B-Vitamine in der Geriatrie – was bestimmen, was ersetzen?

2021 ◽  
Vol 146 (03) ◽  
pp. 152-156
Author(s):  
Marija Djukic ◽  
Christine A.F. von Arnim

Was ist neu? Klinische Manifestation eines B-Vitamin-Mangels Ein Vitamin-B1-Mangel kann sich als Wernicke-Enzephalopathie oder als Beriberi manifestieren. Geriatrische Patienten mit den Diagnosen Demenz oder Delir haben niedrigere Vitamin-B1-Spiegel als solche ohne diese Diagnosen. Ebenso zeigen sich bei geriatrischen Patienten mit höherem Vitamin-B1-Spiegel bessere Ergebnisse in der Funktionalität (Barthel-Index) bei Entlassung. Vitamin B6 ist an über 100 Reaktionen als Koenzym beteiligt und ein Mangel kann daher mit vielen Symptomen einhergehen. Klinische Manifestationen des Vitamin-B12-Mangels reichen von frühen neuropsychiatrischen bis zu hämatologischen Symptomen, wobei die makrozytäre Anämie als später Indikator eines Vitamin-B12-Mangels gilt. Neurologische Symptome treten sehr häufig schon vor oder ohne hämatologische Manifestationen auf. Diagnostik von B-Vitamin-Mangelzuständen Die Bestimmung des Vitamin-B1-Spiegels im Blut ist wenig aussagekräftig. Die Wernicke-Enzephalopathie ist eine klinische Diagnose. Zur Diagnose eines Vitamin-B6-Mangels wird die Bestimmung von Pyridoxin (Pyridoxal-5′-Phosphat) im Plasma empfohlen. Ein erniedrigter Holo-TC-Spiegel im Serum gilt als frühester Marker eines Vitamin-B12-Mangels. Eine kombinierte Bestimmung von Vitamin B12, Holo-TC, MMA und Homozystein scheint die diagnostische Zuverlässigkeit bei Vitamin-B12-Mangel zu erhöhen. Therapie Für Empfehlungen zur Substitutionstherapie bei allen B-Vitaminen liegen kaum bzw. keine evidenzbasierten Daten vor. Durch die Substitution von 0,8 mg Folsäure, 0,5 mg Vitamin B12 und 20 mg Vitamin B6 konnte in einer randomisierten kontrollierten Studie bei Patienten mit einer leichten kognitiven Störung eine Verlangsamung der Hirnatrophie bewirkt werden.

2021 ◽  
Vol 46 (05) ◽  
pp. 312-316
Author(s):  
Marija Djukic ◽  
Christine A. F. von Arnim

ZusammenfassungEin Vitamin-B1-Mangel kann sich als Wernicke-Enzephalopathie oder als Beriberi manifestieren. Geriatrische Patienten mit den Diagnosen Demenz oder Delir haben niedrigere Vitamin-B1-Spiegel als solche ohne diese Diagnosen. Ebenso zeigen sich bei geriatrischen Patienten mit höherem Vitamin-B1-Spiegel bessere Ergebnisse in der Funktionalität (Barthel-Index) bei Entlassung. Vitamin B6 ist an über 100 Reaktionen als Koenzym beteiligt und ein Mangel kann daher mit vielen Symptomen einhergehen. Klinische Manifestationen des Vitamin-B12-Mangels reichen von frühen neuropsychiatrischen bis zu hämatologischen Symptomen, wobei die makrozytäre Anämie als später Indikator eines Vitamin-B12-Mangels gilt. Neurologische Symptome treten sehr häufig schon vor oder ohne hämatologische Manifestationen auf. Die Bestimmung des Vitamin-B1-Spiegels im Blut ist wenig aussagekräftig. Die Wernicke-Enzephalopathie ist eine klinische Diagnose. Zur Diagnose eines Vitamin-B6-Mangels wird die Bestimmung von Pyridoxin (Pyridoxal-5′-Phosphat) im Plasma empfohlen. Ein erniedrigter Holo-TC-Spiegel im Serum gilt als frühester Marker eines Vitamin-B12-Mangels. Eine kombinierte Bestimmung von Vitamin B12, Holo-TC, MMA und Homozystein scheint die diagnostische Zuverlässigkeit bei Vitamin-B12-Mangel zu erhöhen. Für Empfehlungen zur Substitutionstherapie bei allen B-Vitaminen liegen kaum bzw. keine evidenzbasierten Daten vor. Durch die Substitution von 0,8 mg Folsäure, 0,5 mg Vitamin B12 und 20 mg Vitamin B6 konnte in einer randomisierten kontrollierten Studie bei Patienten mit einer leichten kognitiven Störung eine Verlangsamung der Hirnatrophie bewirkt werden.


