Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011991 (diarrhea)
 57,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Complex zinc tannate salts of heroin, hydromorphone and l-alpha-acetylmethadol were synthesized and injected in a slow-release vehicle, into rats. One, 3, 7, 10 and 14 days after the drug was administered rats were injected with naloxone hydrochloride (10 mg/kg) and during the following 4 hours body weights, core temperature and behavioral signs such as diarrhea, writhing, teeth chattering and wet dog shakes were recorded. On every naloxone testing day the narcotic-treated groups presented behavioral signs of abstinence, but weight loss and temperature changes were much less consistent. Reduction of core temperature following naloxone administration seems to be an earlier indicator of physical dependence than weight loss. According to the parameters tested a level of physical dependence can persist for at least two weeks after a single injection of these narcotic salts.
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PMID:Dependence in rats after one injection of heroin-, LAAM- or hydromorphone-zinc tannate. 9 35

Zinc deficiency was observed in an infant receiving total parenteral nutrition (TPN) for chronic untractable diarrhoea. Clinical findings included low zinc plasma levels, skin lesions and loss of all the advantages of TPN such as weight gain, serum proteins and albumin increase and normalization of intestinal mucosa. Oral administration of zinc sulphate was the decisive factor making possible both the improvement of clinical and laboratory findings and alimentation by natural route.
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PMID:The role of zinc in total parenteral nutrition. 10 61

A child with hypogammaglobulinemia and intractable diarrhea underwent parenteral alimentation for five months. A clinical syndrome of acrodermatitis enteropathica subsequently developed associated with a depression in thymus-dependent lymphocyte (T cell) numbers, abnormal T-cell mitogen-induced blast transformation, and anergy to skin test antigens. Plasma zinc levels were found to be abnormally low. Zinc therapy resulted in dramatic resolution of the clinical manifestations of acrodermatitis enteropathica. Cell-mediated immune function was also restored to normal, suggesting an important role for zinc and possibly other trace metals in cellular immune responses.
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PMID:Zinc therapy of depressed cellular immunity in acrodermatitis enteropathica. Its correction. 11 58

The effects of orally administered zinc sulfate in 52 patients with mild to moderate acne vulgaris were compared to those of a placebo capsule. The numbers of comedones, papules, pustules, infiltrates, and cysts were counted at each visit over a 12-week period. Forty patients completed the study. Zinc appeared to have a somewhat beneficial effect on pustules but not on comedones, papules, infiltrates, or cysts. Fourteen patients (50%) in the zinc group had side effects of nausea, vomiting, or diarrhea. Six patients (21%) in the zinc group could not tolerate the nausea and withdrew from the study.
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PMID:Zinc sulfate in acne vulgaris. 15 30

Ultrastructural and biochemical changes in the intestinal epithelium during the process of active triglyceride absorption were studied in rats fed a zinc-deficient diet as compared with those of pair-fed and ad libitum-fed zinc-supplemented controls. The rate of triglyceride absorption markedly decreased in zinc-deficient rats. Despite a significant reduction in pancreatic lipase activity, the digestion of triglycerides proceeded normally in the zinc deficient rats, as evidenced by no apparent signs of diarrhea (or steatorrhea) and by the appearance of the hydrolytic products such as free-fatty acids and monoglycerides in the intestinal mucosa. The mucosa uptake of digested lipids and resynthesis of triglycerides in the mucosa from deficient rats were normal. Ultrastructural and chromatographic analysis of the mucosal lipids indicated a massive accumulation of lipid droplets, predominantly in the form of triglycerides. The primary defect in lipid absorptive processes in zinc-deficient rats occurred in the formation of chylomicrons. The lipid droplets in the mucosa of deficient rats were physically unstable. This instability was shown by coalescence of droplets which did not appear to be membrane-bound. Coalescing lipid droplets ranged from 2.0 to 4.0 micron in diameter. The absorptive cells were not able to discharge lipid droplets of this size into the intercellular spaces and hence into the lamina propria, resulting in the accumulation of the large droplets within the mucosa. This exit block to the movement of lipid droplets out of the mucosal cell appeared to be due to the failure, in zinc-deficiency, of the mucosal synthesis of proteins required for the formation of chylomicrons. Ultrastructural observations demonstrated changes in the subcellular organelles related to protein synthesis, including a marked reduction in granular endoplasmic reticulum and a quiescent appearance of the Golgi-complex.
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PMID:Effect of zinc deficiency on intestinal transport triglyceride in the rat. 19 62

