Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036474 (scurvy)
 685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The goal of this study was to test the hypothesis that the ratio of liver to bone alkaline phosphatase in blood plasma reflects the ascorbate status in scurvy-prone teleost fish (rainbow trout [Oncorhynchus mykiss]). The studies focused on finding a method for distinguishing bone alkaline phosphatase present in blood plasma from other alkaline phosphatase isoforms. We tested temperature optima and thermostability of liver, kidney, gill cartilage, and intestinal alkaline phosphatases. We did not observe differences among liver, bone, and kidney enzymes with respect to temperature optima and thermostability. We partially purified alkaline phosphatase from juvenile rainbow trout vertebrae and liver using n-butanol solubilization and ammonium sulfate fractionation. We found a difference between bone alkaline phosphatase, which precipitated in 0%-20% ammonium sulfate saturation, and liver enzyme, which required 40%-50% ammonium sulfate saturation to precipitation. We conducted a series of urea inactivation studies on partially purified enzymes from liver and vertebrae. Urea differentially inhibited the enzymes with t 1/2 = 1.1 and 0.4 min, for bone and liver, respectively. Subsequently, we subjected blood plasma alkaline phosphatase to urea inhibition, and using regression analysis we calculated the ratio of liver to bone alkaline phosphatase. We found that thus obtained ratios of bone enzyme in blood plasma correlated with liver ascorbate concentration. Bone alkaline phosphatase declined in ascorbate deficiency 10-fold, whereas low ascorbate status resulted in a 3.5-fold decrease. In order to draw a general conclusion on the linearity of the response of blood plasma/bone alkaline phosphatase as an indicator of ascorbate deficiency in fish, further studies must include analysis of individual fish followed in the process of developing avitaminosis.
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PMID:Utilization of the bone/liver alkaline phosphatase activity ratio in blood plasma as an indicator of ascorbate deficiency in salmonid fish. 861 50

Eating disorders are significant causes of morbidity and mortality in adolescent females and young women. They are associated with severe medical and psychological consequences, including death, osteoporosis, growth delay and developmental delay. Dermatologic symptoms are almost always detectable in patients with severe anorexia nervosa (AN) and bulimia nervosa (BN), and awareness of these may help in the early diagnosis of hidden AN or BN. Cutaneous manifestations are the expression of the medical consequences of starvation, vomiting, abuse of drugs (such as laxatives and diuretics), and of psychiatric morbidity. These manifestations include xerosis, lanugo-like body hair, telogen effluvium, carotenoderma, acne, hyperpigmentation, seborrheic dermatitis, acrocyanosis, perniosis, petechiae, livedo reticularis, interdigital intertrigo, paronychia, generalized pruritus, acquired striae distensae, slower wound healing, prurigo pigmentosa, edema, linear erythema craquele, acral coldness, pellagra, scurvy, and acrodermatitis enteropathica. The most characteristic cutaneous sign of vomiting is Russell's sign (knuckle calluses). Symptoms arising from laxative or diuretic abuse include adverse reactions to drugs. Symptoms arising from psychiatric morbidity (artefacta) include the consequences of self-induced trauma. The role of the dermatologist in the management of eating disorders is to make an early diagnosis of the 'hidden' signs of these disorders in patients who tend to minimize or deny their disorder, and to avoid over-treatment of conditions which are overemphasized by patients' distorted perception of skin appearance. Even though skin signs of eating disorders improve with weight gain, the dermatologist will be asked to treat the dermatological conditions mentioned above. Xerosis improves with moisturizing ointments and humidification of the environment. Acne may be treated with topical benzoyl peroxide, antibacterials or azaleic acid; these agents may be administered as monotherapy or in combinations. Combination antibacterials, such as erythromycin with zinc, are also recommended because of the possibility of zinc deficiency in patients with eating disorders. The antiandrogen cyproterone acetate combined with 35 microg ethinyl estradiol may improve acne in women with AN and should be given for 2-4 months. Cheilitis, angular stomatitis, and nail fragility appear to respond to topical tocopherol (vitamin E). Russell's sign may decrease in size following applications of ointments that contain urea. Regular dental treatment is required to avoid tooth loss.
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PMID:Dermatologic signs in patients with eating disorders. 1594 93