2018 ◽  
Vol 1 (1) ◽  
pp. 18-25
Author(s):  
Diane Paparang ◽  
Nurpudji A. Taslim ◽  
Haerani Rasyid ◽  
A. Yasmin Syauki

Pendahuluan Proses penyembuhan luka post amputasi dan luka bakar dengan luas 25% dan kedalaman derajat III serta hipoalbuminemia sedang (albumin 2,6g/dL) dan status gizi kurang memerlukan terapi gizi spesifik tinggi protein. Laporan Kasus Tn.I, laki-laki, 28 tahun dikonsul oleh bagian bedah dengan luka post amputasi dan  luka bakar listrik derajat III luas 25%. Keluhan utama asupan makan kurang sejak 16 hari terakhir karena nafsu makan kurang akibat nyeri pada luka post amputasi dan luka bakar. Ada nyeri ulu hati dan demam menggigil. Asupan 24 jam 1000kkal. Pasien didiagnosis dengan status gizi kurang (LLA=80,7%), status metabolik anemia normositik normokrom (Hb 9.7 g/dl), deplesi sedang sistem imun (TLC 940/µL), hipoalbuminemia (albumin 2,6g/dL) dan status gastrointestinal fungsional. Terapi nutrisi dengan energi 2500 kkal, protein 2 gr/kgBBI/hari (23%), karbohidrat 57% dan lemak 20 %, melalui oral berupa makanan biasa 1250 kkal, ONS glutamine 2.5g/hari, suplementasi 6 butir putih telur (protein 31,5g/hari), vitamin C 1g/24jam, vitamin A 6.000IU/12jam, vitamin B1-100mg, vitamin B6-200mg, vitamin B12-200mg, Zinc 50mg/24jam, selenium 55µg, Curcuma 400mg/8jam dan ekstrak ikan gabus 2 kapsul/8 jam. Setelah perawatan 30 hari, terjadi perbaikan dalam penyembuhan luka, peningkatan LLA menjadi 23,5cm, peningkatan hemoglobin 9.3g/dl, peningkatan sistem imun (TLC 2064/µL), peningkatan albumin 3.9g/dL. Kesimpulan Terapi nutrisi spesifik dengan protein 2 gr/kgBBI dapat meningkatkan kadar albumin dan mempercepat penyembuhan luka pada pasien luka bakar.


2019 ◽  
Vol 104 (10) ◽  
pp. 4837-4847 ◽  
Author(s):  
Kirsty M Porter ◽  
Mary Ward ◽  
Catherine F Hughes ◽  
Maurice O’Kane ◽  
Leane Hoey ◽  
...  

