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Prenatal Care
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Gabriele Saccone, Kerri Sendek
In pregnancy, some extra vitamin A is required for growth and tissue maintenance in the fetus, for providing fetal reserves, and for maternal metabolism. However, vitamin A in its synthetic form as well as in large doses as retinol (preformed vitamin A found in cod liver oil and chicken or beef liver) is teratogenic. It is recommended that pregnant women ingest vitamin A as β-carotene and limit the ingestion of retinol during pregnancy. In vitamin A–deficient populations (where night blindness is present) and in HIV-positive women, vitamin A supplementation reduces maternal night blindness and anemia. Excess vitamin A intake can cause birth defects and miscarriages at doses >25,000 IU/day. Vitamin A supplements should be avoided, with maximum daily intake prior to and during pregnancy probably 5000 IU and certainly ≤10,000 IU, respectively. Vitamin A supplementation may be beneficial in women with vitamin A deficiency, especially in prevention of night blindness, in developing countries. Optimal duration of supplement use cannot be evaluated. One large population-based trial in Nepal shows a possible beneficial effect on maternal mortality after weekly vitamin A supplements. Night blindness, associated with vitamin A deficiency, was assessed in a nested case-control study within this trial and found to be reduced but not eliminated. There is insufficient evidence to support vitamin A supplementation as an intervention for anemia [83, 84].
Crocus sativus and the Prized Commodity, Saffron
Published in Raymond Cooper, Jeffrey John Deakin, Natural Products of Silk Road Plants, 2020
Jeffrey John Deakin, Raymond Cooper
β-Carotene is cleaved by the action of an enzyme in the human body to form retinol, which functions as a form of storage for retinal in the body. Subsequent chemical reduction of the alcohol functional group readily occurs in the body to give the visually active and corresponding aldehyde, retinal. Vitamin A is needed by the retina of the eye in the form of retinal, which influences low-light and color vision. Night blindness, an inability to see well in dim light, is one of the earliest signs of vitamin A deficiency followed by decreased visual acuity.
Neurodegeneration, ataxia, and retinitis pigmentosa (NARP)
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Night blindness is often the first symptom of these patients [6]. This is followed by loss of peripheral vision and, in some, loss of central vision. The index patient at 47 years could just perceive light. Examination of the retina reveals evidence of retinitis pigmentosa (Figures 53.1 and 53.2). The appearance of the clumps of pigment in the retina typically resembles spicules of bone [1, 7]. Some retinas may have a salt-and-pepper appearance [8]. The electroretinogram may be abnormal, as may visual fields. Others have optic atrophy [9]. There may be nystagmus on horizontal or vertical gaze and esotropia [8]. Progression of retinal disease has been described from the appearance of salt and pepper in the retina in the absence of symptoms to constriction of visual fields along with the appearance of bone spicules in the retina, optic nerve pallor, and arteriolar attenuation [10].
Management of a case of Enhanced S-cone syndrome with massive foveoschisis treated with pars plana vitrectomy with silicone oil tamponade
Published in Ophthalmic Genetics, 2021
Lorane Bechet, Raphaël Atia, Christina Zeitz, Saddek Mohand-Saïd, José-Alain Sahel, Pierre-Oliver Barale, Isabelle Audo
The main symptoms are night blindness due to the absence of functional rods, a variable loss of VA, and an altered visual field. Many clinical phenotypes have been described (10–13). One typical feature seen in the fundus, is pigmentary alteration that is present in the pigment epithelium, distributed annularly along the vascular arcades. GFS is a more severe form of ESCS with degenerative vitreous changes and both peripheral and macular retinoschisis (14). Retinoschisis is identified on OCT as a separation in the retinal layers or foveal cysts. Full field electroretinogram (ffERG) in ESCS is pathognomonic and shows undetectable rod response and a similar wave form in both scotopic and photopic conditions for the same flash intensities in relation with cone-dominated scotopic response. The 30 Hz flicker responses are markedly delayed and are of lower amplitude than the photopic a-wave to a single flash in relation to an excess of S-cones (3,11).
Oliver McFarlane syndrome: two new cases and a review of the literature
Published in Ophthalmic Genetics, 2021
Kristian Lisbjerg, Mette K. G. Andersen, Mette Bertelsen, Agnes G. Brost, Frederik F. Buchvald, Rikke B. Jensen, Anne-Marie Bisgaard, Thomas Rosenberg, Zeynep Tümer, Line Kessel
Parents noticed visual difficulties from the age of two. At the age of three years, the patient underwent an ophthalmological examination at which point poor visual acuity equivalent to 20/200 (binocular) and a pale fundus with peripheral pigmentations was noted. The signs of severe chorioretinal degeneration were confirmed with ff-ERG that showed extinguished dark-adapted single flash and only a slight residual flicker response indicating absent rod function and very limited cone function. Complete night blindness was reported. The diagnosis at this point was early-onset retinitis pigmentosa. Fundoscopic findings were described as choroideremia-like. Due to dysmorphic features (Figure 1), growth retardation, and retinal degeneration a syndrome was suspected, and in the following years several clinical investigations were performed in the pursuit of a more exact diagnose. Chromosome analysis showed a normal female karyotype, 46,XX. The hair was examined for suspected Menkes disease or trichothiodystrophy but with no conclusive findings. At the age of three, thyroidal parameters were normal and clonidine stimulation of growth hormone (GH) also showed a normal result. Growth retardation persisted and by the age of 10, treatment with GH was initiated and she ended up with an adult height of 158 cm.
Differential effect of a carotenoid-rich diet on retina function in non-diabetic and diabetic rats
Published in Nutritional Neuroscience, 2020
Kathleen J. McClinton, Michel Aliani, Sharee Kuny, Yves Sauvé, Miyoung Suh
Carrots, a well-known health food for the eyes, are one of the richest sources of β-carotene and α-carotene.1,2 Carotenoids are essential for retina function, as precursors of vitamin A, the very substrate of the only chromophore of photoreceptors (rods and cones), 11-cis retinal.3 The aldehyde form of vitamin A (11-cis retinal), converted solely from the diet, covalently binds to the photopigment opsin, and initiate phototransduction cascade when photoisomerized from cis to trans in response to photon catch.4 While 11-cis retinal is recycled by the retina, a continuous supply remains essential for the first steps of vision. Vitamin A deficiency can cause night blindness if sustained.5 Numerous studies have examined the role of supplementation of purified vitamin A, and β-carotene respectively on healthy vision and visual disorders; however, the impact of a whole food containing several carotenoids has been never tested.