Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

Thiamin is a water-soluble vitamin also known as vitamin B1. Its biologically active form, thiamin pyrophosphate (TPP), is a cofactor in macronutrient metabolism. In addition to its coenzyme roles, TPP plays a role in nerve structure and function as well as brain metabolism. Signs and symptoms of thiamin deficiency (TD) include lactic acidosis, peripheral neuropathy, ataxia, and ocular changes (eg, nystagmus). More advanced symptoms include confabulation and memory loss and/or psychosis, resulting in Wernicke's encephalopathy and/or Wernicke's Korsakoff syndrome, respectively. The nutrition support clinician should be aware of patients who may be at risk for TD. Risk factors include those patients with malnutrition due to 1 or more nutrition-related etiologies: decreased nutrient intake, increased nutrient losses, or impaired nutrient absorption. Clinical scenarios such as unexplained heart failure or lactic acidosis, renal failure with dialysis, alcoholism, starvation, hyperemesis gravidarum, or bariatric surgery may increase the risk for TD. Patients who are critically ill and require nutrition support may also be at risk for TD, especially those who are given intravenous dextrose void of thiamin repletion. Furthermore, understanding thiamin's role as a potential therapeutic agent for diabetes, some inborn errors of metabolism, and neurodegenerative diseases warrants further research. This tutorial describes the absorption, digestion, and metabolism of thiamin. Issues pertaining to thiamin in clinical practice will be described, and evidence-based practice suggestions for the prevention and treatment of TD will be discussed.
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PMID:Thiamin in Clinical Practice. 2556 26

Wernicke's encephalopathy (WE) is a potentially fatal neuropsychiatric syndrome precipitated by thiamine deficiency due to a variety of causes such as chronic severe alcoholism, starvation, and prolonged intravenous feeding. WE has also been observed rarely in the clinical setting of hyperemesis gravidarum. Here, we report the case of a 34-year-old pregnant woman who presented with reduced vision, gaze-evoked nystagmus, and postural imbalance preceded by 2 weeks of hyperemesis. Fundus examination showed features consistent with papillitis. Magnetic resonance imaging (MRI) showed T2WI, FLAIR, and diffusion-weighted imaging MR images showing hyperintensity in dorsomedial thalami and periaqueductal grey matter with diffusion restriction. She was diagnosed with WE based on history, clinical examination findings, and MRI findings and was treated with injectable thiamine. She showed marked improvement in vision and nystagmus within 3 days. Our case is a rare presentation of WE in a pregnant woman with hyperemesis gravidarum.
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PMID:Visual loss and optic neuropathy associated with Wernicke's encephalopathy in hyperemesis gravidarum. 3104 Dec 82