AbstractContextEmerging evidence suggests that deficiencies of folate-related B vitamins can arise with metformin treatment and are independently linked with cognitive dysfunction, a comorbidity of diabetes.ObjectiveTo determine the impact of hyperglycemia and metformin use on relevant B vitamin biomarkers and cognitive outcomes in older adults.Setting and ParticipantsCommunity-dwelling older adults (74.1 ± 8.3 years, n = 4160) without dementia, recruited to the Trinity, Ulster and Department of Agriculture cohort study in 2008 to 2012, were classified as normoglycemic (n = 1856) or hyperglycemic, based on HbA1c ≥5.7% (39 mmol/mol), either with (n = 318) or without (n = 1986) metformin treatment.Main Outcome MeasuresBiomarkers of folate, vitamin B12, vitamin B6, and riboflavin were measured. Cognitive assessments included the Repeatable Battery for Assessment of Neuropsychological Status (RBANS) and the Frontal Assessment Battery (FAB).ResultsMetformin use was associated with higher risk of deficiency of vitamin B12 (combined B12 index ≤−1; OR 1.45; 95% CI, 1.03 to 2.02) and vitamin B6 (plasma pyridoxal 5-phosphate <30.0 nmol/L; OR 1.48; 95% CI, 1.02 to 2.15). Fortified foods when eaten regularly had a positive impact on all relevant B vitamin biomarkers, even with hyperglycemia. After adjustment for relevant covariates, metformin use was associated with an increased risk of cognitive dysfunction as assessed with the RBANS (OR 1.36; 95% CI, 1.03 to 1.80) and FAB (OR 1.34; 95% CI, 1.03 to 1.74).ConclusionsUse of metformin by older adults is associated with poorer cognitive performance; B vitamin deficiency may be implicated. Fortified foods can optimize B vitamin status and may be beneficial for maintaining better cognitive health in older people with or at risk for diabetes.


2003 ◽  
Vol 49 (1) ◽  
pp. 155-161 ◽  
Author(s):  
Mustafa Vakur Bor ◽  
Helga Refsum ◽  
Marianne R Bisp ◽  
Øyvind Bleie ◽  
Jorn Schneede ◽  
...  

Abstract Background: Vitamin B6 has attracted renewed interest because of its role in homocysteine metabolism and its possible relation to cardiovascular risk. We examined the plasma B6 vitamers, pyridoxal 5′-phosphate (PLP), pyridoxal (PL), pyridoxine (PN), and 4-pyridoxic acid (4-PA) before and after vitamin B6 supplementation. Methods: Patients (n = 90; age range, 38–80 years) undergoing coronary angiography (part of the homocysteine-lowering Western Norway B-Vitamin Intervention Trial) were allocated to the following daily oral treatment groups: (A), vitamin B12 (0.4 mg), folic acid (0.8 mg), and vitamin B6 (40 mg); (B), vitamin B12 and folic acid; (C), vitamin B6; or (D), placebo. EDTA blood was obtained before treatment and 3, 14, 28, and 84 days thereafter. Results: Before treatment, PLP (range, 5–111 nmol/L) and 4-PA (6–93 nmol/L) were the predominant B6 vitamers identified in plasma. During the 84-day study period, the intraindividual variation (CV) in patients not treated with vitamin B6 (groups B and D) was 45% for PLP and 67% for 4-PA. Three days after the start of treatment, the increases in concentration were ∼10-, 50-, and 100-fold for PLP, 4-PA, and PL, respectively. No significant additional increase was observed at the later time points. The PLP concentration correlated to the concentrations of 4-PA and PL before treatment, but not after treatment. The PL concentration correlated with 4-PA before and after treatment. Conclusions: Vitamin B6 treatment has an immediate effect on the concentrations and the forms of B6 vitamers present in plasma, and the changes remain the same during prolonged treatment. Our results suggest that the B6 vitamers in plasma reflect vitamin B6 intake.


2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Simone Baltrusch

Damage and regeneration naturally occur in the peripheral nervous system. The neurotropic B vitamins thiamine (B1), pyridoxine (B6), and cobalamin (B12) are key players, which maintain the neuronal viability in different ways. Firstly, they constantly protect nerves against damaging environmental influences. While vitamin B1 acts as a site-directed antioxidant, vitamin B6 balances nerve metabolism, and vitamin B12 maintains myelin sheaths. However, nerve injury occurs at times, because of an imbalance between protective factors and accumulating stress and noxae. This will result in the so-called Wallerian degeneration process. The presence of vitamins B1, B6, and B12 paves the way out to the following important regeneration by supporting the development of new cell structures. Furthermore, vitamin B1 facilitates the usage of carbohydrates for energy production, whereas vitamin B12 promotes nerve cell survival and remyelination. Absence of these vitamins will favor permanent nerve degeneration and pain, eventually leading to peripheral neuropathy.


