Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was aimed at analysing the epidemiological structure of patients with liver cirrhosis without HBsAg treated in 1980-1988. There were 231 of such cases in this period of time. The most frequent cause of liver cirrhosis in patients under 60 years of life was chronic alcoholism whereas 40% of the diagnosed liver cirrhosis in older persons was of unclear etiology. Patients complaints, clinical examinations, and results of the laboratory tests were analysed. The course of the disease was more severe in alcohol-produced liver cirrhosis leading to the haemorrhage from esophageal varices in 36%, and coma in 8% of cases. Alcohol-produced liver cirrhosis promoted other complications such as: cancer of the liver, hepato-renal syndrome or encephalopathy. Liver cirrhosis of unclear etiology in the elderly may be a consequence of the prolonged exposition to environmental pollutants. More severe course of alcohol-produced liver cirrhosis may depend on simultaneous action of two harmful factors: alcohol and environmental pollutants.
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PMID:[The course of liver cirrhosis not preceded by viral hepatitis with p articular reference to toxic etiology]. 166 47

Ifosfamide is an oxazaphosphorine alkylating agent with a broad spectrum of antineoplastic activity. It is a prodrug metabolised in the liver by cytochrome P450 mixed-function oxidase enzymes to isofosforamide mustard, the active alkylating compound. Mesna, a uroprotective thiol agent, is routinely administered concomitantly with ifosfamide, and has almost eliminated ifosfamide-induced haemorrhagic cystitis and has reduced nephron toxicity. Therapeutic studies, mostly noncomparative in nature, have demonstrated the efficacy of ifosfamide/mesna alone, or more commonly as a component of combination regimens, in a variety of cancers. In patients with relapsed or refractory disseminated nonseminomatous testicular cancer, a salvage regimen of ifosfamide/mesna, cisplatin and either etoposide or vinblastine produced complete response in approximately one-quarter of patients. As a component of both induction and salvage chemotherapeutic regimens, ifosfamide/mesna has produced favourable response rates in small cell lung cancer, paediatric solid tumours, non-Hodgkin's and Hodgkin's lymphoma, and ovarian cancer. Induction therapy with ifosfamide/mesna-containing chemotherapeutic regimens has been encouraging in non-small cell lung cancer, adult soft-tissue sarcomas, and as neoadjuvant therapy in advanced cervical cancer. As salvage therapy, ifosfamide/mesna-containing combinations have a palliative role in advanced breast cancer and advanced cervical cancer. Ifosfamide/mesna can elicit responses in patients refractory to numerous other antineoplastic drugs, including cyclophosphamide. With administration of concomitant mesna to protect against ifosfamide-induced urotoxicity, the principal dose-limiting toxicity of ifosfamide is myelosuppression; leucopenia is generally more severe than thrombocytopenia. Reversible CNS adverse effects ranging from mild somnolence and confusion to severe encephalopathy and coma can occur in approximately 10 to 20% of patients after intravenous infusion, and the incidence of neurotoxicity may be increased to 50% after oral administration because of differences in the preferential route of metabolism between the 2 routes of administration. Other adverse effects of ifosfamide include nephrotoxicity, alopecia, and nausea/vomiting. In general, intravenously administered mesna is associated with a low incidence of adverse effects; however, gastrointestinal disturbances are common following oral administration. Thus, ifosfamide/mesna is an important and worthwhile addition to the currently available range of chemotherapeutic agents. It has a broad spectrum of antineoplastic activity and causes less marked myelosuppression than many other cytotoxic agents. At present, the role of ifosfamide/mesna in refractory germ cell testicular cancer is clearly defined; however, its overall place in the treatment of other forms of cancer awaits delineation in future well-controlled comparative studies.
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PMID:Ifosfamide/mesna. A review of its antineoplastic activity, pharmacokinetic properties and therapeutic efficacy in cancer. 172 Mar 82

Besides general complications of immunosuppression such as increased susceptibility to opportunistic infections or malignancy, individual immunosuppressive agents are associated with specific side effects. Nephrotoxicity is the major side effect of cyclosporine (CsA). Various attempts have been made to minimize this toxicity, such as monitoring drug blood levels, modifying the protocol, and coadministering other agents. Other side effects caused by CsA are hepatotoxicity, hyperkalemia, hypertension, tremor, gum overgrowth, and hirsutism. Azathioprine (AZA) causes dose-related bone marrow suppression, commonly leading to leukopenia. Careful monitoring of complete blood cell count and dosage adjustment according to white blood cell count are usually adequate to prevent serious leukopenia. The side effects of corticosteroids are numerous and include slow wound healing and de novo insulin-dependent diabetes mellitus. Many complications are dose related, and with low dosage or discontinuation of steroids, their frequency rapidly decreases. Antilymphoblast and antithymocyte globulins (P-ALG) are foreign antibodies and may cause allergic-type reactions such as fever, chill, and hypotension. The initial side effect of monoclonal antibody (muromonab-CD3, OKT3) is similar to that of P-ALG. It includes high fever, shaking chills, headache, rigors, and hypotension. To prevent it, acetaminophen, an antihistamine, and a steroid usually are administered before injection. Because this agent is also associated with high frequency of pulmonary edema, it should not be given to any patient who has more than 3% body weight gain during the week prior to therapy. In rare case, it causes aseptic meningitis or encephalopathy, which is manifested by fever, severe headache, and seizure.
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PMID:Complications associated with immunosuppressive therapy and their management. 174 17

