Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

10 patients with anorexia nervosa were compared with controls with normal weight, regarding their peripheral blood polymorphonuclear (PMN) granulocyte reactions. The anorexia patients showed a statistically significant decrease in PMN bactericidal capacity and PMN adherence. The mean chemotaxis did not differ, but in two of the anorexia patients chemotaxis was almost absent. The intracellular activity of alkaline phosphatase was below the reference values in 5 of the 6 patients in whom it was investigated. It is concluded that changes in granulocyte function may be noted in anorexia nervosa, but their clinical significance is uncertain, as no patients had recurrent or severe infectious diseases.
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PMID:Anorexia nervosa and polymorphonuclear (PMN) granulocyte reactions. 91 61

Some aspects of zinc nutritive status in patients suffering from anorexia nervosa were evaluated. Basic anthropometric measurements, Zn levels in serum, urine and hair as well as serum alkaline phosphatase (ALP) and lactate dehydrogenase (LDH; Zn-dependent enzymes) and delayed dermal hypersensitivity were tested both in patients and in control subjects. The patients showed higher Zn levels in serum (123%), hair (85%) and urine (215%) than controls, whereas ALP and LDH values were 38 and 21%, respectively, lower than those from the control group. Half of the patients showed hypoergy, and less than 50% of them were able to show a normal immune response. These results suggest that Zn-dependent functions may be impaired in anorexia nervosa as a consequence of Zn unavailability.
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PMID:Zinc status in anorexia nervosa. 147 56

An emaciated 16-year-old female with anorexia nervosa was hospitalized for treatment of vomiting, epigastralgia and diarrhea. The finding of a taste disorder, low serum alkaline phosphatase activity and relatively low serum zinc level strongly suggested a zinc deficiency. Zinc was initially administered intravenously (40 mumol/day) for 7 days, then orally (15 mg elemental zinc/day) for about 60 days. Her digestive symptoms disappeared after the second day of intravenous treatment and she began to gain weight. She rapidly regained her normal weight after one month of receiving the oral zinc supplementation. Both exocrine pancreatic function and intestinal absorption were improved by the prolonged oral administration of zinc. In such cases zinc supplementation may be a therapeutic option in addition to psychologic and other approaches to management.
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PMID:Anorexia nervosa responding to zinc supplementation: a case report. 152 38

Serum vitamin D metabolites and other parameters of mineral metabolism were measured in 12 patients with anorexia nervosa. Serum concentrations of calcium, phosphate, albumin, alkaline phosphatase, parathyroid hormone, calcitonin, osteocalcin, and 24-hours calcium excretion were normal. Serum 25-hydroxyvitamin D (25OHD) concentration was similar in patients and normal subjects, whereas 1,25-dihydroxyvitamin D (1,25(OH)2D) levels were significantly reduced in patients (62 +/- 17 vs 82 +/- 17 pmol/l); p less than 0.05). The concentration of vitamin D-binding protein (DBP) in patients was normal, but serum binding capacity (Nmax) was diminished in anorectic patients (2.05 +/- 0.50 vs 2.53 +/- 0.51 mumol/l; p less than 0.05). The diminished serum binding capacity, in spite of normal concentrations of albumin and DBP, reflects the presence of qualitative rather than quantitative defects in serum transport proteins. Since the reduction in 1,25(OH)2D and serum binding capacity was quantitatively similar, it is likely that free 1,25(OH)2D levels would be normal.
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PMID:Vitamin D metabolism and serum binding proteins in anorexia nervosa. 190 47

Biochemical analyses of sera from 27 patients with anorexia nervosa were performed and compared with those of normal female volunteers and other anorectic groups including patients who had undergone digestive tract surgery and patients with malignancies. There were significant increases in gamma-glutamyltranspeptidase, lactate dehydrogenase, glutamic pyruvic transaminase, glutamic oxaloacetic transaminase, cholesterol, and amylase activity and significant decreases in total serum protein, blood sugar, albumin, globulins, and cholinesterase in anorexia nervosa patients compared with normal control subjects. At discharge, these values slightly improved. Similar alterations were also observed in two other anorectic groups. Compared with anorexia nervosa patients, the two other anorectic groups showed a severe reduction in the albumin level and increase in the globulin level. In two other anorectic groups cholesterol levels were lower, and in the malignancy group cholinesterase level was lower than in the anorexia nervosa patients. In anorexia nervosa patients, biochemical abnormalities in the serum were more frequent in total serum protein (93%), blood sugar (85%), and globulins (78%) than in other serum factors, such as blood urea nitrogen (15%), uric acid (15%), and alkaline phosphatase (7%). These results suggest that detection of biochemical abnormalities in the above-mentioned serum factors in routine analyses would be valuable in making an early diagnosis of anorexia nervosa from various anorectic disorders.
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PMID:Biochemical abnormalities of the serum in anorexia nervosa. 245 69

