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)

A 3-year-old, spayed, female Boxer was presented because of acute onset of anorexia, vomiting, and hemorrhagic diarrhea. Microangiopathic hemolytic anemia with intravascular hemolysis, thrombocytopenia, and acute renal failure were detected. The dog was treated with fluids, antiemetics, antibiotics, and diuretics. Despite supportive therapy, the dog's condition worsened, and the owners elected euthanasia. Necropsy revealed disseminated petechiae on the parietal peritoneum and serosal surfaces of the intestinal tract. The histologic lesions were consistent with severe arteritis and microvascular thrombosis involving only the renal and intestinal arterioles. The final diagnosis was hemolytic-uremic syndrome (HUS), a rarely described disorder in dogs. The clinical presentation of primarily gastrointestinal clinical signs was similar to that of typical or diarrhea-associated HUS (D+ HUS) in humans (mainly children), which is caused by gastrointestinal proliferation of verocytotoxin-producing Escherichia coli. Bacterial toxins can be adsorbed and cause endothelial injury, activation of hemostasis, and thrombosis, with lesions confined primarily to the kidneys. Although rare, HUS should be considered in the differential diagnosis of dogs with microangiopathic hemolytic anemia.
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PMID:Hemolytic-uremic syndrome in a dog. 1613 76

In August 1994, a 19-year-old woman presented to her dermatologist with a slight fever, arthralgia, and a butterfly rash. Discoid lupus erythematosus was suspected, and serological testing yielded positive results for antinuclear antibody. She was diagnosed with systemic lupus erythematosus without organ failure and was treated with only nonsteroidal antiinflammatory drugs. She became pregnant in June 2001, at age 26. In November her obstetrician noted that she had severe hypertension, edema of the low limbs, and proteinuria. On admission, she was diagnosed with severe preeclampsia, and cesarean section was performed. On hospital day 3 the patient developed sudden epigastric pain and vomiting. Laboratory tests revealed thrombocytopenia, liver dysfunction, and microangiopathic hemolytic anemia, leading to a diagnosis of HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome. Plasma exchange was performed for 5 days. The thrombocytopenia, liver dysfunction, and proteinuria diminished quickly. Later testing revealed a high titer of plasma phosphatidylserine-dependent anti-prothrombin antibody. This case is useful for exploring the relations between SLE, HELLP syndrome, and anti-prothrombin antibody.
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PMID:A case of systemic lupus erythematosus with postpartum hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome and concomitant high phosphatidylserine-dependent anti-prothrombin antibody levels. 1714 1

We report a case of Thrombotic Thrombocytopenic Purpura occurring as an allergic response to trimethoprim-sulfamethoxazole therapy (Bactrim, Septra) in a Jehovah's Witness patient. The patient presented with fulminant microangiopathic hemolytic anemia and thrombocytopenia within 48 hr of initiating therapy with trimethoprim-sulfamethoxazole. Other symptoms of drug hypersensitivity included nausea, vomiting, urticarial rash, and leukopenia. Because of her religious faith, the patient was supported without plasma therapy with use of intravenous immunoglobulin, steroids, rituximab, and erythropoietin.
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PMID:Thrombotic thrombocytopenic purpura induced by trimethoprim-sulfamethoxazole in a Jehovah's Witness. 1792 46

A 26-year-old man was referred to our hospital with vomiting and high fever. He was disoriented and laboratory results showed microangiopathic hemolytic anemia (Hb 7.1 g/dl) and severe thrombocytopenia (15 x 10(3)/microl). The diagnosis of thrombotic thrombocytopenic purpura (TTP) was established. The activity of von Willebrand cleaving protease (ADAMTS13) was found to be remarkably low (<0.5%) and the high activity of the inhibitor (11.0 Bethesda U/ml) was detected, confirming the diagnosis of typical acquired TIP. Although he had been successfully treated with daily plasma exchange and methylprednisolone, he relapsed after a week. To this therapeutic strategy we added four weekly doses of rituximab (375 mg/m2) and two weekly doses of vincristine (1 mg/m2) simultaneously. The response was very rapid and complete, that is, the platelet count recovered to normal seven days after the first rituximab and vincristine treatment. The patient maintains complete remission nine months later under the administration of 17.5 mg prednisolone. Recovery of the plasma ADAMTS13 activity was clearly correlated with the decrease or disappearance of the inhibitor activity. Combination of rituximab and vincristine therapy would appear to be very effective against refractory TTP.
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PMID:[Refractory thrombotic thrombocytopenic purpura successfully treated with a combination of rituximab and vincristine]. 1737 Jun 43

A 2-year-old female neutered Somali cat was presented with vomiting and acute onset jaundice 1 year after diagnosis of pyruvate kinase (PK) deficiency. Diagnostic investigations revealed a moderate regenerative haemolytic anaemia, severe hyperbilirubinaemia and elevated liver enzymes. Ultrasonography revealed marked distension of the gall bladder and common bile duct (CBD), consistent with extrahepatic biliary obstruction (EHBO). At cholecystotomy, the gall bladder contained purulent material, and two obstructive choleliths were removed from the CBD by choledochotomy. The cat recovered from surgery uneventfully, and serum liver enzymes and bilirubin normalised within 10 days. Postoperative treatment consisted of cephalexin, metronidazole and ursodeoxycholic acid (UDCA). Bacterial culture of the gall bladder contents yielded a pure growth of an Actinomyces species. Cholelith analysis revealed that they consisted of 100% bilirubin. Antibiotic treatment was stopped 4 weeks after surgery but UDCA was continued indefinitely. The cat remains clinically well with no recurrence of cholelithiasis 20 months after initial presentation. This is the first report of successful treatment and long-term follow-up of a cat with EHBO due to bilirubin cholelithiasis in association with PK deficiency-induced chronic haemolysis.
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PMID:Treatment and long-term follow-up of extrahepatic biliary obstruction with bilirubin cholelithiasis in a Somali cat with pyruvate kinase deficiency. 1747 29

