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)

Evidence for cobalamin (vitamin B12) deficiency usually involves some combination of low serum cobalamin levels, clinical abnormalities (classically, megaloblastic anemia and neurologic defects), metabolic abnormalities, and response to therapy. However, cobalamin deficiency may often display few of the expected clinical findings. Identification of the underlying cause is also important in the diagnosis of deficiency, and its value may be particularly great when the expression of deficiency is subtle. The cause of cobalamin deficiency is usually malabsorptive, but may sometimes be limited to malabsorption of food cobalamin while free cobalamin is absorbed normally. Nongastroenterologic entities may sometimes also be found. All of these considerations allow the proposal of four patterns of cobalamin deficiency. The first type is classical deficiency; typical megaloblastic anemia with or without neurologic dysfunction occurs because of classical cobalamin malabsorption such as lack of intrinsic factor (pernicious anemia). The second type consists of classical cobalamin malabsorption in which the cobalamin deficiency is expressed subtly rather than in classical fashion. There is no megaloblastic anemia and sometimes the only evidence of deficiency may be metabolic. In the third type, cobalamin deficiency is expressed classically but is attributable to a subtle or atypical cause, such as food-cobalamin malabsorption. In the fourth type, deficiency is both expressed subtly and arises from subtle or atypical causes. Such presentations require further investigation but are a challenging expansion of our understanding and recognition of cobalamin deficiency.
 ...
PMID:Subtle and atypical cobalamin deficiency states. 218 34

Vitamin B12 can bind two carrier proteins in the digestive tract, haptocorrin (R binder) and intrinsic factor, but only its binding to intrinsic factor allows its absorption. A malabsorption of vitamin B12 is observed in about 30% of adult patients with exocrine pancreatic insufficiency, using the Schilling test. None of the hypotheses that have tried to explain this malabsorption are entirely satisfactory. A failure to degrade haptocorrin can prevent the binding of vitamin B12 to intrinsic factor. It has also been suggested that pancreatic secretion could modify the structure of intrinsic factor, enabling the uptake of the vitamin B12-intrinsic factor complex by the ileum. Other factors can also affect the binding of vitamin B12 to intrinsic factor, such as the gastric pH and bile. The Schilling test is abnormal in nearly all cases of cystic fibrosis. One explanation could be the gastric hyperacidity observed in this disease. Despite the frequency of abnormal Schilling tests, vitamin B12 deficiency is very rare in cases of exocrine pancreatic dysfunction, in adults as well as in children with cystic fibrosis. The assimilation of this vitamin with a tracer included in food instead of the crystalline labeled cobalamin used in the Schilling test remains to be investigated.
 ...
PMID:Malabsorption of vitamin B12 in pancreatic insufficiency of the adult and of the child. 223 67

In a group of nine children with postenteritis enteropathy (i.e., persisting small-intestinal mucosal damage and failure-to-thrive after an acute episode of gastroenteritis), absorption capacities for vitamin B12 and folic acid were studied and compared with hematological status in peripheral blood. The fractional absorptions of vitamin B12 (FAB12) and folic acid (FAFol) were determined by means of a double-isotope technique employing a single-stool-sample test. The children were examined when growth retardation was maximal, and examinations were repeated during the late recovery period. In spite of considerable small-intestinal mucosal damage, only the absorption of vitamin B12 was markedly affected, while that of folic acid was almost intact. When growth retardation was maximal, FAB12 was below the normal age-correlated range in half of the children. FAB12 was also severely reduced in all longitudinally observed children when compared with the results obtained during the late recovery period (p less than 0.005). FAFol was below the normal range in one fourth of the children, but the reduction was modest and insignificant when compared with the results of repeated examinations during the late recovery period. A moderate iron deficiency was detected in half the children. High levels of plasma vitamin B12, folic acid, and erythrocyte folate were detected at both early and later examinations, indicating that these parameters were not affected by the reduced absorption capacities. However, if malabsorption and chronic diarrhea are combined with low dietary intake of vitamin B12, as is the case for many children in the Third World, depletion of vitamin B12 stores may result.
 ...
PMID:Vitamin B12 and folic acid absorption and hematological status in children with postenteritis enteropathy. 224 17

