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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diagnosis is often overlooked because symptoms develop slowly and insidiously and many patients don't complain about them. Then too, the giddiness, apathy, confusion, clumsiness, and similar problems may be considered simply signs of "old age." Iron deficiency anemia is the most common type in old people. It's usually due to gastrointestinal bleeding, but there may be a second, less obvious cause. The classic picture of low serum iron, high total iron-binding capacity, and low iron-binding saturation is sometimes distorted. Usually, many studies are needed to confirm the suspicion of a vitamin B12 or folic acid deficiency. A raised mean corpuscular volume in itself signals the need for further investigation. In patients with macrocytosis, the bone marrow must be examined. Tests for intestinal malabsorption must be considered too. Repeated blood tests are essential in patients being treated for any type of anemia. Iron deficiency may hide evidence of folate or B12 deficiency. And iron therapy may lessen bleeding from colonic cancer, delaying diagnosis until it's too late to operate.
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PMID:Anemia--a common but never a normal concomitant of aging. 108 61

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67

The psychiatric symptoms of magnesium deficiency are unspecific, ranging from apathy to psychosis, and may be attributed to other disease processes associated with poor intake, defect absorption, or excretion of magnesium. Serum magnesium should be determined when there are symptoms consistent with magnesium deficiency and/or in conditions which can lead to a deficiency, e.g., malabsorption, malnutrition, alcoholism and diuretic treatment. A low serum value suggests magnesium deficiency, but the diagnosis is reinforced with analyses of magnesium in the urine and a loading test with magnesium. Magnesium can be given orally or intramuscular/intravenously.
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PMID:Depression and magnesium deficiency. 272 6

The classical symptoms of malabsorption syndrome are diarrhea, steatorrhea, weight loss, and fatigue. Tetany, ecchymosis, anorexia, bone pain, pallor, muscle wasting, hyperpigmentation, apathy, digital clubbing, abdominal distention which contrasts in view of the reduced common statement are other signs of malabsorption. Long before the onset of these symptoms there may be a disinterest in regular daily activities often associated with the passage of three soft stools per day and with the remarkable sign of difficulties in flushing bulky stools. Anamnesia, clinical examination in connection with common laboratory findings, small intestinal x-rays and endoscopic investigations associated with biopsies of the small (and large) bowel as well as estimation of stool fat excretion, xylose- and Schilling-test allow the diagnosis in most of the cases.
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PMID:[Clinical aspects and differential diagnosis of malabsorption]. 684 29

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

The human immunodeficiency virus (HIV)-associated dementia complex is characterized by difficulties in concentration and memory followed by apathy, social withdrawal and motor dysfunction. Decreased serum vitamin B12 levels occur in up to 20% of patients with acquired immune deficiency syndrome (AIDS) and may adversely contribute to the haematologic and neurologic dysfunction which is frequently attributed to the human immunodeficiency virus. We describe a patient with AIDS who presented with an apparent advanced AIDS dementia complex. There was an associated low serum vitamin B12 resulting from malabsorption due to low gastric intrinsic factor secretion. Following treatment with vitamin B12 the symptoms resolved over a 2-month period. We believe that the AIDS dementia complex represented a reversible adverse synergistic interaction between the human immunodeficiency virus and vitamin B12 deficiency.
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PMID:Reversal of apparent AIDS dementia complex following treatment with vitamin B12. 850 20