Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024523 (malabsorption)
 7,319 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.
 ...
PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

Chronic tubulointerstitial renal disease and villous atrophy of the small intestine occurred in two first cousins. Both had protracted diarrhea with malabsorption and died despite intensive parenteral alimentation. In one patient signs of generalized proximal tubular dysfunction developed, followed by nephrotic syndrome and progressive renal insufficiency. A renal biopsy specimen disclosed severe tubulointerstitial disease and membranous glomerulopathy. In this patient, circulating immune complexes were detected and granular deposits of IgG and C3 were seen in the intestinal epithelial cells by direct immunofluorescence. Antiintestinal antibodies (IgG class) were demonstrated by indirect immunofluorescence. The other patient had interstitial nephritis but no glomerular abnormality. On direct immunofluorescence, both patients had confluent granular staining of the renal tubular basement membranes. These immunopathologic studies suggest a common immunologic mechanism in the pathogenesis of the renal and gastrointestinal disorders in these infants.
 ...
PMID:Familial occurrence of renal and intestinal disease associated with tissue autoantibodies. 707 66

Timely nutrition assessment and intervention in organ transplant recipients may improve outcomes surrounding transplantation. A pretransplant nutrition assessment should include a variety of parameters including physical assessment, history, anthropometric measurements, and laboratory tests. Malnutrition compromises posttransplant survival; prolonged waiting times worsen outcomes when patients are already malnourished. Severe obesity may decrease graft function and survival in kidney transplant recipients. In the pretransplant phase, nutritional goals include optimization of nutritional status and treatment of nutrition-related symptoms induced by organ failure. Enteral tube feeding is indicated for patients with functional gastrointestinal tracts who are not eating adequately. Parenteral nutrition is rarely needed pretransplant except in cases of intestinal failure. When determining pretransplant nutrient requirements, nutritional status, weight, age, gender, metabolic state, stage and type of organ failure, malabsorption, induced losses, goals, and comorbid conditions must be considered. During the acute posttransplant phase, adequate nutrition is required to help prevent infection, promote wound healing, support metabolic demands, replenish lost stores, and perhaps mediate the immune response. Nutrient recommendations reflect posttransplant metabolic changes. The appropriateness of posttransplant nutrition support depends on the prevalence of malnutrition among patients with a specific type of organ failure and the benefits when nutrition support is given. Organ transplantation complications including rejection, infection, wound healing, renal insufficiency, hyperglycemia, and surgical complications require specific nutritional requirements and therapies. Many potential applications of nutrition in the pre- and posttransplant phases exist and require further study.
 ...
PMID:Nutrition assessment and support of organ transplant recipients. 1133 61

Hypomagnesemia is seen in 11% of the normal hospital population and in up to 65% of severely ill patients, and can have many causes. The clinical picture may comprise the signs of Chvostek and Trousseau, paraesthesias, tremor and convulsions, although asymptomatic hypomagnesemia is seen most often. Hypomagnesemia can be treated by parenteral or oral administration of magnesium, guided by the serum magnesium level. Parenteral magnesium suppletion is indicated if the concentration is below 0.5 mmol/l or in the presence of symptoms of hypomagnesemia. In patients with magnesium concentrations between 0.5 and 0.7 mmol/l and a deficient diet or malabsorption, prolonged therapy is sometimes necessary. In such cases, oral Mg-containing antacids in a normal dosage regimen may be a good choice, but clinical proof is still lacking. In case of renal insufficiency or constipation the magnesium dose should be lowered, while in hypophosphatemia oral antacids are contra-indicated.
 ...
PMID:[The treatment of hypomagnesemia]. 1251 Apr 10

