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)

The tetracycline class of antibiotics is infrequently used in clinical pediatrics due to its side effects: they include anorexia, nausea, vomiting and diarrhea. Hypersensitivity, a photosensibility reaction and a brownish discoloration of teeth is less frequently, a pseudotumor cerebri is rarely seen. Once therapeutic plasma levels are exceeded however, either by overdosage or decreased renal or hepatic clearance of the drug, serious complications like a secondary Fanconi-Syndrom or a nephrogenic diabetes insipidus can occur. The increased toxicity of tetracyclines in pregnant women is well known. We would like to report a fatal case, where serious complications like a secondary Fanconi-Syndrom, toxic degeneration of the liver, a clinically undected pancreatitis and a protein loosing enteropathy are though to be either direct consequences of tetracycline overdosage or the indirect effect of a shocklike syndrom by means of a nonoliguric renal failure induced by tetracycline.
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PMID:[Tetracyclin intoxication versus idiopathic pancreatitis: report of a case with multiple organ involvement (author's transl)]. 47 25

Infantile cystinosis is a metabolic lysosomal storage disease of cystine affecting most of the body cells. The first symptoms appear after 5-6 months of life: anorexia, vomiting, polyuria, polydipsia and failure to thrive, associated with the signs of tubular Fanconi syndrome including glycosuria, proteinuria, loss of bicarbonate, phosphate, potassium, sodium, etc. Treatment with cysteamine is effective if started as early as possible. This treatment delays or prevents the spontaneous evolution toward end-stage renal failure, usually between 6 and 12 years of age, and also prevents growth stunting. In the long term, other organs may be involved like eye, thyroid, endocrine pancreas, muscle and central nervous system. The diagnosis is ascertained by leucocytes cystine assay, also useful for the follow up and the adjustment of the treatment. Prenatal diagnosis is available on chorionic sample. The gene of the disease is not yet identified but is known to map to chromosome 17.
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PMID:[Infantile cystinosis]. 936 13

Tyrosinemia type l is an inherited metabolic disorder attributable to deficiency of fumarylacetoacetate hydrolase, a terminal enzyme in the degradation pathway of tyrosine. Affected individuals may present with any of a number of signs and symptoms, including failure to thrive, fever, vomiting, diarrhea, hepatomegaly, ascites, jaundice, renal Fanconi syndrome, or conditions such as rickets and hepatocellular carcinoma.1 If untreated, the patient may die of acute liver failure before the second year of life, or from chronic liver failure or hepatocellular carcinoma before the end of the second decade of life.2 Although overt liver failure with coagulopathy may be part of the presentation of tyrosinemia, a significant coagulopathy in the absence of overt signs of liver disease has not been emphasized as a clue to the diagnosis of this condition. We report two tyrosinemic infants who presented with severe coagulopathies and no other signs of liver failure to stress this diagnostic point.
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PMID:Tyrosinemia type 1 should be suspected in infants with severe coagulopathy even in the absence of other signs of liver failure. 1004 78

Nephropathic cystinosis is a metabolic disease related to lysosomal cystine accumulation in almost all tissues of the body. The first symptoms set up from 5 or 6 months of age including anorexia vomiting polyurodipsia and failure to thrive associated with a proximal tubulopathy (glycosuria, tubular proteinuria, loss of bicarbonate, potassium, phosphorus, etc.) Treatment by cysteamine dramatically changed the prognostic. If started early this treatment allows to delay and possibly to prevent the spontaneous evolution towards end stage renal disease between 6 and 12 years of age and to avoid the growth failure. On the long term the disease involves other organs: eyes, thyroid endocrine pancreas, muscle and central nervous system. The diagnosis of cystinosis is based on the cystine leukocyte assay allowing also the follow up and the adjustment of the treatment. Prenatal diagnosis is possible on chorionic sample. The gene of this recessive disease, mapping on chromosome 17 was recently identified. This gene encodes a protein of the lysosomal membrane involved in the transport of cystine out of the lysosome. There is a juvenile, late onset, form of cystinosis its main symptom is proteinuria with variable tubular alterations. The so called adult form is asymptomatic its only symptom is corneal deposits most often found by chance examination.
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PMID:[Cystinosis from childhood to adulthood]. 1073 Feb 75

