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)

Alcohol has at least two actions on essential fatty acid (EFA) and Prostaglandin (PG) metabolism. It enhances the conversion of dihomogammalinolenic acid (DGLA) to PGE1 but it blocks the activity of the delta-6-desaturase, an enzyme necessary for replenishment of DGLA stores from dietary precursors. The acute effect of ethanol is therefore an increased production of PGE1 but chronic consumption will lead to depletion of DGLA and PGE1. Withdrawal from alcohol will lead to a precipitous fall in PGE1. PGE1 is known to have profound effects on the nervous system and behaviour. Patients with mania produce more PGE1 than normal while those with depression make less. Alcoholics may drink to maintain a normal PGE1 level, something which will require more and more ethanol as DGLA is depleted. In both animals and humans PGE1 or its precursor, gamma-linolenic acid (GLA) have been shown to attenuate the acute withdrawal syndrome. PGE1 injections prevent the development of fatty liver in alcohol-treated animals. Defective EFA and PGE1 metabolism are known to lead to increased fibrosis, reproductive failure, cardiomyopathy, cardiovascular disorders, gastritis and pancreatitis and could therefore be the basis for these disorders in alcoholics. A PGE1 deficiency could also be responsible for the fetal alcohol syndrome. Three other agents are known to produce constellations of fetal defects very similar to those found in the alcohol syndrome. These other factors are dihphenylhydantoin, lithium, and a deficiency of zinc. These three factors and excessive alcohol consumption all lead to PGE1 deficiency by different routes. If this concept is correct, the key to the management of alcoholism and its medical complications lies in the provision of GLA or DGLA, fatty acids which by-pass the alcohol blocked step and which are unfortunately unlikely to be present in any normal diet. Unlike many concepts of alcoholism and alcohol damage, the EFA/PGE1 idea is very readily testable and already has considerable experimental support.
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PMID:A biochemical basis for alcoholism and alcohol-induced damage including the fetal alcohol syndrome and cirrhosis: interference with essential fatty acid and prostaglandin metabolism. 625 73

Suppurative cholangitis in 5 aged cats was characterized clinically by weight loss, depression, dehydration, icterus, and fever. The major abnormal laboratory findings were a severe left shift of WBC and a high, conjugated bilirubin concentration consistent with an inflammatory process and cholestasis. Gross pathologic findings included periductal biliary fibrosis (4 cats), periductal pancreatic fibrosis (2 cats), cholelithiasis (2 cats), deformation of the gallbladder (2 cats), and chronic interstitial pancreatitis (2 cats). Histopathologic findings in all cases were portal hepatic fibrosis, biliary hyperplasia, and suppurative exudate within dilated intrahepatic biliary ducts. Weight loss and portal fibrosis were suggestive of chronic, intermittent illness. The pathogenesis appeared to involve invasion of the bile duct by enteric bacteria. Cholangitis was observed to occur in association with pancreatitis, cholelithiasis, or anatomic abnormalities of the biliary tract.
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PMID:Suppurative cholangitis in cats. 686 38

Myocardial depression (measured by ventricular function curves on response to a fluid load) has been shown in 10 patients with acute hemorrhagic pancreatitis. Significant inadequate responses were found on evaluation of both the left and right heart. The increased pulmonary vascular resistance associated with adult respiratory distress syndrome (ARDS) of this disease was shown to correlate inversely with pulmonary wedge pressure, thereby excluding myocardial failure and pulmonary edema as mechanisms for the production of the ARDS.
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PMID:The myocardial depressant factor (MDF) in acute hemorrhagic pancreatitis. 724 73

Fifteen patients with acute pancreatitis had 68 physiologic cardiopulmonary assessments performed, and they were compared with 61 performed on normal postoperative patients, and 113 on 41 cirrhotics. It was found that the patients with pancreatitis have an elevated cardiac index (CI), which is not due to the hyperdynamic hemodynamic state found in cirrhotics. In spite of this, the Sarnoff curves demonstrated that pancreatitis was accompanied by a myocardial depression p less than 0.03, not found in hyperdynamic cirrhotics. Cirrhotics are unable to increase their oxygen consumption in response to an increase in CI, as do normal patients or those with acute pancreatitis. In cirrhotics the hemodynamic lesion occurs at the capillary level with the opening of arteriovenous shunts which rob the tissues of their nutritive blood supply, while the patient with acute pancreatitis has a primary myocardial depression and his peripheral vasculature reacts like that of a normal person.
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PMID:Myocardial function in acute pancreatitis. 724 38

The left ventricular function of 24 patients with acute pancreatitis was studied noninvasively using systolic time intervals. Seven of the 24 patients were reevaluated 4-40 days following the onset of acute symptoms. During the acute phase the PEP/LVET ratio was significantly prolonged to 0.470 +/- 0.031 and later declined to 0.376 +/- 0.017 (P less than 0.01). The convalescent value is similar to the low grade abnormality found in noncardiac alcoholics without pancreatitis (0.381 vs 0.312 in age-matched normals). Since serum electrolytes were normal, serum cardiac isoenzymes were not elevated and there was no evidence of volume depletion in the initial stages, the transient cardiac depression produced by acute pancreatitis may be mediated by the postulated myocardial depressant factor from the pancreas.
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PMID:Depression of myocardial function during acute pancreatitis. 724 65

