UMLS:C0042963 - FACTA Search

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Query: UMLS:C0042963 (vomiting)
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A 5-month-old girl with distal renal tubular acidosis (RTA) and hyperammonaemia that had lasted for 12 days, despite metabolic acidosis correction, is presented in this report. The patient showed failure to thrive, poor feeding, hypotonia and vomiting crisis in absence of inborn errors of metabolism. Probably, hyperammonaemia was the result of an imbalance between the increased ammonia synthesis, in response to metabolic acidosis, and the impaired ammonia excretion, typical of distal RTA. Our case confirms that hyperammonaemia may be observed in distal RTA, mimicking an inborn error of metabolism, and it underlines that hyperammonaemia may persist several days after metabolic acidosis correction.
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PMID:Hyperammonaemia in a child with distal renal tubular acidosis. 1613 56

We have reported previously the efficacy of antiprotozoal drugs against canine giardiasis (In press, Journal of Veterinary Clinic, the Korean Society of Veterinary Clinics). Fenbendazole was found to be the most efficacious for the treatment of canine giardiasis. There were no significant differences between the efficacy of albendazole and fenbendazole against canine giardiasis. On the other hand, the efficacy of metronidazole for the treatment of canine giardiasis, the efficacy was lower when compared to that of albendazole and fenbendazole. On the basis of these results, to evaluate clinical effect of silymarin, we evaluated the therapeutic efficacy of metronidazole alone, or combined with silymarin for 2 weeks for canine giardiasis. In addition, to observe effects on nutrition, we investigated the changes of body weight, the serum biochemical indicators for liver inflammation (GOT, GPT, NH3), the liver cell regeneration indicators (total protein, albumin) and the hematological changes during treatment (WBC, RBC, MCV, MCH and MCHC). The dogs were allocated to four groups; one group was treated with silymarin (3.5 mg/kg once a day, oral), another with metronidazole (50 mg/kg once a day, oral), and the other group with silymarin (3.5 mg/kg once a day, oral) plus metronidazole (50 mg/kg once a day, oral), while control group remained nontreated. The fecal samples from all the dogs were examined, using the ZSCT and giardia antigen test kit (SNAP(*) Giardia, IDEXX Laboratories), from each dog of each group for three times a week for 2 weeks. Dogs were considered to have giardiasis when one or more of the fecal samples had positive results for Giardia cysts. Seven days after treatment, the efficacy of silymarin plus metronidazole was found 79%, whereas that of metronidazole was 72%. Ten days post-treatment the efficacy of metronidazole plus silymarin (91%) was significantly different in comparison with that of metronidazole (75%). Two weeks post-treatment no cysts were detected in the fecal samples in the dogs of metronidazole or silymarin plus metronidazole-treated groups. Whereas, the fecal samples of all the dogs of the control and only silymarin-treated groups were giardia positive. Signs of side effects were not observed in silymarin plus metronidazole-treated dogs. But poor appetite and intermittent vomiting signs were observed in two dogs of the metronidazole-treated group that resolved when metronidazole administration was discontinued. The body weight of those treated with metronidazole was significantly decreased in comparison with those treated with silymarin and metronidazole plus silymarin. There were significant differences of body weight between the dogs treated with silymarin and metronidazole. Two weeks after metronidazole treatment, serum concentration of GOT, GPT and NH3 were significantly increased in comparison with those treated with silymarin. On the other hand, the serum concentration of GOT, GPT and NH3 were not significantly increased when treated with silymarin plus metronidazole compared to those treated with metronidazole. Serum total protein and albumin concentrations were decreased after metronidazole treatment as compared to those treated with silymarin and silymarin plus metronidazole. The concentrations of serum total protein and albumin decreased significantly in metronidazole-treated group as compared to that of treated with silymarin. The numbers of WBC and RBC did show significant differences in the dogs treated with metronidazole, while MCV, MCH were significant by different between silymarin and metronidazole-treated dogs. On the other hand, there were no significant differences in MCHC in any groups. These data suggest that silymarin, in supplement with antiprotozoal drugs, can influence the therapy of canine giardiasis.
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PMID:Evaluation of silymarin in the treatment on asymptomatic Giardia infections in dogs. 1615 41