The authors evaluated bone mineralization by single photon absorptiometry and mineral homeostasis in 7 patients with anorexia nervosa. The patients with anorexia nervosa showed a reduction of bone mineralization in respect to age-sex matched normal values. Serum levels of calcium, ionized calcium, phosphate, magnesium, alkaline phosphatase, calcitonin and 25-hydroxyvitamin D were normal as well as phosphate and hydroxyproline urinary excretion. Osteocalcin levels were significantly low as compared to normal values (5.0 +/- 3.0 ng/ml vs 14.3 +/- 5.2 ng/ml, p less than 0.01) as well as urinary calcium excretion (0.02 +/- 1.01 vs 0.08 +/- 0.06, p less than 0.05); 1,25-dihydroxyvitamin D values were low only in 4 patients. Parathyroid hormone means levels were increased in respect to normal values (74.1 +/- 12.7 pg/ml vs 38.0 +/- 12.0, p less than 0.02). We confirm that adolescents with anorexia nervosa showed a reduced bone mineral content and alterations of mineral homeostasis that may contribute to the development of bone mineral loss.
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PMID:[Calciotropic hormones in osteoporosis caused by anorexia nervosa]. 278 86

The intake laboratory data of 46 patients seen between 1970 and 1980 who were less than 19 years of age with a discharge diagnosis of anorexia nervosa were retrospectively reviewed to determine their metabolic profile. The major findings for those who had laboratory data were as follows: 45% (19/42) had serum glutamic oxalacetic transaminase (SGOT) values greater than 36 International Units/liter (IU/L), and 65% (27/41) had alkaline phosphatase levels less than 58 IU/L. We suggest that patients with anorexia nervosa may reflect a state of hepatic dysfunction and/or dehydration before therapy.
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PMID:Metabolic abnormalities in adolescent patients with anorexia nervosa. 398 77

Bone loss is a potentially debilitating condition in women with eating disorders. Complications may include failure to achieve peak bone mass, increased risk of premature fractures, and inability to reach the height potential. We therefore conducted a comprehensive evaluation of 58 women with anorexia nervosa (AN), bulimia (BUL) and anorexia/bulimia (AB), comparing bone mineral density (BMD) to physical parameters, biochemical indices, and markers for bone formation and resorption. BMDs were significantly lower in patients with AN than in those with AB and BUL, and overt osteopenia was uncommon in AB and BUL. Hypercortisolism was the best laboratory marker to assess the risk of osteopenia in patients with AN. However, there were no associated changes in bone formation or resorption parameters. No direct correlation was found between BMD and body mass index, estrogen deficiency, tubular reabsorption of phosphorus, serum vitamin D, PTH, BGP, or alkaline phosphatase levels. Although the prognosis for complete recovery to normal BMD is poor, treatment of the underlying depressive disorder, improvement in nutrition with increased weight, and spontaneous resumption of menses are associated with restoring bone health.
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PMID:Bone metabolism and osteopenia in eating disorders. 756 66

A 32-year-old patient with anorexia nervosa since adolescence was admitted because of diffuse bone pain, increasing during the 2 preceding winters. She had a special aversion to dairy products and all forms of dietary fat. Low normal serum calcium and very low calciuria were noted, with a highly elevated bone fraction of alkaline phosphatase, and severe hypovitaminosis D and B12. Apart from a recent spontaneous fracture of the clavicle, Looser lines and pseudofractures were noted in a finger, fibula and malleolus. In particular, magnetic resonance imaging of the knee showed additional evidence of a pseudofracture in the femur, and medullary changes were found. Evidence for secondary hyperparathyroidism was described. Apart from the well known occurrence of osteoporosis, our case shows that osteomalacia may exceptionally occur in anorexia nervosa.
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PMID:Osteomalacia in a patient with anorexia nervosa. 847 61

Cortical and trabecular bone loss can lead to osteoporosis in chronic forms of anorexia nervosa (AN). As there is some debate about the reversibility of this condition, we performed a longitudinal follow-up study of 27 cases in which clinical, biological, X-ray and lumbar and femoral neck dual photon absorptiometry examinations were conducted every 6 months for up to 30 months. Three groups were distinguished: G1, untreated amenorrheic AN (N = 14, total follow-up 126 months); G2, effectively treated AN (N = 11, total follow-up 192 months), with two subgroups: fluoride (N = 5) and estrogen (N = 6); and G3, remitting AN with normalization of the gonadic function (N = 2, total follow-up 36 months). Results were adjusted for each patient to a 6-month variation. Semestrial variations in lumbar bone mineral density (BMD) were -2.1 +/- 1.3%, +2.8 +/- 1.5%, and -0.3 +/- 1.3% (mean +/- SEM), respectively for G1, G2 and G3; those for femoral neck BMD semestrial variations were -5.9 +/- 2.1%, -3.8 +/- 1.2% and -1.0 +/- 0.6%. Femoral neck and lumbar BMD variations for G1 were mainly correlated positively with bone-forming markers (serum osteocalcin, alkaline phosphatase) and negatively with initial lumbar BMD. Estrogen alone increased lumbar BMD by +1.4 +/- 2.3% every 6 months but did not stabilize femoral neck BMD (-3.5 +/- 1.4%). Fluoride increased lumbar BMD by 4.8 +/- 1.8%. Both lumbar and femoral neck BMD were stabilized in the remission group (-0.3 +/- 1.3% and -1.0 +/- 0.6%), despite half of the follow-up time with amenorrhea. In conclusion, untreated AN is associated with a marked trabecular and cortical bone loss (4-10% per year), which can lead to osteoporotic fractures. In prevention of bone loss, the efficacy of estrogen is difficult to investigate in AN, even with a well-controlled trial. Our study could provide argument that, when the observance of this preventive treatment is assessed, lumbar BMD can be stabilized in chronic forms of AN.
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PMID:Follow-up of bone mineral density in 27 cases of anorexia nervosa. 898 Jan 62


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