FÆCAL EXCRETION OF α1-ANTITRYPSIN IN PROTEIN-LOSING ENTEROPATHY

The Lancet ◽  
1980 ◽  
Vol 315 (8167) ◽  
pp. 711
Author(s):  
N Keaney
The Lancet ◽  
1980 ◽  
Vol 315 (8170) ◽  
pp. 711 ◽  
Author(s):  
NiallP. Keaney ◽  
Jerry Kelleher

2019 ◽  
Vol 61 (9) ◽  
pp. 935-937 ◽  
Author(s):  
Kazuhiro Takahashi ◽  
Kenzo Sakurai ◽  
Kiyotaka Takefuta ◽  
Mami Nakayashiro

1966 ◽  
Vol 50 (3) ◽  
pp. 422-443 ◽  
Author(s):  
Thomas A. Waldmann

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 828
Author(s):  
Karolina Graczykowska ◽  
Joanna Kaczmarek ◽  
Dominika Wilczyńska ◽  
Ewa Łoś-Rycharska ◽  
Aneta Krogulska

Cow’s milk is a key component of a child’s diet. While the consumption of even trace amounts can result in allergy to its proteins and/or hypolactasia, excessive cow’s milk consumption can result in numerous health complications, including iron deficiency, due to the diet being improperly balanced. Although the incidence of iron deficiency has declined, it remains the most widespread nutritional deficiency globally and the most common cause of anemia. One rare consequence of anemia caused by iron deficiency is protein-losing enteropathy; however, the mechanisms of its development are unclear. The following manuscript, based on a literature review, presents two rare cases of children, a 16-month-old boy and a 2.5-year-old girl, who developed severe microcytic anemia, enteropathy with hypoalbuminemia, and anasarca as a result of excessive cow’s milk consumption. It highlights the possible relationship between excessive consumption of cow’s milk in children and severe iron deficiency anemia with accompanying hypoalbuminemia; it may also result in serious clinical conditions, even in children that do not demonstrate food hypersensitivity.


2012 ◽  
Vol 28 (4) ◽  
pp. 224-229
Author(s):  
Kentaro Ueno ◽  
Hideaki Nakamura ◽  
Ryohei Gatayama ◽  
Sadamitsu Yanagi ◽  
Hideaki Ueda ◽  
...  

1979 ◽  
Vol 82 (2) ◽  
pp. 227-234 ◽  
Author(s):  
VIPA BOONNAMSIRI ◽  
J. C. KERMODE ◽  
B. D. THOMPSON

SUMMARY Radio-iodide was administered by prolonged continuous intravenous infusion to rats maintained under iodine-replete conditions and in moderate iodine deficiency. A close approximation to equilibrium labelling was thereby achieved. Labelled iodocompounds extracted from various tissues were analysed by thin-layer chromatography. Moderate iodine deficiency resulted in a slight increase in the ratio of mono-iodotyrosine to di-iodotyrosine in the thyroid. No change in the ratio of tri-iodothyronine (T3) to thyroxine (T4) was found in thyroid, plasma or skeletal muscle. Faecal excretion of T3 declined appreciably relative to that of T4. Under iodine-replete conditions the ratio of thyroidal secretion rates of T3 and T4 was estimated to be more than three times higher than the ratio of these iodocompounds within the thyroid. Heterogeneity of thyroglobulin structure and function may explain these observations.


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