Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Halofantrine is an orally administered blood schizontocide which is active against both chloroquine-sensitive and chloroquine-resistant plasmodia. Dose-finding and noncomparative clinical trials have confirmed the efficacy of halofantrine in the treatment of falciparum malaria in areas of chloroquine- and sulfonamide/pyrimethamine-resistant malaria and vivax malaria. However, poor results obtained in patients who failed mefloquine prophylaxis suggest that the efficacy of halofantrine may not extend to mefloquine-resistant P. falciparum, although more studies are needed to confirm this. Data concerning halofantrine in the treatment of P. ovale and P. malariae infections are still limited. One comparative study indicates that halofantrine has an efficacy equivalent to that of mefloquine and may be better tolerated. Halofantrine is generally well tolerated in both adults and children, the most common drug-associated effects being abdominal pain, pruritus, vomiting, diarrhoea, headache and rash, although it is difficult to distinguish between disease- and treatment-related events. The development of parasite resistance to halofantrine, like other blood schizontocides, is inevitable. Poor absorption resulting in variable peak plasma halofantrine concentrations, and possible cross-resistance with mefloquine, may accelerate the emergence of resistance to halofantrine. Thus, it is of primary importance that halofantrine is used only in areas where chloroquine- and sulfonamide/pyrimethamine-resistance are established in order to preserve and sustain its efficacy. If used with care, halofantrine will provide an important treatment option for falciparum malaria, a widespread parasitic disease associated with considerable morbidity against which the number of effective drugs available is being increasingly compromised by the spread of resistance.
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PMID:Halofantrine. A review of its antimalarial activity, pharmacokinetic properties and therapeutic potential. 137 21

Mefloquine is an orally administered blood schizontocide. Initial dose-finding and comparative studies performed between 1977 and 1989 demonstrated efficacy of mefloquine as prophylaxis in nonimmune individuals and in the suppression and treatment of malaria in adults and children caused by multidrug-resistant Plasmodium falciparum. It was also effective against P. vivax infection, while data concerning the treatment of P. ovale and P. malariae infections were limited. In an attempt to delay the emergence of resistance to this promising antimalarial agent, mefloquine was combined with sulfadoxine and pyrimethamine. Although initial clinical trials indicated that this regimen was effective in preventing and treating falciparum malaria, recent treatment failures, the potential for severe dermatological reactions and lack of therapeutic advantage over mefloquine alone has prompted the World Health Organization to recommended that the combination be no longer used for treatment or prophylaxis of malaria. Mefloquine is generally well tolerated in both adults and children, with nausea, vomiting, diarrhoea, headache, dizziness, rash, pruritus and abdominal pain being the most common adverse effects, although it is difficult to distinguish between disease- and treatment-related events. The incidence of these adverse effects is similar to or lower than those observed with other antimalarial agents. Cardiovascular changes, such as bradycardia, occasionally occur. The most notable adverse effects associated with mefloquine are neuropsychiatric disturbances; precipitation of such events should be closely monitored and requires termination of prophylaxis or therapy. The eventual emergence of resistance to mefloquine, as with many other antimalarial agents, was inevitable. Mefloquine resistance is established in certain areas of Thailand and may be becoming a growing problem in other regions of the world. In order to preserve the efficacy of mefloquine in non-resistant areas, this useful agent should be used with care and only prescribed for prophylaxis in travellers and treatment in areas of multidrug-resistant plasmodia. Future options to combat mefloquine resistance may include the combination of mefloquine with other antimalarial agents such as qinghaosu derivatives. Thus, with cautious use and possible combination with other agents, mefloquine is likely to remain an important treatment option for falciparum malaria, a widespread parasitic disease for which an increasing number of drugs have proved inadequate.
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PMID:Mefloquine. A review of its antimalarial activity, pharmacokinetic properties and therapeutic efficacy. 768 11

Artesunate is an antimalarial agent, available in oral, rectal and parenteral formulations, that provides a rapid clinical effect in patients with Plasmodium falciparum malaria. The rapidity of effect, availability of an intravenous and intramuscular formulation and convenient dosage regimen make artesunate an ideal candidate for the treatment of severe malaria, including cerebral disease. While some results have been promising, there is no clear evidence to date that artesunate reduces mortality in patients with cerebral malaria to any greater extent than standard quinine therapy. When given as monotherapy, treatment should be continued for at least 5 to 7 days to prevent recrudescence. Combination therapy with mefloquine allows artesunate to be administered over 3 days or less, with a satisfactory clinical outcome maintained. Although optimal dosages remain to be determined, this combination continues to provide the rapid onset of clinical effect observed with artesunate monotherapy, but decreases the rate of recrudescence to 2% (i.e. radical cure rate of 98%) when used as treatment in patients with uncomplicated malaria from areas with a high risk of multidrug-resistance falciparum malaria. Although assessment of tolerability is complicated by the difficulty of distinguishing between disease- and treatment-related events, artesunate and artesunate-mefloquine combinations appear to be well tolerated in adults and children. Indeed, it is possible that prior administration of artesunate may reduce the incidence of mefloquine-induced vomiting. Clinical findings to date have not revealed any pattern of resistance to artesunate after use of the drug. However, given the history of the development of resistance to other antimalarial drugs, the use of artesunate should be restricted to areas of multidrug resistance, the drug should be used in combination with a longer acting agent such as mefloquine, and it should be used in regimens that provide radical cure rates of 90 to 100%. If used according to these treatment principles, artesunate will provide a well tolerated and valuable addition to the current extremely limited treatment options for multidrug-resistant falciparum malaria, a widespread parasitic disease associated with considerable mortality.
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PMID:Artesunate. A review of its pharmacology and therapeutic efficacy in the treatment of malaria. 853 55