A 9-year-old spayed female Labrador Retriever was evaluated for anorexia, lethargy, and vomiting of 5 days' duration. Laboratory abnormalities included azotemia, high liver enzyme activities, hyperchloremic metabolic acidosis, glucosuria, ketonuria, proteinuria, and aminoaciduria. These laboratory abnormalities were diagnostic of proximal renal tubular acidosis and Fanconi syndrome. Results of initial and convalescent serologic tests for leptospirosis were negative. The dog was treated with amoxicillin, sodium bicarbonate, and potassium citrate at discharge. Repeated evaluations revealed resolution of the acidosis, azotemia, proteinuria, glucosuria, ketonuria, and high liver enzyme activities. Alkali administration was gradually discontinued, and the dog was clinically normal 8 months after discharge. The dog's clinical condition appeared to have been transient in nature, a phenomenon that is rarely seen in human or veterinary medicine.
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PMID:Transient proximal renal tubular acidosis and Fanconi syndrome in a dog. 1515 30

We present a 5-years old boy with acquired Fanconi-de Toni-Debre syndrome being a effect of therapy for Ewing's sarcoma. At the age of 3 years, this boy was diagnosed as suffering from Ewing sarcoma of his right femur. The boy received a course of 8-month pre-surgery (6 VIDE--Vincristine, Ifosfamide, Doxorubicin, Etoposide cycles and 2 VAI--Vincristine, Actinomycin, Ifosfamide cycles) and 6-month post-surgery (6 VAI--Vincristine, Actinomycin, Ifosfamide cycles) cytostatic therapies according to EWING, EURO 99 protocol. In forth month of post-surgery cytostatic therapy, progressive malaise, polyuria, polydypsia, and recurrent vomiting occurred. The association between those symptoms and malignancy was excluded. Laboratory studies revealed hypokaliemia, hypophosphatemia, proximal tubular acidosis, proteinuria, glucosuria, aminoaciduria, hyperkaliuria and hyperphosphaturia. Acquired Fanconi-de Toni-Debre syndrome due to toxic effect of cytostatic therapy on renal proximal tubules was diagnosed. At present, two years after the time the diagnosis was made, despite constant substitution of potassium, phosphates and bicarbonates, deficit of body mass and height, and bone mineral density abnormalities are observed.
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PMID:[Acquired Fanconi-de Toni-Debre syndrome due to therapy for Ewing's sarcoma in 5-years old boy]. 1689 36

We evaluated efficacy and toxicity profiles of fludarabine, Ara-C, idarubicin, and G-CSF (Ida-FLAG) combination chemotherapy in 56 refractory and/or relapsed acute leukemia patients. Patients were treated with fludarabine phosphate 25 mg/m2/d (d1-5), Ara-C 2 g/m2/d (d1-5), idarubicin 12 mg/m2/d (d1-3), G-CSF was given subcutaneously from sixth day until absolute neutrophil count (ANC) >500/microL. One third of the acute myeloblastic leukemia (AML) and 45% of acute lymphoblastic leukemia (ALL) cases were primary refractory disease. In AML patients, complete remission (CR) was achieved in 15 cases (53.6%). One case showed partial remission (PR) (3.6%) and 12 cases (42.8%) had resistant to this regimen (RD). Grade IV hematologic toxicity occurred in all AML cases. Leukocyte recovery time was 16 days. Nonhematologic complications were mild to moderate nausea, vomiting, and mucositis and could be controlled by routine measures. Stem cell transplantation was performed in 5 patients and all achieved CR, 2 autologous and 3 allogeneic. In ALL patients, CR and PR were obtained in 8 (42.2%) and 2 (10.5%) of 22 cases; disease was resistant to Ida-FLAG in 9 (47.3%) cases. Grade IV hematologic toxicity occurred in all ALL cases. Leukocyte recovery time was 17 days. Nonhematologic toxicity consisted of nausea, vomiting, and mucositis and could be controlled by supportive therapy. Autologous transplantation was performed in 1 patient, but relapse disease occurred after 5 weeks. There was no correlation between response rate and leukemia subtype (AML versus ALL), leukocyte count, age, sex, disease status (de novo versus secondary), and RFS (early versus late relapse) (P > 0.05). Median survival was 16 weeks in all cases (22 weeks in AML versus 13 weeks). At present, only 3 patients are alive and 2 of these are in continuous remission. The rest of the patients died. In conclusion, Ida-FLAG is a good choice in cases with refractory/relapsing acute leukemia for salvage chemotherapy. High efficacy and a low-toxicity profile are preferable properties of this regimen, and this regimen has been found to be useful for cytoreduction, especially in candidates for allo-SCT.
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PMID:IDA-FLAG regimen for the therapy of primary refractory and relapse acute leukemia: a single-center experience. 1698 32

