Premature infant syndrome. This term, which is also known as Vitamin E Deficiency , was defined in the mid- 1960s by Hassan, Oski, Ritchie and other collaborators, respectively. Prior to this time, biochemical vitamin E deficiency, recognized for many years, was an interesting biochemical finding, looking for a disease .
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- 1 Incidence
- 2 Associated common pathologies
- 3 Etiology
- 4 Diagnosis
- 5 Treatment
- 6 Sources
Another disease of progress, clinical vitamin E deficiency, probably does not occur in breastfed infants. It is exclusively a disease of small premature infants, and both the production of cow’s milk to create our current commercial formula and the supplementation of this formula with iron, have increased the risk of clinical sequelae, in fact, in 1968Ritchie’s group observed evidence of biochemical or clinical abnormalities of sensitivity to vitamin E in two-thirds of the infants weighing less than 1,500 g they investigated. This figure is undoubtedly high and perhaps has been reduced due to the alterations that the infant formula has suffered since then, however, when dealing with small premature infants, this clinical entity must be kept in mind.
Associated common pathologies
Babies born prematurely are at high risk for a series of complications. These are the most common complications seen immediately after birth. Although many of these complications can be diagnosed and treated, they can often lead to long-lasting problems as the baby grows, including the following:
- Hypothermia .
- Respiratory distress syndrome (SDR).
- Apnea .
- Bleeding in the brain (intraventricular hemorrhage).
- Patent ductus arteriosus (CAP).
- Necrotizing enterocolitis (NEC).
- Retinopathy of prematurity (ROP).
Vitamin E, a fat-soluble vitamin ( tocopherol ∞), crosses the placenta , but fetal serum levels are less than a quarter of that of the mother. Leonard has suggested that fetal levels change gradually throughout the course of pregnancy , although previous studies have reported lower serum levels in the premature infant. After birth, vitamin E must be absorbed from the gastrointestinal tract. Full-term infants absorb the vitamin well , but premature infants have a marked reduction in absorptive capacity .
Linoleic acid and other polyunsaturated fatty acids (PUFAs) common in plant acids that are used to supplement many commercial formulas, reduce the absorption of vitamin E, therefore, as the amount of PUFA in the diet increases, so does the amount of vitamin E necessary to maintain an adequate serum level. The breast milk , which is low PUFA, has an E / PUFA ratio high and therefore is suitable to promote absorption of vitamin E. It is considered that the E / PUFA ratios higher than 0.6 are suitable for absorption of vitamin E.
The premature infant, in whom the poor absorption of vitamin E is aggravated by a diet with a high content of PUFA and by the presence of Nutritional Iron , is at great risk of vitamin E deficiency. Cordal vitamin E levels tend to be 0.2 to 0.3 mg per 100 ml, a level above 0.5 is accompanied by metabolic defects. Normal levels are achieved in the full-term infant during the first 2 weeks of life, but in the premature infant without adequate vitamin E supplementation, levels may continue to decrease during the first 6 to 8 weeks.
Although sterility and muscle necrosis can be observed in experimental animals deficient in vitamin E and in severe deficiencies of vitamin E accompanied by prolonged steatorrhea outside the neonatal period, the main effect of vitamin E in the neonate seems to be on the stability of the erythrocyte membrane . It is well known that tocopherols are antioxidants, and it has been assumed that vitamin E contributes to the stability of the RBC membrane, preventing the oxidation of lipids and sulfhydryl groups.
More recent work has suggested that the vitamin E-selenium complex may be an important step in stabilizing the red cell membrane. Apart from this mechanism, the vitamin E-deficient red blood cell is subject to hemolysis in vivo, stimulated by hydrogen peroxide in vitro.
The classic work by Oski and Barnes established the association of vitamin E deficiency and hemolytic anemia in the premature infant. In their cases, the diagnosis was determined between 6 and 8 weeks of age. Anemia accompanied by mild reticulocytosis and pycnocytosis was found to be directly related to low serum tocopherical levels.
Red cell survival was shortened to a half-life of 11 to 15 days. No other clinical signs were observed and anemia immediately responded to vitamin E administration.
They also observed that patients used to have subcutaneous edema of the legs and genitalia with inflammation of the eyebrows. The electrolytes and proteins serum were normal. In cases, a papular erythomatous rash was observed. These findings disappeared 2 to 3 weeks after administering vitamin E.
A major problem is the differentiation of this benign hemolytic anemia from the physiological anemia of prematurity. The peroxide hemolysis test at 2 weeks of age is helpful. The increase in hemolysis seems to be directly related to the degree of vitamin E deficiency, although the test is not completely specific for this vitamin effect. But a normal peroxide hemolysis test makes vitamin E deficiency unlikely.
Once vitamin E deficiency has been demonstrated, treatment with 75 to 100 IU of tocopherol α should be instituted daily. Hematological indices show a response within the first 2 weeks. Within a few days, an improvement in RBC survival and a reduction in peroxide hemolysis are observed. After one week, the dose of tocopherol α can be reduced to a maintenance dose.
Most standard formulas contain 10 to 13 IU of α-tocopherol per liter and have an adequate E / PUFA ratio. This supplementation appears to be correct to suppress vitamin E deficiency in infants weighing more than 2,000 g. lighter infants, especially those who receive an iron supplement, require higher doses of vitamin E, between 15 and 25 IU daily. Recently Gross and Melhorn have presented data showing more effective absorption of a water-soluble form of the vitamin, which achieved (sufficient) serum levels with 25 IU daily, and prevented clinical evidence of deficiency in all infants studied.