Author(s):  
Trung Vinh Hoàng

Bài tổng quan sau đây nói về mối liên quan giữa đái tháo đường typ 2 (ĐTĐT2) với từng loại vitamin nói chung cũng như vitamin tổng hợp. Nồng độ các vitamin có tác dụng chống gốc tự do như vitamin A, C và E đều giảm ở BN ĐTĐ làm gia tăng các stress oxi hóa, góp phần gây bất thường chuyển hóa glucose. Mặt khác các protein mang retinol (vitamin A) còn có tác dụng điều biến tương tự như các adipokin. Mặc dù cơ chế gây giảm nồng độ các vitamin nhóm B như thiamin (vitamin B1), vitamin B6 và biotin là hoàn toàn chưa rõ song nếu bổ sung các loại đó lại có tác dụng cải thiện kiểm soát chuyển hóa ở BN ĐTĐ. Hấp thu acid folic và vitamin B12 sẽ bị giảm đi nếu sử dụng merformin kéo dài trong khi đó đây lại là thuốc lựa chọn hàng đầu để điều trị ĐTĐ chưa có biến chứng. Chính vì vậy nồng độ hai loại này bị thiếu hụt, rất cần bổ sung thường xuyên. Vitamin D đóng vai trò như là yếu tố nguy cơ (YTNC) gây biến chứng ở BN trong đó có biến chứng tim mạch. Cũng có ý kiến cho rằng vitamin K có liên quan đến chuyển hóa glucose song cần phải có thêm bằng chứng trong nghiên cứu. Việc sử dụng vitamin tổng hợp cho hiệu quả chưa rõ rệt. Tuy vậy hiện nay vẫn chưa có một chỉ định thống nhất nào về bồi phụ vitamin thiếu hụt ngoại trừ sử dụng acid folic và vitamin B12 nếu điều trị bằng metformin kéo dài.


Fermentation ◽  
2021 ◽  
Vol 7 (3) ◽  
pp. 178
Author(s):  
Wilawan Palachum ◽  
Wanna Choorit ◽  
Yusuf Chisti

Nutritionally enhanced probioticated whole pineapple juice (WPJ, comprising juice of pineapple pulp and peel) beverages were produced by fermentation of WPJ with the probiotic bacterium Lactobacillus plantarum WU-P19. The 12 h fermented juice contained between 2.1 × 109 and 3.7 × 109 live cells of the probiotic per milliliter, depending on the beverage formulation. The beverage had a pH of around 4.1 and a lactic acid content of ~12.8 g L−1. It had a total sugar (glucose, sucrose, fructose, maltose) content of ~100.2 g L−1. During fermentation, some of the initial glucose and fructose were consumed by the probiotic, but sucrose and maltose were not consumed. The original WPJ was free of vitamin B12, but fermentation enhanced vitamin B12 content (~19.5 mg L−1). In addition, fermentation enhanced the concentrations of vitamins B2, B3, and B6, but the bacterium consumed some of the vitamin B1 originally present. From a nutritional perspective, the final probioticated beverage was a good source of vitamin B12, vitamin C and vitamin B6. In addition, it contained nutritionally useful levels of vitamins B1, B2, and B3. The calorific value of the final beverage was 56.94 kcal per 100 mL. The product was stable during 21-day refrigerated (4 °C) storage.


2002 ◽  
Vol 48 (10) ◽  
pp. 1768-1771 ◽  
Author(s):  
Ebba Nexo ◽  
Anne-Mette Hvas ◽  
Øyvind Bleie ◽  
Helga Refsum ◽  
Sergey N Fedosov ◽  
...  

