A suspected hypervitaminosis A.

BACKGROUND AND AIM: Vitamin A toxicity is uncommon, but when it occurs can be serious and even fatal. A case vitamin A intoxication with high levels in liver tests, thrombocytopenia and appearance virosis. Laboratory testing is one of the most widely used diagnostic interventions supporting medical decisions of this phenomenon are necessary. CASE REPORT: Here, we report a case vitamin A intoxication with high levels in liver tests, thrombocytopenia and appearance virosis. The patient showed several clinical signs abdominal pain, including mild anemia and thrombocytopenia. CONCLUSIONS: We believe that Laboratory testing is one of the most widely used diagnostic interventions supporting medical decisions, and further investigations regarding the etiology and prevalence of this phenomenon are necessary. (www.actabiomedica.it).

Hypercarotenemia / Hipercarotenemia

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Serum retinyl esters are positively correlated with analyzed total liver vitamin A reserves collected from US adults at time of death.

Background: Minimal human data exist on liver vitamin A (VA) compared with serum biomarkers. Cutoffs of 5% and 10% total serum VA as retinyl esters (REs) suggest a VA intoxication diagnosis. Objectives: We compared total liver VA reserves (TLRs) with the percentage of total serum VA as REs to evaluate hypervitaminosis with the use of US adult autopsy samples. Secondary objectives evaluated serum retinol sensitivity, TLRs among lobes, and hepatic α-retinol concentrations, an α-carotene cleavage product. Design: Matched serum and liver samples were procured from cadavers (n = 27; mean ± SD age: 70.7 ± 14.9 y; range: 49-101 y). TLRs and α-REs were quantified by ultra-performance liquid chromatography. Pearson correlations showed liver and serum associations. Sensitivity and specificity were calculated for >5%, 7.5%, and 10% total serum VA as REs to predict TLRs and for serum retinol <0.7 and 1 µmol/L to predict deficiency. Results: Serum RE concentrations were correlated with TLRs (r = 0.497, P < 0.001). Nine subjects (33%) had hypervitaminosis A (≥1.0 µmol VA/g liver), 2 of whom had >7.5% total serum VA as REs; histologic indicators corroborated toxicity at 3 µmol/g liver. No subject had >10% total serum VA as REs. Serum retinol sensitivity to determine deficiency (TLRs <0.1 µmol VA/g) was 83% at 0.7 and 1 µmol/L. Hepatic α-retinol was positively correlated with age (P = 0.047), but removing an outlier nullified significance. Conclusions: This study evaluated serum REs as a biomarker of VA status against TLRs (gold standard), and abnormal histology suggested that 7.5% total serum VA as REs is diagnostic for toxicity at the individual level in adults. The long-term impact of VA supplements and fortificants on VA status is currently unknown. Considering the high prevalence of hypervitaminotic TLRs in this cohort, and given that many countries are adding preformed VA to processed products, population biomarkers diagnosing hypervitaminosis before toxicity are urgently needed. This trial was registered at clinicaltrials.govas NCT03305042.

Insights of hypercarotenaemia: A brief review.

Carotenoids are generally 40-carbon tetraterpenoids responsible for most of the yellow, orange and red colours throughout the natural world. Pro-vitamin A carotenoids serve as the precursors of vitamin A. In addition to that, carotenoids exhibit range of important protective mechanisms in human health. Hypercarotenaemia is characterized by carotenodermia resulting in yellowing of the skin specially palms and soles. Hypercarotenaemia develops in subjects consuming high levels of carotenoid rich foods or ß-carotene supplements (>30 mg day-1) over a period of months. Less or normal intake of carotenoids very rarely gives rise to metabolic carotenaemia due to genetic defects of the enzyme 15-15'-carotenoid dioxygenase. Moreover, it is known that those with hypothyroidism and diabetes mellitus tend to develop hypercarotenaemia with the normal intake of carotenoid rich foods. Further, hypercarotenaemia has been reported in anorexia nervosa. However, recently some studies have been shown that there is no major correlation between carotenoid intake and hypercarotenaemia indicating that a genetic factor is at play in development of hypercarotenaemia. Therefore, the subjects appear to need to be genetically pre-disposed to hypercarotenaemia.

Hipercarotinemia tras cirugía bariátrica / Hypercarotinemia after bariatric surgery

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High provitamin A carotenoid serum concentrations, elevated retinyl esters, and saturated retinol-binding protein in Zambian preschool children are consistent with the presence of high liver vitamin A stores.

