Relationship between weight gain and clinical improvement in subjects with a manic episode in the first month of treatment

2011 ◽  
Vol 26 ◽  
pp. e1
Author(s):  
N. Sam Calvin ◽  
Sunita Simon Kurpad
PEDIATRICS ◽  
1961 ◽  
Vol 28 (3) ◽  
pp. 399-409
Author(s):  
John H. Menkes ◽  
George A. Jervis

An infant with seizures, spasticity, and failure in weight gain was shown to excrete p-hydroxyphenylpyruvic acid, p-hydroxyphenyllactic acid, and p-hydroxyphenylacetic acid, indicating the likelihood of an impairment in the oxidation of p-hydroxyphenylpyruvate. Institution of a phenylalanine-free diet coincided with marked clinical improvement and disappearance of the abnormal urinary metabolites. The cause of the temporary enzyme defect is discussed, and it is concluded that it represents a persistence into extrauterine life of the relative enzyme inactivity observed in fetal tissues.


2021 ◽  
pp. 1-9
Author(s):  
David J. Bond ◽  
Leonardo E. Silveira ◽  
Ivan J. Torres ◽  
Raymond W. Lam ◽  
Lakshmi N. Yatham

Abstract Background We previously reported that bipolar disorder (BD) patients with clinically significant weight gain (CSWG; ⩾7% of baseline weight) in the 12 months after their first manic episode experienced greater limbic brain volume loss than patients without CSWG. It is unknown whether CSWG is also a risk factor for progressive neurochemical abnormalities. Methods We investigated whether 12-month CSWG predicted greater 12-month decreases in hippocampal N-acetylaspartate (NAA) and greater increases in glutamate + glutamine (Glx) following a first manic episode. In BD patients (n = 58) and healthy comparator subjects (HS; n = 34), we measured baseline and 12-month hippocampal NAA and Glx using bilateral 3-Tesla single-voxel proton magnetic resonance spectroscopy. We used general linear models for repeated measures to investigate whether CSWG predicted neurochemical changes. Results Thirty-three percent of patients and 18% of HS experienced CSWG. After correcting for multiple comparisons, CSWG in patients predicted a greater decrease in left hippocampal NAA (effect size = −0.52, p = 0.005). CSWG also predicted a greater decrease in left hippocampal NAA in HS with a similar effect size (−0.53). A model including patients and HS found an effect of CSWG on Δleft NAA (p = 0.007), but no diagnosis effect and no diagnosis × CSWG interaction, confirming that CSWG had similar effects in patients and HS. Conclusion CSWG is a risk factor for decreasing hippocampal NAA in BD patients and HS. These results suggest that the well-known finding of reduced NAA in BD may result from higher body mass index in patients rather than BD diagnosis.


2011 ◽  
Vol 186 (1) ◽  
pp. 155 ◽  
Author(s):  
Eesha Sharma ◽  
Naren P. Rao ◽  
Ganesan Venkatasubramanian ◽  
Rishikesh V. Behere ◽  
Shivarama Varambally ◽  
...  

2008 ◽  
Vol 42 (5) ◽  
pp. 30
Author(s):  
Kerri Wachter
Keyword(s):  

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