The Role of Nutraceuticals in Gestational Diabetes Mellitus
Priyanka Bhatt, Maryam Sadat Miraghajani, Sarvadaman Pathak, Yashwant Pathak in Nutraceuticals for Prenatal, Maternal and Offspring’s Nutritional Health, 2019
Pyridoxine or vitamin B6 is found generally in foods and can be used as a dietary supplement to increase dietary intake or partially reduce disease risk (53). Some clinical examinations have indicated far-reaching beneficial effects of using pyridoxine in the prevention or amelioration of GDM. Early studies showed that blood concentration of vitamin B6 is significantly decreased in diabetic animals and patients54–57. Bennink and colleagues demonstrated that pregnant women with GDM who were treated with vitamin B6 (pyridoxine), 100 mg/day for two weeks, improved oral glucose tolerance considerably (58). Vitamin B6 deficiency is found to reduce circulating insulin levels and has been related to degenerative changes in pancreatic β-cells (59, 60). Beyond that, the health benefits of pyridoxamine (amine form of vitamin B6) can be attributed to the inhibition of the production of oxidative stress markers or scavenging the reactive oxygen species (61). There seems to be an increased requirement/utilization of vitamin B6 in GDM, accordingly various studies are needed to reach a definitive and overall conclusion regarding adjuvant therapy of vitamin B6 in the prevention of GDM complications.
Additional Supplements That Support Glycemic Control and Reduce Chronic Inflammation
Robert Fried, Richard M. Carlton in Type 2 Diabetes, 2018
According to the U.S. Department of Agriculture, Agricultural Research Service, USDA National Nutrient Database for Standard Reference, Release 24 Vitamin (2011), vitamin B6 is found in a wide variety of foods. The richest sources include fish, beef liver and other organ meats, potatoes and other starchy vegetables, and fruit (other than citrus). In the United States, adults obtain most of their dietary vitamin B6 from fortified cereals, beef, poultry, starchy vegetables, and some noncitrus fruits (Subar, Krebs-Smith, Cook et al. 1998). About 75% of the vitamin from a mixed diet is bioavailable.
Macular Degeneration/ Age Related Macular Degeneration (AMD)
Charles Theisler in Adjuvant Medical Care, 2023
Pyridoxine deficiency has been identified in two observational studies in AMD populations. Folate deficiency has been identified in one of the studies. The B vitamins, in general, are important for nerve conduction, and the methylators (B4, B6, and B12) reduce homocysteine levels. Christen et al. reported a reduction in AMD development in 5,205 women observed for 7.3 years who were given daily supplementation consisting of 2,500 mcg B9 (folate), 500 mg B6 (pyridoxine), and 1,000 mcg B12 (cyanocobalamin).10
Peritoneal tuberculosis caused by intravesical instillation with Bacillus Calmette-Guérin (BCG) following nephroureterectomy in a patient with bladder and upper tract urothelial cancer: a case report
Published in Acta Clinica Belgica, 2023
Charlotte Allaeys, Pieter De Backer, Karel Decaestecker, Camille Berquin, Karen Decaestecker, Steven Callens, Charles Van Praet
A percutaneous ascites punction demonstrated an initial negative culture and normal creatinine count, ruling against persistent urinary leak. An exploratory robot-assisted laparoscopy was performed 2 days later. A large amount of ascites was extracted and sent for culture. The peritoneum was found to be intact with no urinary leak present. However, the peritoneum was diffusely thickened and white plaques were seen and biopsied (see Figure 3). The peritoneum overlying the left internal iliac artery was opened and the bladder was filled, exposing a small residual bladder leak that was sutured using a V-loc 3.0 suture (©Medtronic, Minneapolis, USA). A bladder catheter and an abdominal drain were left in place. While the acid-fast staining of the ascites was negative, biopsy of the suspicious plaques confirmed peritoneal tuberculosis based on the presence of acid-fast rods and a positive GeneXpert M. tuberculosis molecular assay. More specific, rifampicin-sensitive Mycobacterium bovis was detected in culture. A two-month triple treatment with isoniazid, rifampicin and ethambutol was initiated, followed by a 7-month dual treatment with isoniazid and rifampicin. Weekly pyridoxine was started to prevent vitamin B6 deficiency.
Neonatal pyridoxine administration long lastingly accelerates cortical spreading depression in male rats, without affecting anxiety-like behavior
Published in Nutritional Neuroscience, 2021
Kelly Rayanne Gondim-Silva, Joselma M. da-Silva, Laís A. V. de Souza, Rubem C. A. Guedes
However, little is known about the brain effects of excessive pyridoxine; in animals, behavioral alterations, denoted by expressive vocalization, aggressiveness against another rat of the same cage and behavior of postural instability have been reported under conditions of excessive pyridoxine administration [9]. The amount of the pyridoxine present in the body is essential for the balance between the states of excitation and neuronal inhibition. Pyridoxine deficiency causes significant effects on different electrophysiological variables [4]. In brain excitability-related diseases, pyridoxine supplementation has been used in the treatment of infant seizures, to reduce seizures in neonatal epileptic encephalopathy, in isoniazid-induced epilepsy and ALDH7A1 mutation or pyridoxine-dependent epilepsy. These conditions do not respond to conventional anticonvulsant therapy, and the treatment consists of pyridoxine monotherapy, the main cofactor for the enzymatic conversion of the neurotransmitter glutamate to GABA [11,12]. Therefore, the development of experimental models to study the pyridoxine/brain excitability relationship is highly desirable.
Isoniazid-induced neuropathy in a pre-pubertal child
Published in Paediatrics and International Child Health, 2019
Naman S. Shetty, Ira Shah
INH induces pyridoxine deficiency by the following mechanisms. It combines with pyridoxine to form isonicotinylhydrazide which is excreted in urine and INH also inhibits pyridoxal phosphokinase which is required to convert pyridoxine to its active form [4]. Patients with INH-induced neuropathy complain initially of tingling and numbness of the feet. If the drug is continued, the tingling and numbness spread up to the knees and also develop in the hands and fingers in a bilateral stocking and glove distribution. Frequently these symptoms are accompanied by myalgia which is made worse by activity. While sensory complaints are such as myalgia and ostealgia dominate, motor symptoms include ataxia, reduction in vibratory and position sense, exaggerated or reduced tendon reflexes and muscle paralysis in the later stages of the syndrome. Unless the syndrome has progressed to evident myalgia, all symptoms are reversible within a few weeks of stopping the INH, although the longer the symptoms are present, the longer they take to resolve [3,4]. Children remain asymptomatic during pyridoxine deficiency because the tissue levels of pyridoxine are maintained by nutrition even when the serum levels are deficient. Symptoms appear once the tissue levels of pyridoxine are deficient [8]. This patient was symptomatic and responded to pyridoxine supplementation and the cessation of INH. Other side-effects of INH therapy are encephalopathy, psychosis, optic atrophy and pyridoxine-responsive anaemia [3].