BACKGROUND: Biomarkers of micronutrient status are needed to best define deficiencies and excesses of essential nutrients. OBJECTIVE: We evaluated several supporting biomarkers of vitamin A status in Zambian children to determine whether any of the biomarkers were consistent with high liver retinol stores determined by using retinol isotope dilution (RID). DESIGN: A randomized, placebo-controlled, biofortified maize efficacy trial was conducted in 140 rural Zambian children from 4 villages. A series of biomarkers were investigated to better define the vitamin A status of these children. In addition to the assessment of total-body retinol stores (TBSs) by using RID, tests included analyses of serum carotenoids, retinyl esters, and pyridoxal-5'-phosphate (PLP) by using high-pressure liquid chromatography, retinol-binding protein by using ELISA, and alanine aminotransferase (ALT) activity by using a colorimetric assay. RESULTS: Children (n = 133) were analyzed quantitatively for TBSs by using RID. TBSs, retinyl esters, some carotenoids, and PLP differed by village site. Serum carotenoids were elevated above most nonintervened reference values for children. α-Carotene, ß-carotene, and lutein values were >95th percentile from children in the US NHANES III, and 13% of children had hypercarotenemia (defined as total carotenoid concentration >3.7 µmol/L). Although only 2% of children had serum retinyl esters >10% of total retinol plus retinyl esters, 16% of children had >5% as esters, which was consistent with high liver retinol stores. Ratios of serum retinol to retinol-binding protein did not deviate from 1.0, which indicated full saturation. ALT activity was low, which was likely due to underlying vitamin B-6 deficiency, which was confirmed by very low serum PLP concentrations. CONCLUSIONS: The finding of hypervitaminosis A in Zambian children was supported by high circulating concentrations of carotenoids and mildly elevated serum retinyl esters. ALT-activity assays may be compromised with co-existing vitamin B-6 deficiency. Nutrition education to improve intakes of whole grains and animal-source foods may enhance vitamin B-6 status in Zambians.

A Case Report of Acute Vitamin A Intoxication due to Ocean Perch Liver Ingestion.

BACKGROUND: Chronic vitamin A intoxication is well known; however, there are few reports of acute vitamin A intoxication due to the ingestion of food rich in vitamin A, particularly in adults. CASE REPORT: We report a case of a 27-year-old man presenting with chief complaints of flushing, headache, nausea, and joint pain. He had consumed 800 g of grilled ocean perch liver the day before and had experienced numbness shortly after. Although physical examination revealed only facial flushing, we suspected acute vitamin A intoxication due to his diet history. On day 2 after ingestion, his serum retinol levels were elevated at 1577 ng/mL, which confirmed vitamin A intoxication. He returned for follow-up on day 4 after ingestion, by which time his presenting symptoms had improved, but he had developed desquamation of his facial skin. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Emergency physicians should consider acute vitamin A intoxication in the differential diagnosis of patients with headache, flushing, desquamation, nausea, and vomiting of unknown etiology. Complete diet histories and checking vitamin A levels are essential for diagnosis. This report highlights the diagnostic difficulties associated with vitamin A intoxication and the importance of an accurate diet history.

Comparisons among Equations Used for Retinol Isotope Dilution in the Assessment of Total Body Stores and Total Liver Reserves.

Vitamin A plays an essential role in animal biology and has negative effects associated with both hypo- and hypervitaminosis A. Many notable interventions are being done globally to eliminate vitamin A deficiency, including supplementation, fortification, and biofortification. At the same time, it is important to monitor vitamin A status in nations where preformed vitamin A intake is high because of consumption of animal source foods (e.g., liver, dairy, eggs), fortified foods (e.g., milk, cereals, oil, sugar, margarine), or vitamin supplements (e.g., one-a-day multivitamins) to ensure the population does not reach hypervitaminosis A. To accurately assess population status and evaluate interventions aimed at improving vitamin A status, accurate assessment methods are needed. The primary storage site of vitamin A is the liver; however, routinely obtaining liver samples from humans is impractical and unethical. Isotope dilution using deuterium- or (13)C-labeled retinol is currently the most sensitive indirect biomarker of vitamin A status across a wide range of liver reserves. The major drawback to its application is the increased technicality in sample analysis and data calculations when compared to less sensitive methodology, such as serum retinol concentrations and dose response tests. Two main equations have emerged for calculating vitamin A body pool size or liver concentrations from isotope dilution data: the "Olson equation" and the "mass balance equation." Different applications of these equations can lead to confusion and lack of consistency if the underlying principles and assumptions used are not clarified. The purpose of this focused review is to describe the evolution of the equations used in retinol stable-isotope work and the assumptions appropriate to different applications of the test. Ultimately, the 2 main equations are shown to be fundamentally the same and differ only in assumptions made for each specific research application.

Acute hypervitaminosis A in a young lady.

Acute vitamin A toxicity from a large dose has been reported to cause pseudotumour cerebri. Usually it is common in children. Herein we present the case of a young lady of 18 years old with the complaints of headache, vomiting, back pain and diplopia after ingestion of high dose (about 10 million international units) vitamin A capsule intentionally at a time due to some family problems. She gave no history of fever, convulsion, unconsciousness, pain in eyes, difficulties in walking and jaundice or any urinary problem during this illness. On query she gave no history of taking any other drugs including oral contraceptive and tetracycline & steroids. She also gave no history of sleep disorder. There was bilateral papilloedema, pupils were a bit dilated symmetrically but reacting to light, visual acuity 6/60 on left eye and 6/18 on right eye and bilateral 6th cranial nerve palsy more marked on left side. MRI of brain and orbits showed normal study. Patient improved after giving acetazolamide.

