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 major benefits of the perioperative administration of nonsteroidal anti-inflammatory drugs (NSAIDs) are related to the ability of these agents to provide analgesia without cardiovascular or respiratory depression. However, there are several possible adverse effects of NSAIDs. All NSAIDs reduce the synthesis of prostaglandins by the kidneys, but their administration in the perioperative period appears to have little potential for renal toxicity when adequate hydration is maintained and renal function is not dependent on renal prostaglandins. However, NSAIDs may cause impairment of renal function in patients with conditions such as hypovolaemia, congestive cardiac failure, or hepatic cirrhosis, since renal function in these patients may be dependent on the vascular effects of prostaglandins. Platelet aggregation is inhibited by the administration of NSAIDs, and most studies of their haematological effects report that NSAIDs are associated with an increase in bleeding times. In patients with normal haemostatic function before NSAID administration, almost all indices of coagulation remain within the normal range after NSAID treatment. Most studies of perioperative blood loss have reported no significant difference between the effects of NSAIDs and placebo in this regard. The incidence of major allergic reactions in the general population appears to be small with NSAIDs. Overall, NSAIDs appear to be safe and well tolerated drugs with a valuable role to play in the treatment of postoperative pain.
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PMID:Potential renal, haematological and allergic adverse effects associated with nonsteroidal anti-inflammatory drugs. 128 59

Causes of death in 8 of 235 drunkenness offenders each followed up for two years, have been described. The subjects followed up were a heterogenous population of alcohol abusers. The majority were alcohol dependent irregular heavy drinkers. The main causes of death were suicide, road traffic accident, domestic accident, liver cirrhosis, hypothermia (from exposure) and ischaemic heart disease. More than one cause of death was listed in all cases. Chronic alcoholism was frequently listed. Depression was another sub-ordinate cause of death. The overall observed rate of mortality was 30 times the expected rate which was many times higher than those reported by earlier workers for alcoholics generally. These findings were discussed and it was concluded that drunkenness offenders are a particular at risk sub group of alcoholics. In view of the appreciable post mortem blood alcohol levels, it was further concluded that chronic alcoholism and the actual state of being drunk were the two major causes of death in this group of alcohol abusers.
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PMID:Causes of mortality in drunkenness offenders followed-up for 2 years. 130 84

Cardiac function is studied with regular hemodynamic determinations and 2D-doppler echocardiography, in 22 patients with massive ascites. Patients were divided in two groups: 1. Hepatic cirrhosis (n = 12) and 2. Peritoneal carcinomatosis (n = 10). Patients with carcinomatosis showed lowered heart-beat volume, cardiac output, ventricular work and ejection fraction in comparison with cirrhotic patients. In cirrhotic patients the hemodynamic study was done before and after an evacuatory paracentesis, following which an improvement in cardiac function was shown, with significant increments in heart-beat volume, cardiac output, ventricular work, and ejection fraction. 42% of the cirrhotic patients showed an hyperdynamic circulatory status in the baseline study, but after paracentesis this hyperkinetic status was present in 100% of the patients. It is suggested that tension ascites influences negatively in cardiac function because it difficult the venous return. This depression in the ventricular function is more obvious in patients with carcinomas that in cirrhotic patients due to the fact that the former do not have a previous circulatory status.
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PMID:[Hemodynamic impact of tension ascites and evacuatory paracentesis]. 147 38