An analysis was made of 41 cases of disseminated intravascular coagulation in dogs, with the objective of evaluating routine and nonroutine laboratory tests used in making the diagnosis. The dogs were grouped on the basis of underlying disease, which included neoplasia (39%), pancreatitis (30%), chronic active hepatitis (15%), heat stroke (12%), and sepsis (4%). Of the diagnostic tests evaluated, those for determination of activated partial thromboplastin time, antithrombin III activity, prothrombin time, and the platelet count were the most valuable. Of the clotting factors, factor V activity was decreased more frequently than the activity of factor VIII:C (factor VIII: procoagulant). The factor VIII:C activity was in conflict with prevailing dogma that reflects depression of this factor in disseminated intravascular coagulation. Factor VIII:C activity was decreased in only 29% of dogs studied. Activation of the fibrinolytic system was manifested by decreased plasminogen activity in 49% of the dogs studied. Sixty-one percent of the dogs had increased amounts of fibrin (ogen) degradation products.
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PMID:Disseminated intravascular coagulation: antithrombin, plasminogen, and coagulation abnormalities in 41 dogs. 726 67

Graft-versus-host disease developed in two dogs injected with lymphocytes from BCG immunized donors. The disease was characterized by bone marrow depression, ulcerative enteritis, necrotizing cholangiohepatitis, thymic atrophy, pancreatitis, lymphadenopathy, inflammation of mucous membranes and weight loss. In one of the two dogs repopulation of bone marrow and lymphoid tissue by donor cells was demonstrated by cytogenetics. The development of GVHD was considered unusual because both animals received on immunosuppressive treatment and both responded well to PHA in lymphocyte transformation assays indicating they were immunocompetent. It was hypothesized that stimulation of donor lymphocytes by BCG enhanced their ability to induce a graft-versus-host reaction.
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PMID:Graft-versus-host disease in two immunocompetent dogs. 746 Oct 47

We show Escherichia coli derived L-asparaginase complications observed in 14 of 136 acute lymphoblastic leukemia patients during remission induction therapy according to St. Jude Children's Hospital Total XI Protocol. We observed hyperglycemia in six patients; two of them had accompanying ketoacidosis. One of the cases with ketoacidosis had peritonitis and pancreatitis. Central nervous system symptoms such as convulsions and depression with personality changes (in one case) were observed in four of these six hyperglycemic patients. Intracranial bleeding and ischemic infarction were shown in cranial computed tomographies in two cases. Hypersensitivity reactions were observed in seven patients. Patients were randomly assigned into two groups and treated with conventional dose steroids or high dose methylprednisolone. Although the frequency of hypersensitivity reactions were lower in the high dose methylprednisolone group, one patient in this group had an anaphylactic reaction. These findings once again high-light L-asparaginase complications which are not dose dependent and can be life threatening.
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PMID:Hyperglycemia, ketoacidosis and other complications of L-asparaginase in children with acute lymphoblastic leukemia. 799 65

Transient electrocardiographic changes in patients with acute cholecystitis, pancreatitis, and pneumonia have been reported in the past. These changes usually are in the form of T-wave inversion, ST-segment depression, and rarely ST-segment elevation in the absence of coronary artery disease. To the authors' knowledge, this is the first report documenting both left ventricular segmental wall motion abnormality and electrocardiographic changes of myocardial injury in the presence of acute pancreatitis.
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PMID:Electrocardiographic and segmental wall motion abnormalities in pancreatitis mimicking myocardial infarction. 772 Feb 88

Most antiviral drugs are nucleoside analogues with potential teratogenic, embryotoxic, carcinogenic and antiproliferative activities. They must be administered with caution during pregnancy, because some are known teratogens (e.g. amantadine) and a similar propensity cannot be entirely excluded for others (e.g. aciclovir). Their adverse effects mostly involve bone marrow depression (e.g. granulocytopenia with ganciclovir, anaemia with zidovudine) or neurotoxicity (e.g. seizures with interferon-alpha, peripheral neuropathy with zalcitabine), although gastrointestinal effects are also seen. Idiosyncratic reactions include didanosine-induced acute pancreatitis. Only inosine pranobex is largely free from toxicity. Idoxuridine must be administered topically, given the severity of its systemic adverse effects. Drug interactions involving antiviral agents mostly reflect shared toxicity with other agents (e.g. neutropenia with ganciclovir and zidovudine, pancreatitis with didanosine and alcohol), although renal excretion or hepatic metabolism may be implicated. Given the possibility of severe adverse reactions and drug interactions, antiviral chemotherapy should only be used for potentially serious virus infections. Topical administration avoids systemic adverse effects but not mutagenic risks, and may result in exposure of individuals other than the patient (e.g. aerosolised ribavirin).
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PMID:Adverse effects and drug interactions of clinical importance with antiviral drugs. 801


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