Abstract Background: We examined the effect of oral vitamin B12 treatment on fluctuations in plasma total cobalamin and its binding proteins transcobalamin (TC) and haptocorrin (HC). Methods: Patients (n = 88; age range, 38–80 years) undergoing coronary angiography (part of the homocysteine-lowering Western Norway B-Vitamin Intervention Trial) were allocated to daily oral treatment with (a) vitamin B12 (0.4 mg), folic acid (0.8 mg), and vitamin B6 (40 mg); (b) vitamin B12 and folic acid; (c) vitamin B6; or (d) placebo. EDTA blood was obtained before treatment and 3, 14, 28, and 84 days thereafter. Results: The intraindividual variation for patients not treated with B12 was ∼10% for plasma total cobalamin, total TC, apo-TC, and apo-HC, and &lt;20% for holo-TC and TC saturation. In B12-treated patients, the maximum change in concentrations was observed already after 3 days for total TC (−16%), holo-TC (+54%), and TC saturation (+82%). At this time holo-HC (+20%) and plasma total cobalamin (+28%) showed an initial burst, but had increased further at 84 days. All changes were highly significant compared with the control group (P &lt;0.0001). Conclusions: Oral vitamin B12 treatment produces maximal effects on total TC, holo-TC, and TC saturation within 3 days, whereas maximal increases in holo-HC and plasma total cobalamin occur later. The results support the view that holo-TC is an early marker of changes in cobalamin homeostasis.


Author(s):  
T.M. Scott ◽  
G. Rogers ◽  
D.E. Weiner ◽  
K. Livingston ◽  
J. Selhub ◽  
...  

Background: Objectives: Elevated plasma total homocysteine (tHcy) is associated with increased risk of cardiovascular disease, stroke and dementia. Results of clinical trials using B-vitamins to reduce the cognitive risks attributed to tHcy have been inconsistent. The high prevalence of both hyperhomocysteinemia and cognitive impairment among kidney transplant recipients makes them an important population in which to evaluate the effect of lowering homocysteine on cognitive function. We therefore evaluated whether B-vitamin therapy to lower tHcy would prevent cognitive-decline in a cohort of stable kidney transplant recipients. Design: The study was a longitudinal ancillary of the FAVORIT trial, a randomized, placebo-controlled multi-site trial of high-dose B vitamins to reduce cardiovascular and cerebrovascular events in clinically stable kidney transplant recipients with elevated tHcy. Participants: 584 participants from 18 sites across North America. Intervention: The intervention consisted of a daily multivitamin containing high-doses of folate (5.0 mg), vitamin B12 (1.0 mg) and vitamin B6 (50 mg). The placebo consisted of a daily multi-vitamin containing no folate and recommended daily allowances of vitamins B12 and B6 (0 mg folate; 2.0 µg vitamin B12; 1.4 mg vitamin B6). Measurements: Annual neuropsychological assessment for up to 5 years (mean 3.3 years) using a standardized test battery. Efficacy was analyzed on an intention-to-treat basis using end-of-trial data. Subgroup analyses included stratification for baseline plasma B-vitamin and tHcy concentrations. Results: At baseline, cognitive impairment was common with 61% of participants falling more than one standard deviation below published norms for at least one cognitive test. Fewer than 1% of participants had insufficient plasma folate < 5 ng/ml or vitamin B12 < 148 pmol/L. However, 44.6% had plasma B6 concentrations < 30 nmol/L. At follow-up, processing speed and memory scores were modestly but significantly better in the B-vitamin supplement group than in controls (p≤0.05). There was no interaction between baseline tHcy, B-vitamin status and treatment on the cognitive outcomes. Conclusions: High-dose B-vitamin supplementation provided modest cognitive benefit for kidney transplant recipients with elevated baseline tHcy. Since nearly all participants were folate and vitamin B12 sufficient at baseline, the potential cognitive benefits of folate and B12 supplementation in individuals with poor B-vitamin status remains to be determined.


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