We studied hypoxic pulmonary vasoconstriction (HPV) and pulmonary gas exchange in unanesthetized rats with biliary cirrhosis induced by chronic bile duct ligation (BDL) (5 to 6 wk) and compared pulmonary vascular reactivity in perfused lungs isolated from BDL and control rats. Awake, catheter-implanted, cirrhotic rats exhibited increased cardiac output, normal systemic and pulmonary arterial pressures, and decreased total systemic (TSR) and pulmonary (TPR) vascular resistances in comparison with those in sham-operated control rats. HPV was markedly depressed in cirrhotic rats (percent increase in TPR while breathing 8% O2: 42.3 +/- 13.7% in control and 0.9 +/- 3.6% in cirrhotic rats, p less than 0.05), and this was associated with an increased AaPO2 (control rats, 15.7 +/- 1.1 mm Hg; cirrhotic rats, 23.1 +/- 1.9 mm Hg; p less than 0.05). In contrast, the pulmonary pressor response to angiotensin II was intact, and the depression of HPV in cirrhotic rats was ameliorated after angiotensin II infusion. These changes in cirrhotic rats were not due to the accompanying cholestasis since noncirrhotic rats with severe cholestasis had intact HPV and normal AaPO2. Lungs isolated from cirrhotic rats and perfused with blood from normal rats exhibited two patterns of response to hypoxia. In one group, HPV was blunted compared with that in control rats (change in pulmonary arterial perfusion pressure after 3% O2: control rats, 23.2 +/- 2.8 mm Hg; cirrhotic rats, 4.8 +/- 1.4 mm Hg; p less than 0.01). Similar to the result in intact rat, angiotensin-II-induced vasoconstriction was preserved in lungs from cirrhotic rats, and HPV increased significantly after angiotensin II infusion (to 17.3 +/- 4.8 mm Hg). In the second group, baseline pulmonary arterial pressure progressively increased during normoxia, and this increase was attenuated by hypoxic ventilation (hypoxic vasodilation).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary circulatory dysfunction in rats with biliary cirrhosis. An animal model of the hepatopulmonary syndrome. 155 5

The hemodynamics during hemodilution occurred after hepatectomy for hepatocellular carcinoma with liver cirrhosis and its influences on the liver functions were studied. The hematocrit value gradually decreased about 10% until the 4th postoperative day owing to hemodilution after hepatectomy. While anemia progressed, cardiac index inversely increased. Under such a condition, oxygen consumption was maintained so that acidosis did not develop. Arterial blood ketone body ratio was also kept within a normal range except for a case whose hematocrit value decreased to 17.1%. Although the escaped hepatic enzymes such as GOT and GPT increased in the serum after hepatectomy, hemodilution was not responsible for their increase. While total bilirubin increased in the severe hemodiluted group, the increase was not due to hemodilution but caused by blood transfusion. The protein synthesis of the liver measured by rapid turnover protein levels in plasma was depressed after surgery, and this depression prolonged to the 14th postoperative day in the group whose hematocrit value decreased below 20%. These results suggest that it is better to keep hemodynamics without blood transfusion unless the hematocrit value decrease below 20%, and also better to maintain the hematocrit above 20% for liver regeneration after hepatectomy.
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PMID:[The hemodynamics during hemodilution and its influence on the liver functions after hepatectomy for hepatocellular carcinoma with liver cirrhosis]. 165 85

The interferons (IFN) act too slowly to arrest acute viral infections, but interferon-alpha (IFN alpha) preparations have proved useful in some chronic infections and will clearly be used increasingly in these in the future. In the preparations derived from human leucocytes or cultured B lymphoblastoid cells, which are in routine clinical use, mixtures of a number of distinct subtypes of human IFN alpha have been identified. There are also 3 slightly different versions of the same single subtype, IFN alpha-2, made by recombinant DNA procedures in bacteria. IFN alpha preparations are injected intramuscularly or subcutaneously. Dose-related side effects are common but usually tolerable, but prolonged treatment may cause increasing fatigue and depression. Some patients form neutralising antibodies which block the effects of the IFN; these appear to be relatively more common after recombinant IFN alpha-2 than after IFN derived from human cells. Given intranasally, IFN alpha can prevent a subsequent experimental rhinovirus infection, or the spread of natural colds within a family. Repeated administration progressively damages the nasal mucosa, so that long term prophylaxis is not possible. IFN alpha has proved useful in patients with papillomavirus warts of the larynx, ano-genital region (condyloma acuminata) and skin (common warts). Treatment regimens remain to be optimised and are likely to include surgery or other treatments. IFN alpha and zidovudine (azidothymidine) synergistically inhibit the growth of HIV in vitro, and combination are on trial in patients with early AIDS. Very large doses of IFN alpha are effective against Kaposi's sarcoma in some AIDS patients. In chronic hepatitis B, continuing virus replication may lead to cirrhosis or primary liver cancer. Earlier clinical trials with IFN alpha gave inconclusive results, but recent large studies have confirmed that 25 to 40% of patients obtain benefit; this probably results from both the antiviral and the immunomodulatory effects of IFN alpha. In patients with chronic hepatitis C, the biochemical markers usually improve rapidly during IFN alpha administration, but relapse if treatment is stopped after only a few months; to increase the chances of sustained cure, the treatment period is now being prolonged.
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PMID:The use of interferon-alpha in virus infections. 172 72