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.
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PMID:[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. 896 84

Anisakidosis is a parasitic disease of the human gastrointestinal tract caused by ingestion of marine nematode larvae such as anisakis simplex or, rarely, Pseudoterranova, present in raw or undercooked fish. Frequent sites of involvement by anisakis are the stomach, small intestine, rarely the colon, or the peritoneum, liver, pancreas, lung and tonsils, anisakidosis is a self-limiting disease; the symptoms arise 12-24 hours after ingesting raw fish and include nausea, diarrhoea, and severe abdominal pain, but also anaphylactic reactions. At the site of penetration, anisakis causes marked oedema, eosinophilic infiltration and granuloma formation. There are haematological abnormalities such as marked leukocytosis of the peripheral blood, eosinophilia, and positive PCR and serum antibodies to the larva's surface antigens. The diagnosis of anisakidosis can be made by endoscopy, radiology and US, but the disease is often diagnosed at surgical intervention. In the gastric form of anisakidosis, EGIDS has both a diagnostic role and a therapeutic one because it is possible to remove the worm using biopsy forceps. We report on one case of gastric anisakidosis, in a women, hospitalised for intense epigastric pain and vomiting after ingesting raw fish. She underwent gastroscopy. A worm was extracted from the gastric mucosa using biopsy forceps. This was followed by clinical improvement. The worm was identified by its macroscopic and microscopic characteristics as an anisakis larva. At laboratory examination, marked leukocytosis and eosinophilia of the patient's peripheral blood were observed 3-4 days after ingestion of anisakis.
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PMID:[Gastric anisakidosis: personal experience]. 1515 28

Mesenteric inflammatory veno-occlusive disease (MIVOD) is a relatively recently known and not very often diagnosed form of ischemic bowel disease of low incidence und unknown etiology. We present the case of a patient who after presentation of inconclusive signs of epigastric pain and rectal bleeding suddenly developed right abdominal pain with local peritonism. Suspecting intestinal ischemia or perforated appendicitis we first performed laparoscopy, which showed an inflammable tumor of cecum, ascending colon and appendix with massive adhesions to the abdominal wall. We performed an open right hemicolectomy with primary anastomosis. The patient developed a deep vein thrombosis of the vena tibialis post. and vena saphena parva. After 12 months our patient is free of complaints and recurrence. Investigations carried out showed no evidence of hypercoagulopathy. The presentation of MIVOD can range from chronic inflammatory bowel disease with recurrent abdominal pain in combination with nausea, emesis and bloody diarrhea to acute abdomen. Therefore diagnostic misinterpretation and mistherapy as well as underdiagnosis is common. Histologic investigation shows a variable inflammatory infiltration of multiple veins of the intestinal wall and the mesentery as well as thrombotic vessel occlusion in different stages without involvement of the arteries. All forms of hypercoagulopathy, parasitic disease, sepsis and malignancy have to be excluded. Therapeutic success can only be achieved with surgical resection of the affected bowel, whereon in general no recurrence will occur.
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PMID:[Mesenteric inflammatory veno-occlusive disease (MIVOD)--a rare cause of intestinal ischemia]. 1639 91

