Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied 12 patients with chronic persistent hepatitis and persistent or intermittent mild unconjugated hyperbilirubinemia. Maximum serum total bilirubin concentration ranged from 2.1 to 3.6 mg/dl. Hemolysis was not evident. Hepatic bilirubin UDP-glucuronyltransferase activity assayed in each patient ranged from 0.16 to 0.39 U (mean +/- SEM = 0.27 +/- 0.02) compared to 0.68-1.99 (1.35 +/- 0.08) in 23 normals, 0.78-2.28 (1.41 +/- 0.05) in 53 patients with acute hepatitis, 0.34-1.74 (0.81 +/- 0.09) in 16 patients with anicteric chronic persistent hepatitis, and 0-0.62 (0.24 +/- 0.03) in 33 patients with Gilbert's syndrome. The mean UDP-glucuronyltransferase activity was significantly lower in anicteric chronic persistent hepatitis compared to normals, but higher than in Gilbert's syndrome. The incidence of unconjugated hyperbilirubinemia among first degree relatives was 0:32 in icteric chronic persistent hepatitis compared to 24:85 (28%) in Gilbert's syndrome. These results show that the likely cause for the unconjugated hyperbilirubinemia associated with chronic persistent hepatitis is an acquired depression of hepatic bilirubin UDP-glucuronyltransferase activity. The data suggest that the enzyme defect is related to chronic persistent hepatitis.
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PMID:Chronic persistent hepatitis and unconjugated hyperbilirubinemia. 10 75

Hyperbilirubinaemia in newborn infants is generally regarded as a problem, and bilirubin itself as toxic metabolic waste, but the high frequency in newborn infants suggests that the excess of neonatal bilirubin may have a positive function. To investigate the hypothesis that bilirubin has a role as a free-radical scavenger, the rate of rise in serum bilirubin in the first few days of life was measured in 44 infants with five illnesses thought to enhance free-radical production and in 58 control infants. The infants were selected from 2700 consecutive births by exclusion of those with factors known to affect bilirubin metabolism, including enteral feeding. The control infants were those who seemed to be ill and received treatment, including restriction of enteral feeds, but in whom no illness, or disorders not related to free-radical production, were found. The mean serum bilirubin rise was significantly lower in the combined illness group than in the control group (36.1 [95% Cl 26.9-45.3] vs 66.7 [55.9-77.5] mumol.l-1.day-1; p less than 0.0001). In subgroup analyses the mean rises in infants with circulatory failure, neonatal depression/asphyxia, aspiration syndromes, and proven sepsis were significantly lower than in controls matched for gestational age and birthweight, but rises in infants with respiratory distress and their matched controls did not differ. These findings are consistent with the hypothesis that bilirubin is consumed in vivo as an antioxidant. Such consumption may operate in vivo in addition to the standard pathways for bilirubin metabolism (production, isomerisation, and excretion).
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PMID:Variation of initial serum bilirubin rise in newborn infants with type of illness. 167 69

Acute Francisella tularensis infection in 3 domestic cats was presumptively diagnosed on the basis of clinical signs and lesions and confirmed by culturing or immunofluorescent demonstration of the organism. Clinical findings include marked signs of depression, oral/lingual ulceration, regional or generalized lymphadenomegaly, hepatosplenomegaly, panleukopenia with severe toxic change of neutrophils, and hyperbilirubinemia with bilirubinuria. Lesions found at necropsy included icterus, oropharyngeal and lingual ulceration, multiple foci of necrosis in lymph nodes, spleen, liver, and lung, and severe segmental or diffuse enterocolitis. Results of serologic testing for F tularensis was positive in only 1 of the 3 cats. The organism was cultured aerobically from several tissues, including aspirated bone marrow obtained before death in 1 cat. Results of an indirect fluorescent antibody test, performed on fresh and formalin-fixed tissues of all cats, were positive. Because of the severe clinical course, opportunity to evaluate therapeutic regimens was not possible. Until now, confirmed diagnosis of feline tularemia only has been made retrospectively, in instances when cats were suspected to have transmitted infection to human beings in whom the primary diagnosis was made. The findings in this report provide a basis for presumptive diagnosis that will help to minimize public health risk associated with this potentially fatal zoonotic disease.
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PMID:Acute tularemia in three domestic cats. 177 44

