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

A woman of 30 with Simmonds--Sheehan syndrome is described that developed after delivery by vacuum-extraction of the fetus, due to powerless labour. The clinical picture was dominated by suprarenal cortical insufficiency, manifested with pains in the abdomen, vomiting, hypotonia and severe asthenic-adynamic syndrome. The substitutional hormonal treatment completely restored the general state and the working capacity of the patient.
 ...
PMID:[Simmonds-Sheehan syndrome]. 118 88

Intussusception is the most frequent cause of intestinal occlusion in children aged 3-5 years. Diagnosis is easy to perform in cases with typical clinical presentation. However diagnosis may be difficult in rare cases with atypical symptoms characterized by SNC involvement, that could delay a convenient treatment. We report 4 cases of intussusception presenting initially with consciousness abnormalities, hypotonia and vomiting. In these cases differential diagnosis with other conditions associated with comatose states has to be performed. Some hypothesis may be considered to explain these clinical pictures: 1. increased endorphins excretion during abdominal pain; 2. neurotoxins of bacterial origin released and absorbed by altered bowel; 3. intestinal hormones abnormally produced during the disease. As recommended by Rachmel, the condition should be suspected in all children presenting with the association of vomiting and lethargy and a radiological or tomographic study of abdomen should be performed also in cases without intussusception typical symptoms.
 ...
PMID:[Changes in the consciousness state as a symptom of intestinal invagination onset]. 129 38

The neuroleptic effect and tolerability of roxindole (EMD 49,980), an agonist of the dopamine-D2 autoreceptor, was studied during a 4 week treatment period in 7 patients with paranoid-hallucinatory schizophrenia (ICD-9: 295.3). In patients with a daily dosage of up to 4.5 mg/day, there was no improvement as measured with the total score of the BPRS scale. In contrast, patients with a daily dosage of up to 30 mg/day showed a slight improvement, especially in items associated with negative symptoms. In 3 patients there were slight adverse events (dizziness, hypersalivation, hypotonia, nausea/vomiting, miction disturbance) which were probably connected with the intake of roxindole.
 ...
PMID:Early clinical results with the neuroleptic roxindole (EMD 49,980) in the treatment of schizophrenia--an open study. 135 88

A number of inherited metabolic disorders are diagnosed by means of the nationwide newborn screening programme, usually before the first clinical signs occur. As for the rest of the varied metabolic disorders, knowledge and intuition of the paediatrician is a prerequisite for selection of patients for further metabolic investigation (selective screening procedure). Clinical symptoms of the most important metabolic diseases can be classified according to their pathophysiological background as: "intoxication type, energy deficiency type, storage type, neurodegenerative type". Especially in the first year of life, clinical features are unspecific: psychomotoric retardation, muscular hypotonia, cerebral convulsions, recurrent vomiting, sepsis-like conditions. In these cases indication for metabolic screening is broad. Especially in older children some clinical symptoms can be specific for a metabolic disorder: distinctive odour of urine, changes in hair, skin or eyes, organomegaly, skeletal changes. Recently, Reye-like syndrome, stridor, macrocephaly and vague, cerebral ischaemic episodes have been described in association with a metabolic defect. In conclusion, experience has shown that only a small number of metabolic disorders will be diagnosed from the typical clinical picture alone. In most cases a selective screening procedure leads to diagnosis because initial symptoms are unspecific.
 ...
PMID:[Clinical suspicion of inborn errors of metabolism]. 141 7

A 3-month-old girl was admitted to the hospital because of hypotonia and frequent vomiting. She had severe metabolic acidosis and her liver function was abnormal. Hepatomegaly and rapidly progressive liver failure developed, and she died at 4 months of age. Two half-siblings from a different mother had died in infancy of an undiagnosed myopathy. The liver was fatty and hepatocytes were filled with large and small lipid droplets. Other tissues were morphologically normal. The respiratory chain enzymes containing subunits encoded by mitochondrial DNA were markedly decreased in liver, partially decreased in muscle, but normal in other tissues. Southern blot analysis showed 90% depletion of mitochondrial DNA in liver, 53% depletion in muscle, and normal amounts in other tissues. This is the second case of fatal infantile liver failure associated with mitochondrial DNA depletion. This pathogenetic mechanism should be considered in infants with multiple respiratory chain defects and variable tissue expression.
 ...
PMID:Fatal infantile liver failure associated with mitochondrial DNA depletion. 144 52

A 6-month-old girl was hospitalized on three occasions for irritability, vomiting, acidosis, and hypotonia. During the third hospitalization hyperglycinemia and urinary glycolic acid were detected. Ethylene glycol was discovered in the infant's blood and bottled formula. Clinicians must consider ethylene glycol intoxication as a cause of recurrent infantile metabolic acidosis.
 ...
PMID:Intentional infantile ethylene glycol poisoning presenting as an inherited metabolic disorder. 153 89

