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)

The appropriate choice of treatment for infants with diarrhea has long provoked debate. Growth of infants with diarrhea is adversely affected by associated diseases including anorexia, malabsorption, catabolic response to infection, and iatrogenic starvation. To prevent the negative effects of diarrhea on the nutrition of infants, continued feeding during the active and early convalescent phases has been recommended. Although this concept is not new, until recently it has been little used in the treatment of diarrhea. In this article we examine the current knowledge about, and trends in, feeding infants with diarrhea. We will discuss treatments for the well-nourished infant with acute diarrhea, the infant with prolonged diarrhea, and the malnourished infant. Information regarding the use of local staples will also be provided.
 ...
PMID:Nutritional therapy for infants with diarrhea. 209 32

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.
 ...
PMID:Consequences of phosphate imbalance. 306 Jan 61

In young broiler chicks inoculated with 2 x 10(6) sporulated oocysts of Eimeria acervulina per bird, total plasma lipids were significantly depressed compared with controls in the first week after inoculation. The lowest level observed was at 5 days post-inoculation (d.p.i.), at which time the chick host is known to experience malabsorption in the chick host (Ruff and Wilkins, 1980). Analysis of plasma components of infected chicks at 4 and 7 d.p.i. showed that triglycerides, total cholesterol, free fatty acids, pigments and total protein were significantly decreased compared with controls. At 7 d.p.i., reduction of total cholesterol reflected mainly reduction in high density lipoprotein (HDL) cholesterol. However, the ratio of HDL cholesterol/total plasma cholesterol was not significantly different from the control ratio. Density gradient ultracentrifugation of chick plasma separated lipoproteins into three main fractions: portomicrons plus very low density lipoproteins (PM + VLDL), low density lipoproteins (LDL) and HDL. These fractions were analyzed for lipid content. Infection with E. acervulina caused (1) significant reduction in the triglyceride and cholesterol contents of the PM + VLDL fraction at 3 and 5 d.p.i., (2) significant reduction of LDL cholesterol at 9 d.p.i. and LDL phospholipid at 5-9 d.p.i., and (3) significant reduction of HDL cholesterol at 3-9 d.p.i. and HDL phospholipid at 5-9 d.p.i. Starvation of uninfected chicks for 48 h caused significant reduction in plasma triglycerides and phospholipids, but an increase in total cholesterol. Density gradient ultracentrifugation showed that the changes in these components reflected mainly reduction of the lipids in the PM + VLDL fraction. The LDL fractions, however, appeared more intense than those of the controls and contained more cholesterol and phospholipids. These results suggest that changes at 3 and 5 d.p.i. in the plasma lipoprotein pattern of chicks infected with E. acervulina most closely resemble changes seen in chicks starved for 48 h as far as PM + VLDL fraction is concerned. However, changes seen from 7 to 9 d.p.i. involve the LDL and HDL fractions and may reflect alterations in lipid and/or lipoprotein synthesis in the liver and intestine.
 ...
PMID:The effect of Eimeria acervulina infection on plasma lipids and lipoproteins in young broiler chicks. 321 27

Two anorectic, emaciated infants with central nervous system (CNS) neoplasms are reported. Diagnosis in each case was delayed, because computed tomography of the head was initially falsely negative, and because primary gastroenterologic illness was suggested by the presence of mild inflammation and villous atrophy of the small intestine. This experience indicates that the diagnosis of CNS neoplasm must be aggressively pursued in cachectic infants who refuse to eat, regardless of the results of the initial radiologic studies. Mild histologic abnormalities of the small intestine that may be present in infants with brain tumors probably represent a nonspecific response to starvation and, if unassociated with malabsorption, should not be considered the cause of illness.
 ...
PMID:Intestinal abnormalities with central nervous system malignancy. 373 19

The many causes of clinical magnesium deficiency can be placed into 2 categories: diminished intake of magnesium, and enhanced losses of magnesium, either through the gastrointestinal tract or through the kidneys. Examples of the first category include alcoholism, starvation, anorexia due to neoplastic disease and/or chemotherapy. Examples of the second category include severe diarrhoeal states, gastrointestinal fistulae, malabsorption, diuretic therapy and gentamicin therapy. Estimates of the prevalence of clinical hypomagnesaemia range from 6 to 11% in hospitalised patients. Serum predictors of associated clinical magnesium depletion include hypokalaemia (42%), hyponatraemia (23%), hypophosphataemia (22%) and hypocalcaemia (20%). Experimental and clinical observations strongly support the view that magnesium and potassium are closely linked at the cellular level. Magnesium has been demonstrated to be important in cell energetics (Mg++-activated ATPase), in maintenance of the integrity of cell membranes, retardation of cell loss of potassium, as well as enhancing repletion of cell potassium. While translation of these experimental observations into clinical terms encompasses a wide spectrum of illnesses, there is special relevance in considering the role of magnesium in repletion and maintenance of cell potassium in 2 clinical instances: (a) patients treated with digitalis and diuretics; and (b) hypertensive patients. In these types of patients not only potassium but also magnesium should be administered together to avoid the problem of cell potassium depletion and refractory potassium repletion associated with coexisting and uncorrected magnesium depletion.
 ...
PMID:Magnesium deficiency. Causes and clinical implications. 649 96