A 39-yr-old male with hepatorenal syndrome type 1 and refractory ascites was treated with continuous renal replacement therapy (CRRT) resulting in clinical improvement. He was positive for antibodies to hepatitis B, C, and human immunodeficiency viruses, and had a history of chronic alcohol and iv drug abuse. The patient had 4 hospital admissions during a 12-wk period. He first presented with advanced liver disease including pedal edema and a serum ammonia level of 56 micromol/L (reference range: 11 - 35 micromol/L). In subsequent admissions, he had asterixis, nausea, vomiting, jaundice, and worsening pedal edema. On his 4th admission, there was lethargy, tense ascites, decreased urinary output, bilateral edema of the lower extremities and scrotum, serum creatinine of 6.2 mg/dl (reference range: 0.6 - 1.5 mg/dl), and weight gain of 16 kg during the prior 8 wk. During the first 3 hospitalizations, he was treated with lactulose with slight improvement. On the 4th admission, he was started on low-dose dopamine (3 microg/kg/min) and 25% salt-poor albumin without clinical improvement. A pulmonary artery catheter was placed and hemofiltration by CRRT was performed for 5 days, with removal of 26.7 L of fluid and a net reduction of 11 kg of body weight. Serum creatinine decreased to 4.2 mg/dl during CRRT and was 2.2 mg/dl at hospital discharge 2 weeks later. His PaO(2) improved from 66 to 78 mmHg and his systemic vascular resistance increased from 571 to 799 dyne.sec/cm(5). CRRT was effective in relieving severe fluid retention and producing marked clinical improvement. We suggest that CRRT should be considered for the treatment of refractory ascites including that caused by hepatorenal syndrome.
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PMID:Hepatorenal syndrome: resolution of ascites by continuous renal replacement therapy in an alcoholic coinfected with hepatitis B, C, and human immunodeficiency viruses. 1650 Dec 43

We report a male patient with a history of recurrent idiopathic vomiting, normal plasma ammonia and glutamine concentrations in acute phase, who died at 3 years of age. Ornithine transcarbamylase deficiency was diagnosed after detecting elevated urinary orotate concentrations in a sample collected just before death, and the diagnosis was confirmed by DNA analysis.
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PMID:An unusual clinical and biochemical presentation of ornithine transcarbamylase deficiency in a male patient. 1660 86

A previously healthy 5 1/2-year-old male had Reye syndrome. He presented in coma with apnea 1 week after a viral infection and following 2 days of vomiting and progressive obtundation. He was in coma with dystonic posturing and intact brainstem function. Laboratory evaluation revealed initial hypoglycemia, and markedly elevated liver enzymes, prolonged clotting times, and elevated ammonia levels. No underlying metabolic disorder was present, and the patient completely recovered. On a modified diffusion-weighted image magnetic resonance imaging scan, restriction of diffusion in the thalamus and midbrain was observed. While abnormalities of the thalamus and midbrain have previously been reported, this is the first report of diffusion-weighted imaging indicating early impairment of water diffusion, a finding more commonly observed with stroke.
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PMID:The thalamus and midbrain in Reye syndrome. 1664 4

