Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017536 (giardiasis)
 1,714 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Giardia lamblia localize and multiply in the small intestine and may cause acute or chronic diarrhoea with malabsorption of fat, protein and other nutrients. Abnormal pancreatic function has been documented in giardiasis and trophozoites directly inhibit pancreatic lipase activity in vitro. The aim of this study was to examine the effect of Giardia trophozoites on pancreatic trypsin, chymotrypsin and amylase activity in vitro. Axenically cultured Giardia trophozoites (Portland-1 stock) were incubated with a range of concentrations of trypsin, chymotrypsin and amylase and enzyme activity assayed over time. Tryptic activity was decreased after incubation with Giardia trophozoites. This reduction was time dependent and linear over the incubation period of 2 h. At a trypsin concentration of 18 BAEE units/ml, there was a 35.5 +/- 4% reduction in enzyme activity after 2 h compared to controls. The total amount of activity lost was proportional to the initial trypsin concentration up to 185 BAEE units/ml. At this initial concentration, the activity was reduced by 46.5 +/- 3 units/ml after 2 h. Above this concentration, little further loss of enzyme activity was seen. To investigate the nature and specificity of this effect, similar experiments were conducted using killed trophozoites and with a related protozoan, Trichomonas vaginalis. No loss of enzyme activity was evident. Media previously incubated for 2 h with trophozoites did not diminish tryptic activity. Trophozoites had no effect on chymotrypsin or amylase activities over the range of concentrations tested.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of Giardia lamblia trophozoites on trypsin, chymotrypsin and amylase in vitro. 848 60

Giardia lamblia undergoes surface antigenic variation. The variant-specific surface proteins (VSPs) are a distinct family of cysteine-rich proteins. Characteristically, cysteine residues occur mostly as CXXC tetrapeptides. Four of the reported five VSPs contain a putative metal-binding domain that resembles other metal-binding motifs; the fifth is closely related but lacks an essential histidine. Three different native VSPs bound Zn2+. Co2+, Cu2+, and Cd2+ inhibited Zn2+ binding. Analysis of recombinant VSP fusion proteins showed that the putative binding motif bound Zn2+. Surprisingly, peptide fragments from other regions of the VSP contain numerous CXXCXnCXXC motifs that also bound Zn2+. Analysis of deduced amino acid sequences showed well-conserved CXXC spacing in three out of five VSPs, suggesting conservation of structure despite amino acid sequence divergence. The function of VSPs is unknown, but by binding Zn2+ or other metals in the intestine, VSPs may contribute to Zn2+ malnutrition or inhibition of metal-dependent intestinal enzymes, which would lead to malabsorption, a well-known consequence of giardiasis.
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PMID:Variant-specific surface proteins of Giardia lamblia are zinc-binding proteins. 851 91

We report a case of isolated levothyroxine malabsorption in the course of chronic intestinal giardiasis, leading to severe hypothyroidism. Infection with Giardia lamblia was proved histologically by jejunal biopsy. Treatment with metronidazole resulted in complete elimination of parasites and recovery of regular intestinal thyroid hormone absorption. Stable euthyroidism was accomplished with common replacement doses of orally administered levothyroxine.
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PMID:Chronic intestinal giardiasis with isolated levothyroxine malabsorption as reason for severe hypothyroidism--implications for localization of thyroid hormone absorption in the gut. 874 Sep 44

Despite rapid progress in understanding the biology of Giardia, several questions remain unanswered. First, there is no adequate explanation for the diverse clinical spectrum of giardiasis. Second, the mechanisms by which Giardia produces diarrhea and malabsorption are poorly understood, although some progress has been made. Finally, despite extensive studies in animal models and human infections, the key immunologic determinants for clearance of acute infection and development of protective immunity remain ill defined. This article discusses the epidemiology, pathology, diagnosis, treatment, and prevention of giardiasis.
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PMID:Giardiasis. 886 37