[Hypercarotenaemia in an infant]. / Hypercaroténémie chez un nourrisson.

BACKGROUND: Hypercarotenaemia is the consequence of high serum carotenoid levels, which are deposited in the stratum corneum and give a yellowish coloration to the skin. It can be distinguished from jaundice by the absence of colouring of the conjunctivae as well as orange discolouration of the palms and soles. CASE REPORT: We report a rare case of hypercarotenaemia in a child that began at the age of three months. Clinical signs and symptoms included yellowish discolouration of the skin, orange palms and soles, xerosis and pruritus. Hypercarotenaemia was confirmed by high levels of serum carotenoids. Serum vitamin A was normal. Dietary and drug-induced causes of hypercarotenaemia were excluded in this case, as well as other classical metabolic causes (renal insufficiency, malabsorption syndrome, diabetes, hypothyroidism). The child was placed on a low-carotenoids diet for six months, resulting in decreased serum carotenoid levels and regression of cutaneous signs and symptoms, especially pruritus. DISCUSSION: Although pruritus has never been reported in isolated hypercarotenaemia it is a classical sign of hypervitaminosis A. The mechanism of pruritus is not understood in this instance since vitamin A levels were normal. This case report is also unusual in that no classical cause of hypercarotenaemia was found, as a result of which we concluded on a likely defect in beta-carotene 15, 15'oxygenase, an enzyme involved in vitamin A production.

Dysphagia and hypervitaminosis A: cervical hyperostosis.

UNLABELLED: Vertebral hyperostosis typically predominates at the thoracic spine and causes only minor symptoms. Involvement of the cervical spine may cause dysphagia due to pressure on the esophagus. We report three cases of dysphagia revealing cervical hyperostosis. CASE REPORTS: The patients were 3 men aged 54-73 years. Dysphagia was moderate in 2 patients and severe in 1 patient who had lost 4 kg over 6 months. Stiffness of the neck with mild pain was present. One patient reported a neck injury in childhood and another had a brother and father with similar symptoms. Radiographs showed exuberant anterior cervical hyperostosis. Two patients also had hyperostotic changes at the thoracic spine and pelvis. The skin and neurological evaluation were normal. Findings were normal from standard blood tests (C-reactive protein, calcium, and vitamin D). Tests were negative for the HLA-B27 antigen in all 3 patients. Serum vitamin A levels were high, ranging from 894 to 1123 microg/L (normal, 489-720). None of the patients reported taking retinoids or having unusual eating habits. DISCUSSION: Dysphagia can result from anterior cervical hyperostosis. A role for hypervitaminosis A in the genesis of hyperostosis has long been suspected. In our patients, the absence of vitamin A supplementation suggests an abnormality in vitamin A metabolism.

[Hypercalcemia revealing iatrogenic hypervitaminosis A in a child with autistic troubles]. / Hypercalcémie révélant une hypervitaminose A iatrogène chez un enfant atteint de troubles autistiques.

UNLABELLED: Hypervitaminosis A is an unusual cause of infant hypercalcemia. The way it occurs can be very surprising, as one can notice from the following case report. CASE REPORTS: A three-year-old boy, presenting important behavioral disorders, was hospitalized because of a deterioration of his general state of health associated with vomiting, cephalgias, fever and cutaneous abnormalities. A 168 mg/L hypercalcemia was found. The only etiology is a deviant consumption of vitamin A within the framework of an "autistic diet": 100000 UI/d during three months, and then 150000 UI/d the three following months. Intoxication was confirmed by the increased vitamin A plasmatic level, and vitamin A/RBP molar ratio and by the presence of plasmatic retinyl palmitate. An emergency treatment by rehydration, biphosphonates and furosemide led to effective calcemia normalization. CONCLUSION: In the case of nonobvious causes of hypercalcemia, a thorough cross-examination must look for vitamin A intoxication. Our observation illustrates the danger of certain diets suggested for autistic children.

Vitamin A toxicity in a physical culturist patient: a case report and review of the literature.

Excessive intake of vitamin A may produce acute or chronic toxicity. Vitamin A can be consumed in foods, fortified products and supplements. We present a case of a young physical culturist man who was referred to our Unit because of chronic liver disease of unknown origin. The patient had a history of increased vitamin A intake from natural source with the addition of high dose of vitamin A supplements with the purpose of improving his muscular development. Our patient showed chronic liver disease with severe fibrosis, signs of portal hypertension and marked hyperplasia of Ito cells. In conclusion, chronic vitamin A toxicity may produce severe liver damage and should be recognized in the differential diagnosis of chronic liver diseases.