Anorexia is associated with disorders of all systems. Long-term anorexia during chronic disease, however, is deleterious to an organism and may be associated with cachexia, which can ultimately result in death.
Cachexia may result not only from anorexia and a decreased caloric intake, but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions), or a change in body metabolism.
Nutritional modifications and the use of specific steroids (such as megestrol acetate) are being tested in the clinical setting.
Plata-Salam?n CR: Anorexia during acute and chronic disease. Nutrition, 1996 Feb, 12:2, 69-78.
Observations on nutritional disorders were made by a physician inmate in a concentration camp before and during the Great Starvation in China.
Based on therapeutic response, many unique abnormalities should be considered as a part of clinical picture of malnutrition, such as mucocutaneous pigmentation, nail layering phenomena and intranail hemorrhage, palmar/plantar fissures, vegetative system crisis, avitaminostic fevers, multiple premature beats, and enlargement of cartilage, lymph nodes, and submandibular glands.
Lee BY & Thurmon TF: Nutritional disorders in a concentration camp. J Am Coll Nutr, 1997 Aug, 16:4, 366-75.
Identified risk factors for gastrointestinal bleeding (GIB) among users of non-aspirin, non-steroidal anti-inflammatory drugs (NANSAIDs).
A total of 120 patients aged over 60 years and using NANSAIDs were hospitalized between January 1988 and September 1992 for GIB related to erosions or ulceration of the gastroduodenal mucosa.
The adjusted odds ratios (OR) for the risk factors related to the pattern of NANSAID use were 3.39 when the intake of NANSAIDs was followed by decubitus, 3.00 when NANSAIDs were taken before a meal, 6.05 with a high dose of NANSAIDs, 5.87 with recent NANSAID use, 3.35 with NANSAIDs associated with aspirin use, 3.46 with more than one NANSAID, and 10.70 when NANSAIDs were associated with corticosteroids.
This study identified a group at 'high risk' for GIB which would benefit from the development of a prophylactic therapy.
Hochain P et al., Which patients taking non-aspirin non-steroidal anti-inflammatory drugs bleed? A case-control study. Eur J Gastroenterol Hepatol, 1995 May, 7:5, 419-26.
Vitamin K is a substrate for a liver microsomal enzyme that catalyzes the conversion of specific glutamyl residues to gamma-carboxyglutamyl residues in a limited number of proteins. These include the vitamin K-dependent clotting factors: prothrombin (factor II), factor VII, factor IX, and factor X.
In the absence of vitamin K, nonfunctional clotting factors are synthesized and hemorrhage can result.
A Recommended Dietary Allowance of 1 micrograms/kg body weight has been established for vitamin K. Advances in analytic techniques and more sensitive clotting factor assays will make it possible to define the human requirement for this vitamin more accurately. A limited amount of data on the vitamin K content of foods is now available and reasonable estimates of intake can be calculated. Green leafy vegetables constitute the major source of vitamin K in the diet.
Suttie JW: Vitamin K and human nutrition. J Am Diet Assoc, 1992 May, 92:5, 585-90.
Vitamin E (Hemorrhage)
A double-blind study to see if intramuscular "vitamin E" affected mortality and the rate of intracranial hemorrhage (ICH) was evaluated in 149 infants less than 1,000 gm and 24 hours of "age".
There were two weight groups, those between 501-750 g and 751-1000 g. All the neonates, including the controls, were given 100 mg/kg/d of dl-a-tocopheryl acetate of oral Aquasole. The treatment group received intramuscular injections of vitamin E (Ephynal) in 4 doses of 15, 10, 10 and 10 mg/kg on days one, two, three and six of life respectively. The oral dose was adjusted to keep the "serum" levels at .5 to 3.5 mg/dl of vitamin E.
There was no difference in neonatal or total hospital mortality between the groups.
There was a significant reduction of ICH in the vitamin E-treated 501-750-g subgroup.
In the vitamin E-treated neonates there was a significant decrease in ICH of 25% versus 5% in the control group.
Minimal side effects were noted.
It is curious how vitamin E may have had a more profound effect in the 501-750 group and it is suggested that vitamin E may play a significant role in the prevention of severe ICH in premature neonates.
"Effect of Intramuscular Vitamin E on Mortality and Intracranial Hemorrhage in Neonates of 1000 Grams or Less", Fish, Wendy H., MD, et al, Pediatrics, April 1990;85(4):578-584.
Neuropathological examination of 3 patients who were maintained on parenteral nutrition without substitution of thiamine demonstrated an acute haemorrhagic encephalopathy.
The lesions differed substantially from the classic features of thiamine deficient encephalopathy regarding the histopathological alterations and the topographical distribution.
The extreme rapidity of thiamine deprivation may have been responsible for the abrupt clinical onset of the disease and the intensity of the morphological alterations.
Vortmeyer AO et al., Haemorrhagic thiamine deficient encephalopathy following prolonged parenteral nutrition. J Neurol Neurosurg Psychiatry, 1992 Sep, 55:9, 826-9.
Vitamin E And The Newborn
Vitamin E and The Newborn
Twenty mg/kg of vitamin E were given I.M. immediately after "birth", at 24 and 48 hours, and it was found that supplemented babies had lower incidences of intraventricular hemorrhage than controls.
In a single dose (20 mg/kg) trial of vitamin E given soon after birth in preterm babies there was a lower incidence of periventricular hemorrhage.
Vitamin E protects against intraventricular hemorrhage.
"Vitamin E Supplementation and Periventricular Hemorrhage in the Newborn", Chiswick, Malcolm, et al, American Journal of Clinical "Nutrition", 1991;53:370S-372S.
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