Three weeks after initiation of griseofulvin treatment for dermatophytosis (40 mg/kg of body weight, q 12 h), an 8-yr-old domestic shorthair cat developed depression, vomiting, and pyrexia. Abnormalities found during physical examination included bilateral mydriasis, visual impairment, grade-II/V systolic murmur and multiple areas of alopecia. The cat was pancytopenic; serum biochemical abnormalities included hyperbilirubinemia, hyperglycemia, hyponatremia, and hypokalemia, and urinalysis revealed proteinuria, glycosuria, and bilirubinuria. Examination of a bone marrow aspirate revealed profound hypoplasia of all precursors. Griseofulvin toxicosis was diagnosed on the basis of the temporal relationship of drug administration with onset of clinical, hematologic, and biochemical abnormalities and failure to identify an infective or neoplastic cause for the bone marrow hypoplasia. The condition was refractory to treatment and the cat was euthanatized. Pathologic changes in the bone marrow were consistent with severe hypoplasia of all bone marrow precursors.
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PMID:Bone marrow hypoplasia in a cat treated with griseofulvin. 201 Mar 36

To evaluate the clinical value of splenectomy for hepatic resection, a total of 20 patients with hepatocellular carcinoma and hypersplenism were examined focusing on a change of total serum bilirubin values after surgery. Both hepatectomy and splenectomy were simultaneously performed in 12 patients, and in 8 patients as a staged operation. Postoperatively, a significant depression of bilirubin values was observed in a group with the preoperative values between 1.0mg/dl and 2.0mg/ml. Three factors (bilirubin, albumin and prothrombin time) in clinical stage were improved just after splenectomy with a statistical significance (p less than 0.05) in a group received staged operation. In 7 out of 8 patients, clinical stages were getting better as one or two stages prior to the hepatectomies. Therefore, we recommend the addition of splenectomy to hepatectomy in the patients whose hyperbilirubinemia are assumed to be correlated with coexisting hypersplenism.
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PMID:[The role of splenectomy in patients with hepatocellular carcinoma and hypersplenism as an aid to hepatectomy]. 255 82

Thirty cases of neonatal hyperbilirubinemia of varying etiology, severity and duration; and twenty six normal healthy newborns were subjected to various tests of cellular and humoral immunity. The results revealed a significant depression of all the parameters of cellular immunity in neonatal hyperbilirubinemia of greater than or equal to 10 mg/dl as compared to the control values. The depression of immunological profile in these newborns was seen to be more pronounced with increasing duration and severity of jaundice. A limited assessment of the humoral immunity by the B cell count and serum immunoglobulin IgG levels, however, showed no significant difference from the control.
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PMID:Immunological profile in neonatal hyperbilirubinemia. 262 Sep 79

The objective of this investigation was to characterize the acute and short- and long-term toxic potency of orally administered 1,2-dichloropropane (DCP). In the acute and short-term studies, male rats of 250-300 g were gavaged with 0, 100, 250, 500, or 1000 mg DCP/kg in corn oil once daily for up to 10 consecutive days. Although ingestion of DCP caused body weight loss and CNS depression, few other toxic effects were manifest 24 hr after a single dose of the chemical. Morphological changes were limited to liver centrilobular cells in 500 and 1000 mg/kg rats. Similarly, elevated activity of some serum enzymes occurred only at these two highest dose levels. Hepatic nonprotein sulfhydryl (NPS) levels were decreased and renal NPS levels increased at 24 hr. In the short-term study resistance developed to DCP hepatotoxicity over the 10 consecutive days of exposure, as reflected by progressively lower serum enzyme levels and by decreases in the severity and incidence of toxic hepatitis and periportal vacuolization. Nucleolar enlargement in hepatocytes, however, was observed at all dosage levels at 5 and 10 days. There were a number of manifestations of hemolytic anemia, including erythrophagocytosis in the liver, splenic hemosiderosis and hyperplasia of erythropoietic elements of the red pulp, renal tubular cell hemosiderosis, and hyperbilirubinemia. Urinalyses and histopathology revealed no evidence of nephrotoxicity. In the long-term study, male rats initially weighing 180-200 g were gavaged five times weekly for up to 13 weeks with 0, 100, 250, 500, or 750 mg DCP/kg. As over one-half the 750 mg/kg group died within 10 days, the survivors were sacrificed. Histopathological changes in the 750 mg/kg animals included mild hepatitis and splenic hemosiderosis, as well as adrenal medullary vacuolization and cortical lipidosis, testicular degeneration and a reduction in sperm, and increased number of degenerate spermatogonia in the epididymis in some members of the group. Similar testicular and epididymal degenerative change also were observed in some 500 mg/kg animals after 13 weeks of dosing. There was a progressive increase in the number of deaths in the 500 mg/kg group, such that more than 50% were dead by 13 weeks. No deaths occurred in the 100 or 250 mg/kg groups. The DCP dosage regimen also produced a dose-dependent decrease in body weight gain. DCP exhibited very limited hepatotoxic potential and no apparent nephrotoxic potential in the long-term study. Slight elevations in serum ornithine-carbamyltransferase activity, periportal vacuolization, and active fibroplasia in the liver were seen in the 500 mg/kg animals.
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PMID:Oral toxicity of 1,2-dichloropropane: acute, short-term, and long-term studies in rats. 274 74