Fourteen new cases of cytochrome oxidase (COX)-associated Leigh syndrome (LS) are combined with 20 reported cases to describe the clinical, laboratory, and radiological features of this devastating metabolic condition. Three clinical stages are identified. Most patients have normal neurological development during the first 8-12 months (stage I). Somatic complaints are common, including chronic diarrhea, recurrent vomiting, anorexia, and decelerating body and head growth. The second stage evolves during late infancy and early childhood when motor regression becomes evident. Eye signs, altered breathing patterns, pyramidal, extrapyramidal, and cerebellar signs emerge and sudden clinical deterioration occurs during intercurrent infectious or metabolic stress. The last stage may extend from 2 to 10 years and is manifested by extreme hypotonia, swallowing difficulties and undernutrition. Feeding assistance is necessary and seizures may occur. The CSF lactate concentration is consistently elevated and MRI abnormalities are seen in the subcortical structures. COX deficiency affects most tissues, but is not always generalized. For example, 3 patients with a cardiomyopathy had normal COX activity in cultured skin fibroblasts. Nearly normal amounts of cross-reacting material are present by ELISA and immunoblot analyses. Parental consanguinity has been found in several families, the hereditary pattern is recessive and males are affected more commonly (2:1). The biomolecular abnormality causing COX deficiency in LS is unknown, but the available evidence implicates a nuclear-encoded protein that affects the structure or the stability of the holoenzyme complex.
 ...
PMID:Cytochrome c oxidase-associated Leigh syndrome: phenotypic features and pathogenetic speculations. 165 84

This report describes a toddler with chronic diarrhea, vomiting, and hypotonia due to surreptitious administration of syrup of ipecac by his mother (Munchausen's syndrome by proxy). Several features of this case distinguish it from previous reports of chronic ipecac ingestion in childhood: the development of grossly bloody stools; radiologic, endoscopic, and biopsy evidence of a chronic moderate colitis resembling ulcerative colitis; and the histologic finding of pseudomelanosis coli, providing an important clue to toxic ingestion. The significance and possible mechanism for genesis of pseudomelanosis coli is discussed. This case emphasizes the variability in presentation and difficulty in diagnosing long-term ipecac ingestion by proxy. Ipecac toxicity should be considered in children with unexplained colitis and vomiting.
 ...
PMID:Hemorrhagic colitis and pseudomelanosis coli in ipecac ingestion by proxy. 167 9

Alpers disease consists of diffuse cerebral degeneration manifested as developmental delay, seizures, vomiting, and progressive neuromuscular deterioration, with liver disease and death. We report the clinical course of the liver disease, histologic progression of the hepatic lesions, and etiologic investigations in five patients (four girls, three kinships). All had grown and developed normally until seen at 6 to 36 months of age (mean 20 months), with vomiting (n = 5), progressive hypotonia (n = 3), or seizures (n = 2). All had been given anticonvulsants, including valproic acid in three. Liver disease was noted at a mean age of 35 months (range 9 to 67 months), with hepatomegaly (two patients), abnormal hepatic synthetic function (three) or transaminase values (three), and cirrhosis in one. Patients survived for a mean of 4.6 weeks (range 1 to 8 weeks) after the identification of liver disease; all died of hepatic failure. Results of evaluation for infectious and metabolic causes of liver disease and causes of degenerative neuromuscular disease were negative in all patients. Premortem liver biopsy specimens (n = 3) demonstrated an early lesion consisting of lobular disarray, microvesicular steatosis, periportal acute and chronic inflammation, and individual hepatocyte necrosis. Autopsy findings (n = 5) consisted of macrovesicular steatosis, massive hepatocyte dropout, and proliferation of bile ductular elements, with almost complete replacement of hepatocytes by proliferating bile ductular elements in two patients. Brain showed characteristic neuronal degeneration. We conclude that Alpers disease can be a cause of rapidly progressive liver failure in early childhood. Although the cause of this autosomal recessive disease is not known, it does not appear to be related to peroxisomal dysfunction.
 ...
PMID:Liver involvement in Alpers disease. 186 Dec 11

Symptoms and signs were recorded for 1007 infants younger than 6 months of age seen at home (298) or hospital (709) and correlated with four grades of illness severity. Most symptoms, present in the preceding 3 days, were associated with all grades of illness. Only four symptoms were not reported in well infants: a fluid intake less than a third of normal, convulsions, frank blood in the stools, and bile-stained vomiting. By comparison, many signs were seen only in ill infants. Those associated only with moderate or serous illness were marked retraction of the lower ribs, high-pitched or moaning cry, expiratory grunt, loss of alertness, central cyanosis, and severe hypotonia. Although these will not identify all seriously ill infants, parents and professionals should be taught to recognize these important symptoms and signs of serious illness.
 ...
PMID:Symptoms and signs in infants younger than 6 months of age correlated with the severity of their illness. 195 28


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>