Hypocalcification of the enamel is the most common developmental disorder observed in teeth. The prevalence of this kind of hypomineralisation is about 10-19%. These molars are often referred to as cheese molars, because the lesions clinically resemble cheese in color and consistency. Other descriptions are: idiopathic enamel hypomineralisation in the permanent first molars, idiopathic enamel opacities in the permanent first molars, non fluoride enamel hypomineralisation in the permanent first molars, non-endemic mottling of enamel in the permanent first molars. Molar-Incisor Hypomineralisation is today the proposed expression for this disease. Occlusal surfaces of the first permanent molar are most commonly affected. The lesions are more frequent in the upper jaw than in the lower jaw. The incisors are affected to a lesser degree than the molars. Several aetiological factors can cause these defects. Some studies show a relation between intake of dioxins via mother's milk after prolonged breast feeding and developmental defects of the child's teeth. Because the ameloblasts are very sensitive to oxygen supply, complications involving oxygen shortages during birth or respiratory diseases such as asthma or bronchitis and pneumonia are discussed as further aetiological factors. Renal insufficiency, hypoparothyroidism, diarrhoea, malabsorption and malnutrition and high-fever diseases can be other reasons for the occurrence of these defects. Defective enamel can be a locus of lowered resistance for caries. Histologically there are areas of porosity of varying degrees. The affected teeth can be very sensitive to air, cold, warm and mechanical stimuli. Toothbrushing may create toothache in these teeth. We therefore suggest that these patients receive intensified prevention with fluoride varnish, a fissure sealing, GIZ, composits, stainless steel crowns or implants. In some cases an interdisciplinary approach with an orthodontist can result in the extraction of the molars in the age of 8 to 10 years.
 ...
PMID:["Molar-incisor hypomineralization"]. 1510 1

Cardiovascular (CV) complications, associated with space flight (SF), are caused by microgravity, hypokinesia and radiation, particularly beyond earth orbit, with all three conducive to oxidative stress. Except for emergencies, pharmaceuticals appear to be contraindicated, because of unpredictable side effects from malabsorption (M) and potential hepatic and renal impairment. Magnesium (Mg) depletion and elevations of cytokines (interleukin 6) occur during SF, conducive to self-sustaining vascular inflammation mechanisms. There are potential endothelial injuries (EI) and reduced Cyclic GMP (a second messenger of nitric oxide: NO) and elevated urinary excretion of C-peptide (insulin resistance: IR). Recent findings that show reductions in vascular endothelial growth factor (VEGF) suggest that this may result from SF-related thrombocytopenia since platelets (P) are the major source of VEGF, and that NO might play a role. Both VEGF and Mg are vital for angiogenesis, endothelial function and reendothelialization. Insulin is necessary for VEGF expression. To prevent SF-related CV complications in the presence of IR and M and with the potential for renal insufficiency, closely monitored subcutaneous (SC) Mg should be provided. The dosage can be monitored by sublingual intracellular Mg assays. Needed is development of a SC Mg reservoir device, which can be replenished before extra-vehicular activities (EVA) and which must be reliable despite vigorous movements during EVA, that can last up to 8 hours. This could also be protective against decompression sickness and EVA-related 100% oxygen requirements before and during this activity, both of which predispost to EI.
 ...
PMID:The case for a subcutaneous magnesium product and delivery device for space missions. 1546 57

Vitamin K (as phylloquinone and menaquinones) is an essential cofactor for the conversion of peptide-bound glutamate to gamma-carboxy glutamic acid (Gla) residues in a number of specialized Gla-containing proteins. The only unequivocal deficiency outcome is a bleeding syndrome caused by an inability to synthesize active coagulation factors II, VII, IX, and X, although there is growing evidence for roles for vitamin K in bone and vascular health. An adult daily intake of about 100 microg of phylloquinone is recommended for the maintenance of hemostasis. Traditional coagulation tests for assessing vitamin K status are nonspecific and insensitive. Better tests include measurements of circulating vitamin K and inactive proteins such as undercarboxylated forms of factor II and osteocalcin to assess tissue and functional status, respectively. Common risk factors for vitamin K deficiency in the hospitalized patient include inadequate dietary intakes, malabsorption syndromes (especially owing to cholestatic liver disease), antibiotic therapy, and renal insufficiency. Pregnant women and their newborns present a special risk category because of poor placental transport and low concentrations of vitamin K in breast milk. Since 2000, the Food and Drug Administration has mandated that adult parenteral preparations should provide a supplemental amount of 150 microg phylloquinone per day in addition to that present naturally, in variable amounts, in the lipid emulsion. Although this supplemental daily amount is probably beneficial in preventing vitamin K deficiency, it may be excessive for patients taking vitamin K antagonists, such as warfarin, and jeopardize their anticoagulant control. Natural forms of vitamin K have no proven toxicity.
 ...
PMID:Vitamin K in parenteral nutrition. 1987 42