Chagas' disease (American trypanosomiasis) is an endemic parasitic disease in some areas of Latin America. About 16-18 million persons are infected with the aetiological agent of the disease, Trypanosoma cruzi, and more than 100 million are living at risk of infection. There are different modes of infection: (1) via blood sucking vector insects infected with T. cruzi, accounting for 80-90% of transmission of the disease; (2) via blood transfusion or congenital transmission, accounting for 0.5-8% of transmission; (3) other less common forms of infection, eg, from infected food or drinks or via infected organs used in transplants. The acute phase of the disease can last from weeks to months and typically is asymptomatic or associated with fever and other mild nonspecific manifestations. However, life-threatening myocarditis or meningoencephalitis can occur during the acute phase. The death rate for persons in this phase is about 10%. Approximately 10-50% of the survivors develop chronic Chagas' disease, which is characterized by potentially lethal cardiopathy and megacolon or megaoesophagus. There are two drugs available for the aetiological treatment of Chagas' disease: nifurtimox (Nfx) and benznidazole (Bz). Nfx is a nitrofurane and Bz is a nitroimidazole compound. The use of these drugs to treat the acute phase of the disease is widely accepted. However, their use in the treatment of the chronic phase is controversial. The undesirable side effects of both drugs are a major drawback in their use, frequently forcing the physician to stop treatment. The most frequent adverse effects observed in the use of Nfx are: anorexia, loss of weight, psychic alterations, excitability, sleepiness, digestive manifestations such as nausea or vomiting, and occasionally intestinal colic and diarrhoea. In the case of Bz, skin manifestations are the most notorious (e.g., hypersensitivity, dermatitis with cutaneous eruptions, generalized oedema, fever, lymphoadenopathy, articular and muscular pain), with depression of bone marrow, thrombocytopenic purpura and agranulocytosis being the more severe manifestations. Experimental toxicity studies with Nfx evidenced neurotoxicity, testicular damage, ovarian toxicity, and deleterious effects in adrenal, colon, oesophageal and mammary tissue. In the case of Bz, deleterious effects were observed in adrenals, colon and oesophagus. Bz also inhibits the metabolism of several xenobiotics biotransformed by the cytochrome P450 system and its reactive metabolites react with fetal components in vivo. Both drugs exhibited significant mutagenic effects and were shown to be tumorigenic or carcinogenic in some studies. The toxic side effects of both nitroheterocyclic derivatives require enzymatic reduction of their nitro group. Those processes are fundamentally mediated by cytochrome P450 reductase and cytochrome P450. Other enzymes such as xanthine oxidoreductase or aldehyde oxidase may also be involved.
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PMID:Toxic side effects of drugs used to treat Chagas' disease (American trypanosomiasis). 1693 19

Anisakidosis is a parasitic disease of the human gastrointestinal tract caused by ingestion of larvae of marine nematodes such as Anisakis spp. or, rarely, Pseudoterranova spp., present in raw or undercooked fish. We report the first series of gastric Anisakis infection (anisakiasis) from a single centre in Italy. In our department, we observed 3 cases, all in women who were urgently hospitalized following intense epigastric pain and vomiting, developed after the ingestion of raw fish. The patients underwent urgent gastroscopy within a few hours. In each, a worm was extracted from the gastric mucosa by means of biopsy forceps. This was followed by prompt clinical improvement. The worm was identified by its macroscopic and microscopic characteristics as an Anisakis spp. larva (L3). In 2 cases, laboratory tests revealed marked leukocytosis and eosinophilia in the peripheral blood 3-4 days after ingestion of the raw fish. The diagnosis of anisakiasis can be made by endoscopy, radiology and abdominal ultrasound, but is often made only at surgery. In the gastric form of the disease, urgent gastroscopy has both a diagnostic and a therapeutic role, because the worm can be removed by means of biopsy forceps.
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PMID:Acute gastric anisakiasis: an Italian experience. 1728 96

Cutaneous dirofilariasis is a parasitic disease caused by the mosquito-borne filarial nematodes Dirofilaria (Nochtiella) repens, living in the subcutaneous tissue of dogs, cats, wild carnivores, and humans. Cases have been recently reported also from Germany, Czech Republic, Hungary, Ukraine, Russia, Austria, Switzerland, France, The Netherlands, and the Middle East. D. repens is not widely known to cause chronic pruritic dermatitis in animals. Dermatological signs observed in 100 canine clinic cases were pruritus (100%), erythema (79%), papulae (62%), focal or multifocal alopecia (55%), hyperkeratosis (18%), crusting (14%), nodules (12%), acantosis (5%), and eczema (3%). Signs other than dermatological were conjunctivitis (46%), anorexia (35%), vomiting (26%), fever (25%), lethargy (20%), and lymph-adenomegaly (10%). A case imported from Italy to Dubai is described. The opportunistic role of D. repens might explain the presence of asymptomatic carriers, the concurrent observation of nondermatological signs, and the development of dermatitis in a subgroup of parasitized dogs.
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PMID:Clinical Aspects of Dermatitis Associated with Dirofilaria repens in Pets: A Review of 100 Canine and 31 Feline Cases (1990-2010) and a Report of a New Clinic Case Imported from Italy to Dubai. 2220 88

Anisakiasis is a parasitic disease acquired by humans when ingesting raw or undercooked fish infected with L3 larvae of the nematode genus Anisakis or Pseudoterranova. Here we report the first case of human anisakiasis in China. The patient, male, 56 years old, Dalian citizen, was admitted into the hospital with vomiting, peripheral umbilicus and abdominal distension, and frequent mucous diarrhea. The patient was examined using an electronic gastroscope, which displayed a parasite residing in the stomach, and subsequently gastroscope-assisted surgery was implemented. A white round worm was removed from the patient and stained. It was identified as L3 larvae of Anisakis. After the removal of the L3 larvae of Anisakis, the inflammation symptoms disappeared. As the first report of clinical case of Anisakis infection in China, the morphology of L3 Anisakis larvae from the patient is described and discussed. We conclude that anisakiasis should be considered in patients who have a habit of eating raw fish and who display associated symptoms.
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PMID:Anisakiasis in China: the first clinical case report. 2353 84


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