https://doi.org/10.1136/jnnp.50.7.886

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Protein metabolism in acromegaly: differential effects of short- and long-term treatment.

CONTEXT: GH acutely increases body protein by stimulating protein synthesis and reducing protein oxidation. OBJECTIVE: The objective of the study was to determine whether these changes in protein metabolism are sustained in long-term GH excess and reversed by correction. DESIGN: We conducted a cross-sectional study in 16 acromegalic and 18 normal subjects and a longitudinal study in which acromegalic subjects were studied before and after short-term (n=8) or long-term (n=10) treatment. SETTING: The study was conducted at a clinical research center. MAIN OUTCOME MEASURES: Whole-body rates of leucine appearance (leucine Ra; an index of protein breakdown), leucine oxidation, and nonoxidative leucine disposal (NOLD; an index of protein synthesis) estimated using infusion of 1-[13C] leucine were measured. RESULTS: Leucine Ra and NOLD were greater (P<0.01) in acromegalic compared with normal subjects, whereas leucine oxidation did not differ. Leucine oxidation increased significantly (P<0.05) after short-term treatment but returned to baseline after long-term treatment. Both leucine Ra and NOLD decreased significantly (P<0.05) after short- and long-term treatment. Adjustment for body composition did not affect results. CONCLUSIONS: In acromegalic subjects, protein breakdown and synthesis are increased, whereas protein oxidation does not differ from normal subjects. Protein oxidation increases transiently, whereas protein breakdown and synthesis are stably reduced after treatment. Because protein oxidation represents irreversible loss, we conclude that the normal state of protein oxidation found in acromegaly and after long-term treatment represents metabolic adaptation, which maintains protein mass at a steady state after stable changes in GH status.

Acromegaly↗

PubMed2007

Acromegaly.

Explore the source record for details and available documents.

Acromegaly↗

PubMed2007

Carney complex: the first 20 years.

PURPOSE OF REVIEW: The purpose of this review is to comment on the current findings on Carney complex, a dominantly inherited disease and a unique multiple endocrine neoplasia syndrome. RECENT FINDINGS: Sequencing of the PRKAR1A gene in more than 150 kindreds has revealed a number of pathogenic mutations; in more than 90% of the cases, the sequence change was predicted to lead to a premature stop codon and, thus, mutant mRNAs were subject to nonsense-mediated mRNA decay. In Carney complex syndrome cells carrying these mutations, protein kinase A activity is irregularly stimulated by cAMP. Mutations that did not lead to a premature stop codon have also been described; these were also associated with abnormal protein kinase A activity. Animal models of the disease have been recently developed; they reproduced some of the stigmata of Carney complex syndrome but not all. Genetic testing of patients' family members has been introduced in recent years, leading to early detection and a better overall prognosis. SUMMARY: New treatments have yet to be applied; the elucidation of the molecular pathways regulated by PRKAR1A holds the promise of leading to molecularly designed therapies.

Acromegaly↗