Aging is associated with increased incidence and prevalence of both cancer and anemia. Cancer and aging may conspire in making anemia more frequent and more severe. This article reviews the causes and the consequences of anemia in the older individual. The most common causes include chronic inflammation that is a typical manifestation of aging, iron deficiency that may be due to chronic hemorrhage, malabsorption and Helicobacter pylori infection, cobalamin deficiency from malabsorption and renal insufficiency. Other causes of anemia whose prevalence is not well established include myelodysplasia, copper deficiency, hypothyroidism, and sarcopenia. Anemia is associated with increased risk of mortality, functional dependence, dementia, falls, and chemotherapy-related toxicity. When correcting the anemia of older cancer patients one should remember that the erythropoietic stimulating agents (ESA) may stimulate cancer growth and cause thrombosis. These products may be safe when given exclusively to patients receiving chemotherapy and when the hemoglobin levels are maintained below 12 g/dL.
 ...
PMID:Anemia, fatigue and aging. 2106 51

The aims of the present position paper by the Committee on Nutrition of the French Society of Paediatrics were to summarize the recently published data on vitamin D in infants, children and adolescents, i.e., on metabolism, physiological effects, and requirements and to make recommendations on supplementation after careful review of the evidence. Scientific evidence indicates that calcium and vitamin D play key roles in bone health. The current evidence, limited to observational studies, however, does not support other benefits for vitamin D. More targeted research should continue, especially interventional studies. In the absence of any underlying risk of vitamin D deficiency, the recommendations are as follows: pregnant women: a single dose of 80,000 to 100,000 IU at the beginning of the 7th month of pregnancy; breastfed infants: 1000 to 1200 IU/day; children less than 18 months of age, receiving milk supplemented with vitamin D: an additional daily dose of 600 to 800 IU; children less than 18 months of age receiving milk not supplemented with vitamin D: daily dose of 1000 to 1200 IU; children from 18 months to 5 years of age: 2 doses of 80,000 to 100,000 IU every winter (November and February). In the presence of an underlying risk of vitamin D deficiency (dark skin; lack of exposure of the skin to ultraviolet B [UVB] radiation from sunshine in summer; skin disease responsible for decreased exposure of the skin to UVB radiation from sunshine in summer; wearing skin-covering clothes in summer; intestinal malabsorption or maldigestion; cholestasis; renal insufficiency; nephrotic syndrome; drugs [rifampicin; antiepileptic treatment: phenobarbital, phenytoin]; obesity; vegan diet), it may be justified to start vitamin D supplementation in winter in children 5 to 10 years of age as well as to maintain supplementation of vitamin D every 3 months all year long in children 1 to 10 years of age and in adolescents. In some pathological conditions, doses of vitamin D can be increased. If necessary, the determination of 25(OH) vitamin D serum concentration will help determine the level of vitamin D supplementation.
 ...
PMID:Vitamin D: still a topical matter in children and adolescents. A position paper by the Committee on Nutrition of the French Society of Paediatrics. 2228 32

Short bowel syndrome (SBS) occurs in patients who have had extensive resection. The primary physiologic consequence is malabsorption, resulting in fluid and electrolyte abnormalities and malnutrition. Nutrient digestion, absorption, and assimilation may also be diminished by disturbances in the production of bile acids and digestive enzymes. Small bowel dilation, dysmotility, loss of ileocecal valve, and anatomical changes combined with acid suppression and antimotility drugs increase the risk of small intestinal bacterial overgrowth, further contributing to malabsorption. Metabolic changes that occur in SBS due to loss of colonic regulation of gastric and small bowel function can also lead to depletion of calcium, magnesium, and vitamin D, resulting in demineralization of bone and the eventual development of bone disease. Persistent inflammation, steroid use, parenteral nutrition, chronic metabolic acidosis, and renal insufficiency may exacerbate the problem and contribute to the development of osteoporosis. Multiple factors increase the risk of nephrolithiasis in SBS. In the setting of fat malabsorption, increased free fatty acids are available to bind to calcium, resulting in an increased concentration of unbound oxalate, which is readily absorbed across the colonic mucosa where it travels to the kidney. In addition, there is an increase in colonic permeability to oxalate stemming from the effects of unabsorbed bile salts. The risk of nephrolithiasis is compounded by volume depletion, metabolic acidosis, and hypomagnesemia, resulting in a decrease in renal perfusion, urine output, pH, and citrate excretion. This review examines the causes and treatments of small intestinal bacterial overgrowth, bone demineralization, and nephrolithiasis in SBS.
 ...
PMID:Bacteria, Bones, and Stones: Managing Complications of Short Bowel Syndrome. 2992 35


<< Previous 1 2