Several immunologic features were analyzed in mice on a zinc-deficient diet [Zn(-)], in mice pair-fed a diet containing zinc [Zn(+)], in mice fed a Zn(+) diet ad lib, and in mice fed laboratory chow ad lib. When placed on a Zn(-) diet, 6- to 8-week-old A/Jax, C57BL/Ks, and CBA/H mice showed loss of body weight, low lymphoid tissue weight, and profound involution of the thymus within 4-8 weeks after initiation of the regimen. Approximately 50% of the mice on the Zn(-) diet developed severe acrodermatitis enteropathica (lesions on tail and paws) and diarrhea. Pair-fed mice on the Zn(+) diet did not show any of these symptoms. Mice on the Zn(-) diet showed the following immune deficiencies: (i) depressed plaque-forming cells against sheep erythrocytes after in vivo immunization; (ii) depressed T killer cell activity against EL-4 tumor cells after in vivo immunization; and (iii) low natural killer cell activity. However, antibody-dependent cell-mediated cytotoxicity against chicken erythrocytes was normal in the mice on the Zn(-) diet. Deficiency of T killer cell activity was not observed when immunization with EL-4 allogeneic lymphoma cells was carried out in vitro. Progressive loss of relative and absolute number of Thy 1.2+ cells and a proportionate relative increase in cells bearing Fc receptors was seen in spleen and lymph nodes of Zn(-) animals. It appears that zinc is an essential element for maintenance of normal T cell and other immune functions in vivo.
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PMID:Impairment of cell-mediated immunity functions by dietary zinc deficiency in mice. 31 74

1. Multiple sequential changes in zinc metabolism occur during infectious illnesses. These are characterized by early redistribution and by the late occurrence of direct zinc losses. Redistribution is accompanied in many infections by a decline in plasma concentrations before or with onset of illness. Although late losses of zinc have not been confirmed by metabolic balances during infection, losses may be inferred because: a) they accompany the catabolic phase of other illnesses, b) urinary losses have been observed during infections in which they were measured, and c) infections may exaggerate losses via sweat or diarrhea. 2. Leukocytic endogenous mediator (LEM), appears to stimulate the initial changes in zinc redistribution. Although LEM has not been isolated in pure form, it can now be separated by physiocochemical means from endogenous pyrogen and other mediator substances released by activated phagocytic cells. 3. Early zinc redistribution may be a purposeful physiological event which serves as a host defense mechanism. Redistribution may influence the stability of cellular membranes, augment the functional ability of phagocytic cells and certain classes of lymphocytes, aid in the synthesis of nucleic acids and proteins, and contribute to the production of various zinc metalloenzymes. 4. Zinc therapy has not been shown experimentally to produce a beneficial effect in any infectious disease studied in animal models.
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PMID:Zinc metabolism in infection. 60 36

Changes in the plasma levels and urinary excretion of zinc have been studied in a series of adult patients receiving intravenous alimentation. Urinary zinc loss may be very high in this group, but serious plasma depletion does not occur unless there is a concomitant phase of sustained anabolism in the absence of significant exogenous intake. A syndrome of acute zinc deficiency is described consisting of diarrhea, mental apathy and depression, a moist eczematoid dermatitis, most severe in the perioral area and alopecia. The response to intravenous zinc therapy is very striking although alopecia is slower to develop and complete hair regrowth is correspondingly delayed.
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PMID:Acute zinc deficency in man during intravenous alimentation. 81 23

Zinc deficiency was observed in two infants receiving total parenteral alimentation for chronic diarrhea. An acrodermatitis enteropathica-like rash occurred in both of the infants. Staphylococcus aureus was cultured from the rash. Treatment with zinc resulted in rapid cure of the rash and a subsidence of other signs consistent with zinc deficiency.
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PMID:Zinc deficiency in two infants during total parenteral alimentation for diarrhea. 81 5

Changes in the plasma and urine levels of the trace metal zinc have been followed in a series of 37 adult patients totally supported by intravenous alimentation. Copper has also been determined in more recent cases. In such a seriously ill group, although urinary zinc loss may be very high at the height of catabolism, severe plasma depletion does not occur unless there is a subsequent phase of sustained anabolism and weight gain. In four patients plasma zinc fell to very low levels during this phase and three of this group developed a syndrome characterized by diarrhea, mental depression, para-nasal, oral and peri-oral dermatitis, and alopecia. The response to oral or intravenous zinc therapy is striking, except for hair regrowth which is delayed but eventually complete. The syndrome we have recognized in adult man has not been previously described. It resembles however the parakeratosis of zinc deficient swine and it is also very similar to Acrodermatitis enteropathica, a genetically determined disorder of infants very recently linked to zinc deficiency. Zinc is clearly essential to human metabolism and it should be included in all parenteral alimentation regimes particularly during the period of rapid, sustained, weight gain.
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PMID:A syndrome of acute zinc deficiency during total parenteral alimentation in man. 81 77


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