During a five year period, 233 cases of malaria (2.4%) were diagnosed among 9259 children with fever and hepatosplenomegaly seen in Asir Central Hospital, Abha, Saudi Arabia. The majority of these were below four years of age and came from Tihama, a hot, humid valley area in the Asir region. The infection was seasonal and occurred between December and May. Apart from fever, vomiting and hepatosplenomegaly, anemia was a common clinical finding; this was partly due to iron deficiency anemia, probably nutritional. Most of the cases responded to chloroquine therapy; however, three required intravenous quinine and two received Fansidar to effect eradication of the parasitemia. During the study, two patients died, one from cerebral malaria and the other from severe hemolytic anemia and hemoglobinuria. For prevention of malaria in this endemic area, an integrated program is advocated that includes the use of bednets impregnated with permethin, adequate treatment of proven cases and intensive health education on malaria control and nutrition.
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PMID:Malaria in children - experience from Asir region, Saudi Arabia. 1758 50

The major syndromes of mushroom poisoning can be divided by presentation timing: Early syndromes (symptom onset <6 hrs after ingestion) have little probability to cause organ damage. Epigastric pain, nausea, vomiting and diarrhea occur in most cases and treatment includes initial gastrointestinal decontamination with oral activated charcoal and fluid rehydration. In addition, an acute gastrointestinal syndrome can be combined with cholinergic toxicity, epileptiformic response or immuno-hemolytic anemia. Neurotoxic Syndromes may present as dysphoria, delirium, hallucinations or disulfiram-like reactions. Treatment is entirely supportive and if performed in hospital, the prognosis is good. Late syndromes (symptom onset >6 hrs after ingestion) are life-threatening due to liver- and renal failure. Patients who are jaundiced after an acute gastrointestinal episode, are suspected to be poisoned with Amatoxins. Patients with flank pain, hematuria, polyuria or oliguria in the absence of jaundice are suspected to have an intoxication with Cortinarius mushrooms. In both cases an intensive care management is indicated.
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PMID:[Mushroom poisonings: syndromic diagnosis and treatment]. 1803 May 54

We report on an 8-year-old girl with hemolytic anemia because of infection with parvovirus B19 and increased intracranial pressure. She presented acutely with headache, vomiting, and mild scleral and mucosal icterus. Upon evaluation, the patient exhibited profound hemolytic anemia, papilledema, and increased intracranial pressure. The patient was treated with intravenous immunoglobulin, prednisone, and packed red blood cells. Concurrent with an improvement of her anemia, she experienced a gradual resolution of her headache, vomiting, and optic-disc swelling. Signs of idiopathic intracranial hypertension may occur as a consequence of severe anemia, and are reversible upon correction of the underlying hematologic disorder.
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PMID:Hemolytic anemia presenting with idiopathic intracranial hypertension. 1805 95

Gastrointestinal symptoms are extremely common during pregnancy. Increased levels of female sex hormones cause or contribute to symptoms such as heartburn, nausea, vomiting and constipation. If these symptoms do not respond adequately to lifestyle and dietary changes, drug therapy is often warranted to improve quality of life and to prevent complications. Physicians, therefore, need to be familiar with the low-risk treatment options available. Treatment of chronic conditions such as IBD or chronic liver disease during pregnancy can be demanding. In women with IBD, maintenance of adequate disease control during pregnancy is crucial. Most IBD drugs can be used during pregnancy, but the benefits and risks of specific drugs should be discussed with the patient. Liver diseases can be coincidental or pregnancy-specific. Pregnancy-specific liver diseases include not only benign disorders such as intrahepatic cholestasis of pregnancy, but also pre-eclampsia, eclampsia and HELLP syndrome (hemolytic anemia, elevated liver enzymes and low platelet count). Accordingly, the spectrum of therapeutic measures ranges from expectant management to urgent induction of delivery. During pregnancy, lamuvidine therapy for chronic hepatitis B can be continued; however, interferon and ribavirin therapy for chronic hepatitis C is contraindicated. This Review provides an overview of the spectrum and therapy of motility disturbances that occur during pregnancy, and discusses pregnancy-specific aspects of IBD and liver diseases.
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PMID:The spectrum and treatment of gastrointestinal disorders during pregnancy. 1925 5

A Somali cat was presented with recurrent anorexia, lethargy, vomiting and icterus. A macrocytic-hypochromic, regenerative haemolytic anaemia was identified and hereditary pyruvate kinase deficiency was confirmed by means of breed-specific DNA mutation analysis. The case was complicated by the presence of markedly elevated serum liver enzyme activities, hyperbilirubinaemia, coagulopathy and ultrasonographic evidence of gall bladder choleliths and extrahepatic bile duct obstruction. The choleliths consisted of 100 per cent bilirubin, likely because of chronic haemolysis and haeme degradation. In conclusion, haemosiderosis and bilirubin cholelithiasis can be a consequence of chronic haemolysis in pyruvate kinase-deficient cats, as seen in human beings with a variety of chronic haemolytic disorders.
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PMID:Bilirubin cholelithiasis and haemosiderosis in an anaemic pyruvate kinase-deficient Somali cat. 1868 51


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