The haematological status, as well as the fractional absorptions of folic acid-and of vitamin B12 (FAFol and FAB12) were studied longitudinally in 20 coelic children aged 1.2-16.6 yr (mean 7.5 yr) during periods of gluten-free and gluten containing diets. The absorption methods were specially adapted to use in children, and age-related reference limits were established. Also, dietary intakes of iron, folate and B12 were registered. The haemoglobin concentrations did not show any significant differences in relation to shifts in diet. A few had mild anaemia while the haemoglobin concentrations in the other patients remained within normal range. The iron status, as judged from mean corpuscular volume (MCV), serum (S)-iron, S-transferrin and saturation %, appeared to be generally insufficient. However, the only significant change related to shifts in diet was an increase of S-iron during the first period of gluten-free diet. Dietary intakes of iron proved to be insufficient, regardless of the type of diet. Plasma (P)-B12 concentrations demonstrated a wide range of values above the lower normal limit, whereas the level in a single patient was within the "intermediate range" of B12 insufficiency (150-200 pmol/l). The folate status (erythrocyte-folate) showed significant variations related to dietary changes. However, few patients were folate depleted. FAFol and FAB12 demonstrated rapidly occurring, and significant decreases and increases in relation to gluten challenge and gluten-free diet, respectively. Bacterial overgrowth of the small intestinal tract was not found to be a plausible cause of the B12 malabsorption in the case of 5 patients observed.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The impact of gluten on haematological status, dietary intakes of haemopoietic nutrients and vitamin B12 and folic acid absorption in children with coeliac disease. 226 63

Sibling cases of familial vitamin E deficiency accompanied by ataxia, polyneuropathy and mental retardation were reported. Case 1 was a 37-year-old male who developed progressive gait disturbance, deformity of the feet and head tremor from childhood, after normal delivery and development of early childhood. On physical examination, he had cataract, high arched palate and pes cavus. Neurological examination revealed mental retardation (WAIS 68), scanning speech, muscular atrophy of the face and extremities with predominance in the lower limbs, absent Achilles tendon reflex, disturbance of superficial and deep sensation predominant in distal limbs, and marked gait ataxia. Ataxia was both cerebellar and sensory in nature. Laboratory data of the blood showed no significant abnormalities including blood glucose and vitamin B12 except a markedly low level of serum vitamin E. The brain CT scan revealed severe cerebellar atrophy and marked dilatation of the cisterna magna and the subarachnoid space around the cerebellum. Motor nerve conduction velocity in the leg was decreased. Biopsy specimen from the quadriceps muscle showed neurogenic atrophy. Sural nerve biopsy revealed decrease in large myelinated fibers with axonal degeneration and regeneration. Oral administration of alpha-tocopherol acetate, 600 mg per day, diminished ataxia significantly. Based on lysosomal enzyme activity in leukocytes, clinical and laboratory examination, lipidosis or spinocerebellar degeneration was excluded. Chronic lipid malabsorption or beta lipoprotein deficiency which can cause decrease in vitamin E absorption, was not recognized. On oral loading with 2 g of alpha-tocopherol acetate, the decrease rate of serum vitamin E was normal. Consequently the low vitamin E was considered to have resulted from selective impairment of vitamin E absorption.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Familial idiopathic vitamin E deficiency associated with cerebellar atrophy]. 226 7

Low serum vitamin B12 levels are not uncommon in the elderly. Patients with vitamin B12 deficiency manifest a spectrum of clinical findings. Pernicious anemia and malabsorption syndrome are the usual causes of vitamin B12 deficiency. Pernicious anemia is confirmed by the presence of intrinsic factor blocking antibody or abnormal results on the Schilling test. Patients with neuropsychiatric symptoms of vitamin B12 deficiency may have a normal Schilling test and no evidence of macrocytic anemia. In such patients, vitamin B12 deficiency is confirmed by determining serum levels of homocysteine and methylmalonic acid.
 ...
PMID:The spectrum of vitamin B12 deficiency. 227 93