This study evaluated vitamin B-12 status in 113 Guatemalan women and their infants at 3 months of lactation. Findings revealed that plasma vitamin B-12 was deficient or low in 46.7% of the mothers and that holotranscobalamin II (holo TC II) concentrations were low in 32.3%, which may indicate vitamin B-12 malabsorption. Only 9% had deficient or low plasma folate. Breast milk vitamin B-12 was low in 31% and negatively correlated with infant urinary methylmalonic acid (UMMA). UMMA was elevated in 12.2% of the infants, indicating vitamin B-12 deficiency. Mothers of the infants with elevated UMMA had significantly lower concentrations of vitamin B-12 in their breast milk compared with mothers of infants with normal UMMA concentrations. Mean maternal dietary intake of vitamin B-12 was significantly correlated with plasma vitamin B-12 and was the main determinant of plasma vitamin B-12 in a linear regression model. Determinants of maternal holo TC II concentrations included dietary intake of vitamin B-12 and Giardia lamblia infection. There were no statistically significant determinants of infant UMMA concentrations. This study concludes that vitamin B-12 deficiency is highly prevalent in these lactating women and is associated with the depletion of the vitamin in their infants. The cause of the maternal deficiency is unknown, but malabsorption, exacerbated by low dietary intake of the vitamin, is a possibility.
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PMID:Vitamin B-12 deficiency is very prevalent in lactating Guatemalan women and their infants at three months postpartum. 931 52

Malabsorption is a well-known complication of infection with Giardia lamblia. However, selective protein-losing enteropathy is rare. We report a child with anasarca due to hypoalbuminemia as a result of gastrointestinal protein loss. Investigations established giardiasis as the etiology. The child returned to normal health after treatment with metronidazole.
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PMID:Intestinal giardiasis: an unusual cause for hypoproteinemia. 1065 92

Intestinal colonization with the protozoan Giardia causes diffuse brush border microvillous alterations and disaccharidase deficiencies, which in turn are responsible for intestinal malabsorption and maldigestion. The role of T cells and/or cytokines in the pathogenesis of Giardia-induced microvillous injury remains unclear. The aim of this study was to assess the role of T cells and interleukin-6 (IL-6) in the brush border pathophysiology of acute murine giardiasis in vivo. Athymic nude (nu(-)/nu(-)) CD-1 mice and isogenic immunocompetent (nu(+)/nu(+)) CD-1 mice (4 weeks old) received an axenic Giardia muris trophozoite inoculum or vehicle (control) via orogastric gavage. Weight gain and food intake were assessed daily. On day 6, segments of jejunum were assessed for parasite load, brush border ultrastructure, IL-6 content, maltase and sucrase activities, villus-crypt architecture, and intraepithelial lymphocyte (IEL) infiltration. Despite similar parasitic loads on day 6, infected immunocompetent animals, but not infected nude mice, showed a diffuse loss of brush border microvillous surface area, which was correlated with a significant reduction in maltase and sucrase activities and a decrease in jejunal IL-6 concentration. In both athymic control and infected mice, jejunal brush border surface area and disaccharidases were high, but levels of tissue IL-6 were low and comparable to the concentration measured in immunocompetent infected animals. In both immunocompetent and nude mice, infection caused a small but significant increase in the numbers of IELs. These findings suggest that the enterocyte brush border injury and malfunction seen in giardiasis is, at least in part, mediated by thymus-derived T lymphocytes and that suppressed jejunal IL-6 does not necessarily accompany microvillous shortening.
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PMID:Jejunal brush border microvillous alterations in Giardia muris-infected mice: role of T lymphocytes and interleukin-6. 1081 92

Giardiasis is a cosmopolitan parasitosis. Diarrhea, abdominal colic, and flatulence are the main clinical symptoms, however, malabsorption, and impairment of growth of children may occur. The 5-nitroimidazoles are the drugs of choice in the treatment of giardiasis. Methods: The efficacy and tolerability of secnidazole and tinidazole were evaluated in a randomized, open-label, clinical trial performed with 267 Giardia lamblia-positive children. Secnidazole, in a new gel formulation, and tinidazole suspension were prescribed as single oral doses of 30mg/kg and 50mg/kg, respectively. Clinical and parasitological follow-up was carried out before, and at 7, 14, and 21 days after treatment. Results: Clinical cure was observed in 77.3% and 75.7% of the patients in the secnidazole and tinidazole groups, respectively. Parasitological cure was obtained in the 91.3% and 89.6% in the secnidazole and tinidazole groups, respectively. A metallic taste after drug ingestion was more commonly reported in the tinidazole group than in the secnidazole group (p<0.05). Conclusions: The authors conclude that both secnidazole gel and tinidazole administered as a single oral dose are effective treatments for children with giardiasis since both high cure rates and good tolerability were observed.
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PMID:Evaluation of Secnidazole Gel and Tinidazole Suspension in the Treatment of Giardiasis in Children. 1110 44