We have previously reported that monocyte aryl hydrocarbon hydroxylase (AHH) activity is depressed in patients with liver disease and is decreased more in cirrhosis than in early stage liver disease. To determine if monocyte AHH activity reflects liver AHH activity, we studied an animal model of cirrhosis, i.e., yellow phosphorus induced cirrhosis in the pig. AHH activity was detectable in monocytes isolated from peripheral blood of normal pigs (0.32 +/- 0.13 nmol.mg-1 P.h-1, n = 11) and was comparable to the level of AHH activity in hepatic Kupffer cells isolated from wedge or needle biopsies of livers of normal pigs (0.38 +/- 0.21, n = 7). The AHH level in pig Kupffer cells was approximately 10% of the AHH level in hepatocytes and microsomes. To induce liver disease, pigs were administered yellow phosphorus (0.6 mg/kg) 5 days per week for 16 weeks. At 4 weeks of treatment, monocyte AHH activity was not different from control and liver histology was normal. Depression of monocyte AHH activity was evident at 8 weeks of treatment when liver fibrosis was seen histologically. At 12 weeks of treatment when histology revealed extensive liver fibrosis and collagen levels were elevated, the level of monocyte AHH activity was decreased 67% compared with controls. Similar changes were observed at 12 weeks in Kupffer cell AHH activity (86% decrease) and hepatocyte AHH activity (70% decrease) compared with controls. These results suggest that monocyte AHH activity reflects liver AHH activity and may be a good indicator of change in liver enzyme function in liver disease in the pig model of cirrhosis.
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PMID:Monocyte aryl hydrocarbon hydroxylase (AHH) activity mimics Kupffer cell and hepatocyte AHH activity in an animal model of liver disease. 180 52

To evaluate the role of severe liver damage on natural killer cell activity, 29 patients with liver cirrhosis were examined. The natural killer cell activity was measured with a 4-hr chromium release assay, and the K562 cell line was employed as target cells. The natural killer cell activity was significantly decreased in cirrhotic patients compared with normal controls and patients with chronic active hepatitis. Cirrhotic patients with Pugh's C grade of severity of liver disease had lower natural killer cell activity. The depression of natural killer cell activity in cirrhotic patients was inversely correlated with prothrombin time ratios, and the natural killer cell activity in cirrhotic patients with hepatic encephalopathy was lower than in patients without hepatic encephalopathy. Thus, the diminished natural killer cell activity in cirrhotic patients might be related to the severity of liver damage.
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PMID:Natural killer cell activity in patients with liver cirrhosis relative to severity of liver damage. 199 65

Antithrombin III (AT III) levels in 37 healthy people and in 103 patients diagnosed of hepatic cirrhosis (75 due to ethylism, 26 cryptogenic and 7 post-hepatitis) have been studied. Forty seven patients presented a compensation in their cirrhosis and 56 an unbalance. AT III concentration was decreased in cirrhotic patients (14.9 + 1.09 mg/dl), being p less than 0.0005 in relation to healthy patients (24.3 + 0.87 mg/dl). Concentration resulted lesser in patients with unbalance (13.9 + 1.8 mg/dl) than in patients with compensation (18.1 + 1.6 mg/dl). Moreover, statistical study between them showed significant results. AT III, though is a protein whose hepatic synthesis is not clear, decreases in diffuse hepatic disease and so much as more severe is the hepatic damage. Cirrhotic patients did not present thromboembolic phenomena, perhaps because of depression of coagulation factors.
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PMID:[Antithrombin III and liver cirrhosis]. 203 69

To evaluate the significance of natural killer (NK) cell activity in the clinical assessment of patients with hepatocellular carcinoma (HCC), 32 patients combined with liver cirrhosis (LC) and HCC, and 29 LC patients were studied. The NK cell activity was markedly decreased in HCC patients and the LC group as compared with the control group, but there was no statistical difference between the NK cell activity of the HCC group and the LC group. The depression of NK cell activity in HCC patients was inversely correlated with the patient's age, and the HCC patients with venous invasion or with both lobes involved had lower NK cell activity. These results suggest that the decreased NK cell activity in HCC patients might be related to the coexistent liver disease, and marked decrease in NK cell activity might be one of the causes for the early development and invasion of HCC.
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PMID:Natural killer cell activity in patients with hepatocellular carcinoma relative to early development and tumor invasion. 215 37


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