We provide a global assessment, with detailed multi-scale data, of the ecological and toxicological effects generated by inorganic nitrogen pollution in aquatic ecosystems. Our synthesis of the published scientific literature shows three major environmental problems: (1) it can increase the concentration of hydrogen ions in freshwater ecosystems without much acid-neutralizing capacity, resulting in acidification of those systems; (2) it can stimulate or enhance the development, maintenance and proliferation of primary producers, resulting in eutrophication of aquatic ecosystems; (3) it can reach toxic levels that impair the ability of aquatic animals to survive, grow and reproduce. Inorganic nitrogen pollution of ground and surface waters can also induce adverse effects on human health and economy. Because reductions in SO2 emissions have reduced the atmospheric deposition of H2SO4 across large portions of North America and Europe, while emissions of NOx have gone unchecked, HNO3 is now playing an increasing role in the acidification of freshwater ecosystems. This acidification process has caused several adverse effects on primary and secondary producers, with significant biotic impoverishments, particularly concerning invertebrates and fishes, in many atmospherically acidified lakes and streams. The cultural eutrophication of freshwater, estuarine, and coastal marine ecosystems can cause ecological and toxicological effects that are either directly or indirectly related to the proliferation of primary producers. Extensive kills of both invertebrates and fishes are probably the most dramatic manifestation of hypoxia (or anoxia) in eutrophic and hypereutrophic aquatic ecosystems with low water turnover rates. The decline in dissolved oxygen concentrations can also promote the formation of reduced compounds, such as hydrogen sulphide, resulting in higher adverse (toxic) effects on aquatic animals. Additionally, the occurrence of toxic algae can significantly contribute to the extensive kills of aquatic animals. Cyanobacteria, dinoflagellates and diatoms appear to be major responsible that may be stimulated by inorganic nitrogen pollution. Among the different inorganic nitrogenous compounds (NH4+, NH3, NO2-, HNO2NO3-) that aquatic animals can take up directly from the ambient water, unionized ammonia is the most toxic, while ammonium and nitrate ions are the least toxic. In general, seawater animals seem to be more tolerant to the toxicity of inorganic nitrogenous compounds than freshwater animals, probably because of the ameliorating effect of water salinity (sodium, chloride, calcium and other ions) on the tolerance of aquatic animals. Ingested nitrites and nitrates from polluted drinking waters can induce methemoglobinemia in humans, particularly in young infants, by blocking the oxygen-carrying capacity of hemoglobin. Ingested nitrites and nitrates also have a potential role in developing cancers of the digestive tract through their contribution to the formation of nitrosamines. In addition, some scientific evidences suggest that ingested nitrites and nitrates might result in mutagenicity, teratogenicity and birth defects, contribute to the risks of non-Hodgkin's lymphoma and bladder and ovarian cancers, play a role in the etiology of insulin-dependent diabetes mellitus and in the development of thyroid hypertrophy, or cause spontaneous abortions and respiratory tract infections. Indirect health hazards can occur as a consequence of algal toxins, causing nausea, vomiting, diarrhoea, pneumonia, gastroenteritis, hepatoenteritis, muscular cramps, and several poisoning syndromes (paralytic shellfish poisoning, neurotoxic shellfish poisoning, amnesic shellfish poisoning). Other indirect health hazards can also come from the potential relationship between inorganic nitrogen pollution and human infectious diseases (malaria, cholera). Human sickness and death, extensive kills of aquatic animals, and other negative effects, can have elevated costs on human economy, with the recreation and tourism industry suffering the most important economic impacts, at least locally. It is concluded that levels of total nitrogen lower than 0.5-1.0 mg TN/L could prevent aquatic ecosystems (excluding those ecosystems with naturally high N levels) from developing acidification and eutrophication, at least by inorganic nitrogen pollution. Those relatively low TN levels could also protect aquatic animals against the toxicity of inorganic nitrogenous compounds since, in the absence of eutrophication, surface waters usually present relatively high concentrations of dissolved oxygen, most inorganic reactive nitrogen being in the form of nitrate. Additionally, human health and economy would be safer from the adverse effects of inorganic nitrogen pollution.
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PMID:Ecological and toxicological effects of inorganic nitrogen pollution in aquatic ecosystems: A global assessment. 1678 74

Sodium fluoroacetate was introduced as a rodenticide in the US in 1946. However, its considerable efficacy against target species is offset by comparable toxicity to other mammals and, to a lesser extent, birds and its use as a general rodenticide was therefore severely curtailed by 1990. Currently, sodium fluoroacetate is licensed in the US for use against coyotes, which prey on sheep and goats, and in Australia and New Zealand to kill unwanted introduced species. The extreme toxicity of fluoroacetate to mammals and insects stems from its similarity to acetate, which has a pivotal role in cellular metabolism. Fluoroacetate combines with coenzyme A (CoA-SH) to form fluoroacetyl CoA, which can substitute for acetyl CoA in the tricarboxylic acid cycle and reacts with citrate synthase to produce fluorocitrate, a metabolite of which then binds very tightly to aconitase, thereby halting the cycle. Many of the features of fluoroacetate poisoning are, therefore, largely direct and indirect consequences of impaired oxidative metabolism. Energy production is reduced and intermediates of the tricarboxylic acid cycle subsequent to citrate are depleted. Among these is oxoglutarate, a precursor of glutamate, which is not only an excitatory neurotransmitter in the CNS but is also required for efficient removal of ammonia via the urea cycle. Increased ammonia concentrations may contribute to the incidence of seizures. Glutamate is also required for glutamine synthesis and glutamine depletion has been observed in the brain of fluoroacetate-poisoned rodents. Reduced cellular oxidative metabolism contributes to a lactic acidosis. Inability to oxidise fatty acids via the tricarboxylic acid cycle leads to ketone body accumulation and worsening acidosis. Adenosine triphosphate (ATP) depletion results in inhibition of high energy-consuming reactions such as gluconeogenesis. Fluoroacetate poisoning is associated with citrate accumulation in several tissues, including the brain. Fluoride liberated from fluoroacetate, citrate and fluorocitrate are calcium chelators and there are both animal and clinical data to support hypocalcaemia as a mechanism of fluoroacetate toxicity. However, the available evidence suggests the fluoride component does not contribute. Acute poisoning with sodium fluoroacetate is uncommon. Ingestion is the major route by which poisoning occurs. Nausea, vomiting and abdominal pain are common within 1 hour of ingestion. Sweating, apprehension, confusion and agitation follow. Both supraventricular and ventricular arrhythmias have been reported and nonspecific ST- and T-wave changes are common, the QTc may be prolonged and hypotension may develop. Seizures are the main neurological feature. Coma may persist for several days. Although several possible antidotes have been investigated, they are of unproven value in humans. The immediate, and probably only, management of fluoroacetate poisoning is therefore supportive, including the correction of hypocalcaemia.
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PMID:Sodium fluoroacetate poisoning. 1728 93