Heme oxygenase, the rate-limiting enzyme for heme degradation, can be inhibited by several new synthetic metalloporphyrins. Under certain conditions, a depression in heme oxygenase activity has important clinical significance in the treatment of hyperbilirubinemia, and, in this regard, tin-protoporphyrin has been shown to decrease the production of bilirubin in vitro as well as in vivo. Similarly, our study was concerned with finding a new metalloporphyrin which will inhibit heme oxygenase. Many of the synthetic heme analogs that we analyzed were quite effective inhibitors of heme oxygenase, but the most powerful inhibitor was found to be zinc-deuteroporphyrin IX, 2,4-bisglycol. This metalloporphyrin almost completely inhibits liver heme oxygenase at concentrations as low as 0.5 microM. Its potency as an inhibitor was found to be greater than that of tin-protoporphyrin; the Ki of zinc-deuteroporphyrin IX, 2,4-bisglycol was calculated to be 0.003 microM. In conclusion, we demonstrated that zinc-deuteroporphyrin IX, 2,4-bisglycol has potent inhibitory effects on human liver, kidney and brain heme oxygenase so that this metalloporphyrin can be considered as an alternative to tin-protoporphyrin in the treatment of hyperbilirubinemia.
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PMID:Sensitivity of human tissue heme oxygenase to a new synthetic metalloporphyrin. 275 52

Pancreatic abscess was diagnosed by exploratory celiotomy in 6 dogs. The most common clinical signs included acute onset of lethargy (n = 5), anorexia (n = 6), vomiting (n = 5), and diarrhea (n = 2). Physical examination revealed pain response to abdominal palpation (n = 5), depression (n = 5), icterus (n = 3), fever (n = 3), and cranial abdominal mass (n = 2). Consistent preoperative clinicopathologic abnormalities included leukocytosis with left shift, observance of toxic neutrophils on the blood smear, hyperlipasemia, hyperamylasemia, hyperbilirubinemia, and increased serum alkaline phosphatase activity. In 5 of 6 dogs, abdominal radiography revealed increased soft tissue density in the cranial portion of the abdomen. Ultrasonography performed on 4 dogs confirmed pancreatic mass. In all dogs, exploratory celiotomy revealed a cavitary pancreatic mass that contained sterile, mucopurulent material. Histopathologic diagnoses included acute necrotizing or chronic-active pancreatitis and steatitis. Two dogs were euthanatized at the time of diagnosis, and the remaining 4 were treated by use of pancreatic debridement(s), open abdominal drainage, and intensive administration of fluids and antibiotics. One dog was euthanatized 4 days after surgery, because of progressive pancreatic abscessation. Three dogs recovered and were discharged.
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PMID:Pancreatic abscess in dogs: six cases (1978-1986). 319 66

Prospective screening of an extremely high risk group of 137 infants cared for in the Newborn Intensive Care Unit of the James Whitcomb Riley Hospital for Children was undertaken during 1983. Auditory brain stem responses (ABR) were obtained utilizing a clinical evoked potential system (Madsen 2250). Patients were selected for screening prior to discharge or transfer to the referring hospital on the basis of one or more of the following criteria: birth weight less than 1250 grams; birth weight less than 1500 grams and ventilatory support; significant depression at birth (Apgars less than 3 and 6 at 1 and 5 minutes, respectively); seizures, meningitis, and/or sepsis. Of the original 137 infants tested, 82 passed the initial ABR, 22 conditionally passed, and 34 failed. Eighty-two infants had follow-up behavioral and audiometric testing while 20 infants died and 35 were lost to follow-up. Four infants had severe sensorineural hearing loss, each of whom had failed the initial ABR. None of the infants who initially passed or conditionally passed the ABR had sensorineural hearing loss on follow-up testing. High risk factors for sensorineural hearing loss in the neonatal period included: intraventricular/periventricular hemorrhage, apnea, family history, major malformations of the head and neck, and possibly hyperbilirubinemia and congenital infection. No relationship of sensorineural hearing loss with very low birth weight, hyponatremia, infection, seizures, or medications was found. On the basis of these data, it is suggested that electrophysiologic hearing screening of a high risk population may be delayed until 3 to 6 months of age to improve specificity of testing.
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PMID:Hearing screening of high risk newborns. 355 7


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