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

Absorption kinetics of 14C-labelled N-(3-chloro-o-tolyl)-anthranilic acid (tolfenamic acid, 14C-TA, Clotam) from the small intestine was studied in intact rats and in rats with malabsorption states provoked by methotrexate, starvation, and triparanol. 14C-TA was administered intravenously and intraduodenally, and the drug concentrations in the blood were followed up radiometrically. A multi-compartmental model was applied for mathematical analysis. Theoretical model parameters were computed, and absorption parameters were then derived from the theoretical ones. The absorption half-life of 14C-TA was 5.3 min in the controls, 10.8 min in the methotrexate-intoxicated, 7.5 min in the fasted, and 5.3 min in the triparanol-intoxicated rats. The absorbed fraction of the intraduodenal 14C-TA dose was 100% in each experimental group as well as in the controls. It is suggested that the slower transfer of 14C-TA through the intestinal barrier in the methotrexate-intoxicated and fasted rats may be caused by the reduction of the absorptive surface.
 ...
PMID:Intestinal absorption of tolfenamic acid at experimental malabsorption states in rats. 719 4

Critical illness is characterized by the presence of several factors that can cause marked alterations in the structure and function of multiple organ systems (1-2). These factors include injury, ischemia, sepsis, and starvation (Fig. 1). It is common for more than one of these problems to be present in the individual patient. Our current understanding of the effect of these various factors on intestinal structure and function has increased markedly during the past decade (3). Furthermore, the patterns of intestinal dysfunction that occur in response to these conditions have also been better characterized. Although malabsorption and motility disorders have long been recognized as clinical problems, more recently loss of intestinal barrier function and immune dysfunction have gained attention. This improved understanding of the response of the intestine to critical illness may lead to prevention of intestinal failure or permit more specific therapy when it occurs. The goals of this manuscript are to describe the response of the small intestine to critical illness and to identify potential therapeutic strategies for preventing and treating intestinal failure in this setting.
 ...
PMID:The intestinal response to critical illness. 784 84

Wasting may not be an inevitable consequence of HIV infection but may be a consequence of multiple nutritional insults that are additive without periods of replenishment in between. Protein energy malnutrition in AIDS patients may be consequential to underlying illness and concomitant to death as a result of that illness or may hasten a patient's demise, that is, starvation with fatal loss of body cell mass. Mortality is closely related to weight loss. Malnutrition may be a result of decreased intake, malabsorption, altered metabolism, or any combination of the three. Nutritional strategies to prevent PEM include appetite stimulation, early nutritional supplementation with oral supplements, and the diagnosis and treatment of malabsorption and underlying infections. More aggressive measures such as gastrostomy or jejunostomy tube placement and total parenteral feedings are still being evaluated. Nutritional supplementation to enhance the immune system or manipulate metabolism may be adjunctive to the above strategies. Early intervention and attention to nutritional status may have long-term benefits to patients with this disease.
 ...
PMID:Nutritional aspects of HIV infection. 808 74

Nutritional support of patients with HIV or acquired immune deficiency syndrome (AIDS) has many similarities to other disease states in that the same nutritional products and techniques are used. Some patients with HIV, and many with AIDS without secondary infection, experience a metabolic milieu similar to patients with cancer cachexia. In providing dietary counselling to the HIV patient, we encounter many of the obstacles that must be overcome to improve nutrition in cancer: anorexia, gastrointestinal discomfort, lethargy, and poor nutrient utilization, which limit the ability for nutritional repletion. When a secondary infection is superimposed on HIV, patients resemble more highly catabolic trauma patients or patients in the intensive care unit (ICU), where, despite aggressive efforts to feed, there is usually a net nitrogen wasting leading to the more rapid development of cachexia. However, even in this setting, feeding will limit substantially net catabolism when compared to total starvation. Because the nutritional needs of HIV patients vary greatly, individual strategies have to be designed as the patient moves through the stages of disease. Patients are generally able to consume adequate nutrition either as regular food or dietary supplements during the latency period of viral replication. Once secondary infections become prevalent, artificial diets administered by tube or by vein may be required during the period of active secondary infections, with dietary supplements often helpful during more quiescent periods. Patients with HIV are among the most challenging for clinicians providing nutritional support. Knowledge from treatment of patients with other diseases may be useful, but more data must be gathered on the unique aspects of aetiology and treatment of the anorexia, malabsorption, and ultimate wasting associated with AIDS.
 ...
PMID:Nutrition support and the human immunodeficiency virus (HIV). 811 86


1 2 3 Next >>