The urea cycle is the major metabolic pathway for excretion of waste nitrogen. Ornithine transcarbamylase deficiency is the most frequent urea cycle disorder. It is a hereditary-X-linked disease with over 150 mutations described. Ornithine transcarbamylase deficiency causes vomiting, lethargy, hyperventilation, and even death, mainly in the neonatal period. Ammonia, an extremely toxic molecule for the organism, is generated during protein catabolism and is accumulated in patients with this deficiency. Part of the treatment consists of a low-protein diet, to avoid hyperammonemia episodes, which can even have a fatal outcome. Patients can become deficient in several amino acids, either through the low-protein diet or directly through the primary enzyme deficiency; this in turn can cause an acrodermatitis enteropathica-like dermatosis.
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PMID:Acrodermatitis enteropathica-like dermatosis associated with ornithine transcarbamylase deficiency. 1784 64

In the research we included a total of 207 subjects with the dismissal diagnosis of "mycetismus", who were treated at the Department of Infectious Diseases, General Hospital Osijek, during the 1983-1992 period. 32 of them were children. There were 44.93% of men, 39.61% of women and 15.45% of children. The latent time > 6 hours was determined in 51 (25%) and < 6 hours in 75% of subjects. In 156 of patients with the latent time > 6 hours, "false" poisoning occured, while 51 patients experienced real mushroom toxins poisoning. At the admission to the hospital, in patients with the latent time > 6 hours, a pathological PT (protrombine time) was established only in women, leukocytosis in both women and children, increased concentration of GGT (gamma-glutamin-transferase) in men, increased AST (aspartate-aminotransferase) and ALT (alanin-aminotransferase) only in women, and increased urea in both women and children. After 24 hours, control measuring established high values of AST and ALT extended PT uremia and exalted amount of ammonia in blood in 11 of patients (2 men, 7 women and 2 children). They had severe liver and kidney damage, the most probably caused by Amanita phalloides toxins. The latent time lasted 9 to 13 hours. Of the 11 above mentioned patients, 2 women, aged 74 and 43, and one girl, aged 6, died. No pathological laboratory parameters were established in 40 of subjects with the latent time of 6 and more hours, and the disease manifested through vomiting and diarrhea that lasted for several days. These subjects most probably suffered from mushroom toxins poisoning. Mushroom toxins irritate the mucuous membrane of the gastrointestinal tract, and there are many such poisonous mushrooms. There were no mortalities in this group of subjects.
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PMID:Mushroom poisoning. 1821 66

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that may occur in people with normal liver-associated enzyme levels, despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl who had absence seizure and complained about progressive dizziness and general malaise several days after restarting valproate. Then, she presented vomiting and decreased consciousness three weeks after valproate use. Notably, her serum ammonia level was five times the upper limit of normal (184 micrommol/L), with normal liver-associated enzyme and supra-therapeutic valproate level. EEG showed continuous generalized slowing. The tandem mass analysis revealed carnitine deficiency. Consciousness improved after emergent hemodialysis. Ammonia level and EEG also returned to normal. Possible mechanisms, risk factors and the treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.
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PMID:Valproate-induced hyperammonemic encephalopathy treated by hemodialysis. 1879 59

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