A 16-month-old boy was admitted to the clinic because of vomiting and growth failure. His weight and height measurements were under the fifth percentile. He had fair hair and skin, enlarged wrists and rachitic rosaries. The presence of metabolic alkalosis, hypokalemia, hypochloremia, and high renin and aldosterone levels were suggestive of Bartter syndrome. However, in view of the growth failure, fair hair and skin, proteinuria, polyuria and active rickets, cystinosis was considered. Bone marrow smear examination was normal, despite the existence of suspicious crystals in the cornea. Cystine crystals were seen in the conjunctiva biopsy and increased leukocyte cystine level was measured; therefore, definitive cystinosis diagnosis was made. Renal Fanconi syndrome with metabolic acidosis is prominent in cystinosis; however, in rare instances, if sodium-dependent trans-tubular transport defect is present, patients could have Bartter syndrome findings such as hypochloremic metabolic alkalosis. Our case is a good example demonstrating that metabolic alkalosis should not exclude cystinosis and the other signs and symptoms of the patient should be thoroughly evaluated.
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PMID:A patient with cystinosis presenting transient features of Bartter syndrome. 1717 73

This study aimed to retrospectively assess the efficacy of postoperative adjuvant chemotherapy in 77 patients who underwent curative resection for stage III colorectal cancer. They were treated by intravenous administration of 5FU + LV (FL-IV group, 38) or oral administration of UFT + PSK (oral group, 39). The 3-year relapse-free (3Y-RFS), 5-year relapse-free (5Y-RFS) and 5-year overall survival (5Y-OS) were calculated for each group, and clinical results and adverse events (AEs) were compared between the two groups. The 3Y-RFS, 5Y-RFS and 5Y-OS were 65.8, 62.7 and 72.3%, respectively, in the FL-IV group and 63.3 (p=0.7957), 56.3 (p=0.7088) and 60.4% (p=0.5293), respectively, in the oral group. These parameters showed no significant differences between the two groups. As AEs, grade 3 leucopenia, nausea/vomiting, and general fatigue were noted in one patient each (2.6%) in the FL-IV group. Grade 3 or more severe AEs were not noted in the oral group. These results suggest that oral immunochemotherapy is one of the options of postoperative adjuvant therapy for stage III colorectal cancer, because it imposes no financial burden on patients and results in high quality of life.
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PMID:Comparison between intravenous and oral postoperative adjuvant immunochemotherapy in patients with stage III colorectal cancer. 1902 Jul 36

Four small-breed dogs were diagnosed with acquired Fanconi syndrome. All dogs ate varying amounts of chicken jerky treats. All dogs were examined for similar clinical signs that included, but were not limited to, lethargy, vomiting, anorexia, diarrhea, and altered thirst and urination. The quantity of chicken jerky consumed could not be determined; however, based on the histories obtained, the chicken jerky treats were a significant part of the diet and were consumed daily by all dogs. Extensive diagnostic testing eliminated other causes of the observed clinical signs, such as urinary tract infection and rickettsial disease. Glucosuria in the face of euglycemia or hypoglycemia, aminoaciduria, and metabolic acidosis confirmed the diagnosis of Fanconi syndrome. All dogs received supportive care, including IV fluids, antibiotics, gastroprotectants, and oral nutritional supplements. Three dogs exhibited complete resolution of glucosuria, proteinuria, and the associated azotemia; however, one dog remained azotemic, resulting in a diagnosis of chronic kidney disease.
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PMID:Fanconi syndrome in four non-basenji dogs exposed to chicken jerky treats. 2205 68


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