The influence of calcium on vitamin B12 absorption was investigated in two experiments. In the first we investigated whether B12 malabsorption in rats with biliary diversion through choledochocolic fistula is caused by deficiency of calcium in the small intestine. Calcium concentrations were measured in 10 fistula- and 10 sham-operated rats. Fistula rats had steatorrhea, but the concentration of calcium in the intestinal lumen was increased. In the second experiment we studied the effect of calcium deficiency on B12 absorption. Ten young rats were fed a low-calcium diet and 10 rats a control diet for 4 weeks. Rats on the low-calcium diet had moderately reduced calcium concentration in the blood and in the intestinal juice but unaltered calcium concentration in the cytosol fraction of intestinal mucosal scrapings. The absorption of 57CoB12 was unimpaired. This suggests that moderate calcium deficiency does not influence the intestinal absorption of vitamin B12 in the rat.
 ...
PMID:Effect of calcium deficiency on vitamin B12 absorption in rats. 232 Sep 46

A case of 78-year old man with megaloblastic anemia occurring 20 years after partial gastrectomy is reported. Since about 2 years earlier he had an episode of convulsion, and he had been on anti-convulsants (diphenylhydantion, phenobarbital) until admission. Physical examination revealed a pale lean man with polyneuropathy and mental impairment. Laboratory findings revealed WBC 3100/microliters, RBC 187 X 10(4)/microliters, HB 7.9 g/dl, MCV 124.4 microns3, MCH 42.7 micrograms, platelet counts 15.7 X 10(4)/microliters, serum vitamin B12 (VB12) 380 pg/ml, and serum folic acid 5.1 ng/ml. Serum autoantibodies to intrinsic factor (IF) and parietal cells were positive. Bone marrow examination revealed erythroid hyperplasia and megaloblastic changes. Schilling test revealed impaired absorption of VB12 with or without IF, but X-ray study of the small bowels was unremarkable. Treatment with intramuscular cyanocobalamin resulted in a rapid clinical improvement. A repeat Schilling test after 4 months of therapy showed a normal VB12 absorption in the presence of IF. These findings suggest that VB12 malabsorption of the 1st Schilling test was due to intestinal dysfunction caused by the VB12 deficiency state itself, and the improvement of VB12 absorption with IF after therapy suggests a pathogenesis similar to pernicious anemia in this patient.
 ...
PMID:[Postgastrectomy megaloblastic anemia--possible participation of anti-intrinsic factor antibody in its pathogenesis--report of a case]. 236 43

Two patients with ileal conduits underwent planned urinary undiversion; in both patients, the previously constructed ileal conduit was utilized to augment the continent urinary reservoir. Both patients are totally continent with stable upper urinary tracts; neither individual suffers from diarrhea or intestinal absorption abnormalities. This variation in the construction of the continent urinary reservoir allows for the usage of less terminal ileum, and as a result, the risk of intractable diarrhea as well as folate and vitamin B12 malabsorption should be diminished. The criteria that must be met to utilize the ileal conduit in the construction of the continent urinary reservoir include: (1) adequate remaining conduit length after mobilization, and (2) a normal-appearing conduit with sufficient mesenteric length after mobilization.
 ...
PMID:Utilization of ileal conduit in construction of continent urinary reservoir. 236 25

It is possible that the commonly measured serum level of vitamin B12 may miss some cases when used to detect vitamin B12 malabsorption and deficiency in older persons. Serum levels of vitamin B12 and intrinsic factor antibody (IFAB) were determined on 250 consecutive patients over the age of 70 admitted to a rehabilitation hospital. Patients with abnormal results on either test were given the standard Schilling test when possible. Eight patients had documented B12 malabsorption. Of these, five had a low serum B12 level alone and one had a low serum B12 level and a positive IFAB level; however, two patients had positive IFAB and normal serum B12 levels. Serum IFAB level may serve as a useful adjunct to serum B12 level in detecting vitamin B12 malabsorption in older patients.
 ...
PMID:Prevalence of intrinsic factor antibodies and vitamin B12 malabsorption in older patients admitted to a rehabilitation hospital. 237 Mar 93


<< Previous 1 2 3 4 5 6 7 8 9 10