Giardia lamblia is one of the most important causes of waterborne diarrheal disease worldwide, and giardiasis is the most common protozoan infection of the human small intestine. Symptomatic infection is characterized by diarrhea, abdominal pain, and malabsorption, leading to malnutrition and weight loss, particularly in children. The pathogen resides strictly in the lumen of the small intestine, and infection is typically not accompanied by significant mucosal inflammation. Clinical and experimental studies indicate that B cell-dependent host defenses, particularly IgA, are important for controlling and clearing Giardia infection, although B cell-independent mechanisms also contribute to this outcome. In contrast to antigiardial host defenses, much less is known about the pathophysiological mechanisms underlying the clinical symptoms of giardiasis, partly because of the current lack of suitable model systems. In addition to being an important human enteric pathogen, Giardia is an interesting model organism for gaining basic insights into genetic innovations that led to evolution of eukaryotic cells, since it belongs to the earliest diverging eukaryotic lineage known. The completion of the giardial genome project will increase understanding of the basic biology of the protozoan and will help us to better understand host pathogen-interactions as a basis for developing new vaccination and therapeutic strategies.
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PMID:Microbes and microbial toxins: paradigms for microbial-mucosal interactions I. Pathophysiological aspects of enteric infections with the lumen-dwelling protozoan pathogen Giardia lamblia. 1112 91

Several reports have indicated that fecal elastase-1 (EL-1) determination is a new, sensitive, and specific noninvasive pancreatic function test; however, very few patients with malabsorption due to small intestine diseases have been included in the previous studies. The aim of the study was to compare the diagnostic accuracy of fecal EL-1 and fecal chymotrypsin (FCT) in distinguishing between pancreatic maldigestion and intestinal malabsorption. Three groups of subjects were studied: group A included 49 patients with known cystic fibrosis (25 males, median age 5 years); group B included 43 subjects with various small intestine diseases (17 males, median age 6 years); and group C included 45 children without any history of gastrointestinal disease (22 males, median age 5 years). In all patients, stools were collected for 72 h on a standard diet and fecal EL-1, FCT, and steatocrit tests were performed. Both EL-1 and FCT were below normal limits in all CF patients with pancreatic maldigestion not treated with pancreatic enzyme (100% sensitivity for both assays); El-1, but not FCT, was also below normal in all the CF patients with pancreatic maldigestion treated with pancreatic extracts. Both EL-1 and FCT values in the CF group were significantly lower than in subjects with various small intestinal diseases and in children without any history of gastrointestinal disease (P < 0.0001). FCT, but not EL-1, values showed an inverse statistically significant correlation with steatocrit values in the whole CF group (P < 0.001); FCT was below normal in three of four CF patients with steatorrhea on pancreatic enzyme therapy. Both EL-1 and FCT had 100% specificity when calculated in children without any history of gastrointestinal disease; in contrast, specificity was 86% for EL-1 and 76% for FCT if we considered the control group with small intestinal diseases: low EL-1 was observed in two cases of intestinal giardiasis, two cases of short bowel syndrome, one case of celiac disease, and one case of intestinal pseudobstruction; FCT was abnormal in four cases of intestinal giardiasis, three cases of celiac disease, one case of short bowel syndrome, one case of Crohn's disease, and one case of intestinal pseudobstruction. Diagnostic accuracy was 92% for fecal EL-1 and 82% for FCT. Steatocrit values were over the normal limit in 11 patients with small intestine diseases; in 7/11 of these patients at least one of the pancreatic test results was below the normal limit. In conclusions, in patients with CF, fecal EL-1 determination is not more sensitive than FCT in identifying pancreatic maldigestion; however, fecal EL-1 assay is more specific than FCT determination in distinguishing pancreatic maldigestion from intestinal malabsorption.
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PMID:Diagnostic accuracy of fecal elastase 1 assay in patients with pancreatic maldigestion or intestinal malabsorption: a collaborative study of the Italian Society of Pediatric Gastroenterology and Hepatology. 1141 13


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