Neurotoxicity is a common and potential dose-limiting complication of cancer chemotherapy. For most agents, high-dose therapy, combination chemotherapy, concomitant cranial radiotherapy, and intracarotid or intrathecal injection are more likely to produce neurologic complications than standard oral or intravenous therapy. Any portion of the nervous system can be damaged. Encephalopathies (either focal or diffuse) are produced by BCNU, cisplatin, cytarabine, 5-fluorouracil, ifosfamide, L-aspariginase, methotrexate, procarbazine, corticosteroids, and some biological response modifiers (interferon, interleukin-2). Cerebellar syndromes may follow the administration of cytarabine, 5-fluorouracil, and procarbazine. Myelopathy may complicate intrathecal methotrexate, cytarabine, thiotepa, and accidental intrathecal vincristine or doxorubicin injection. Peripheral neuropathy occurs from cisplatin, vincristine, and, sometimes, cytarabine or procarbazine. Myopathy is a common complication of corticosteroids. Strokelike syndromes may occur with L-aspariginase, high-dose methotrexate, and intracarotid BCNU or cisplatin. Differentiating the neurologic complications of chemotherapy from other neurologic complications of cancer is often difficult. As cancer patients are treated more aggressively, receive more chemotherapy, and live longer, and as new chemotherapeutic agents are developed and existing agents are used more intensively or in novel ways, neurologic complications of cancer chemotherapy will become more common, serious, and complex. The recognition and treatment of chemotherapy-induced neurotoxicity will become a frequent and important clinical problem for most neurologists.
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PMID:Neurologic complications of chemotherapy. 175 34

Paraneoplastic neurological syndromes are of two types: some are more often seen without than with cancers and may therefore be called "occasionally para neoplastic" (e.g. chronic sensorimotor polyneuropathy and polymyositis), while others are fairly regularly associated with cancers, and particularly with small cell lung carcinoma. In this category falls subacute encephalomyelitis, an entity of broad anatomico-clinical spectrum including limbic encephalitis and subacute sensory neuronopathy; the patient's serum and cerebrospinal fluid may contain neuronal antinuclear antibodies. One type of subacute cerebellar degeneration is characterized by the presence of antibodies specifically directed against Purkinje cell cytoplasmic antigens, and it is associated with ovarian and mammary cancers. The other type shows no antibodies or different antibodies and sometimes neuronal antinuclear antibodies; the latter case may represent the cerebellar form of subacute encephalopathy. Because it may be either a true autoimmune disease or a true paraneoplastic syndrome, Lambert-Eaton myasthenic syndrome, caused by autoantibodies that block the voltage-dependent calcium channels, stands out as the most convincing argument in support of the autoimmune paraneoplastic syndrome theory. The theory, which refers to cross-antigenicity, cannot be extended to the other syndromes without reservation: there is no evidence that autoantibodies are neurotoxic, and specific autoantibodies in high levels are sometimes detected in patients with cancer but without any neurological symptom. Nevertheless, the finding of circulating antineuronal antibodies in patients with a suggestive clinical syndrome should prompt investigations for cancer perhaps at an early stage.
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PMID:[Paraneoplastic neurologic syndromes]. 182 23

A 72-year-old woman complaining of somnolence and thirst was diagnosed to have a hypercalcemic crisis (corrected serum calcium level, 17.4 mg/dl) associated with encephalopathy and nephropathy. Imaging diagnostic techniques demonstrated a retroperitoneal tumor at the median site of right renal pelvis. Hormonal studies revealed that plasma levels of thromboxane B2, prostaglandin (PG) E2, 6-keto prostaglandin F1 alpha (PGF1 alpha) and prostaglandin F2 alpha (PGF2 alpha) were markedly elevated. The tumor was successfully removed by operation; her serum calcium level and PG levels normalized without any treatment indicating that this case belongs to the category of humoral hypercalcemia of malignancy (HHM). Pathologically, this tumor was diagnosed to be a benign neurilemoma. Parathyroid hormone-related protein (PTHrP) radioimmunoassay and Northern blot hybridization for PTHrP mRNA were negative. The current case demonstrates that hypercalcemic crisis could be induced by a curable benign neurilemoma, and suggests that this HHM-like morbidity was associated with markedly elevated plasma PG levels.
Cancer 1991 Sep 01
PMID:Retroperitoneal neurilemoma presenting with humoral hypercalcemia associated with markedly elevated plasma prostaglandin levels. 191 78

Two rare cases of a spontaneous portacaval shunt occurring in patients with gastric cancer and hepatic cirrhosis are retrospectively reviewed with special attention for the operative indications and techniques. One patient underwent proximal gastrectomy for a IIa cancer in the C region with splenectomy and closure of the splenorenal shunt, and died two years and 3 months later due to hepatic failure. The other patient underwent distal gastrectomy for IIa + IIc, IIc double cancers in the M and A regions with splenectomy through an upper transverse abdominal incision that ligated and divided the paraumbilico-caval shunt, and is alive and well 1 year and 2 months, postoperatively. The ICG-R15 was markedly decreased and the K-ICG and ICG-Rmax were improved following the operation in both cases. The preoperative chronic encephalopathy and hyperammonemia disappeared postoperatively in both cases.
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PMID:Spontaneous portacaval shunts in patients with gastric cancer and hepatic cirrhosis. 194 1

The acquired immunodeficiency syndrome (AIDS) is associated with a broad spectrum of opportunistic infections and neoplasias that differ from those occurring in the general population by their high aggressiveness, unusual location, early tendency to generalization, frequent relapse, and short survival. The severe complications of AIDS, however, represent only the last phase in a prolonged course of progressive dysfunction and destruction of the immune system set in motion by the infection with the human immunodeficiency virus (HIV). While substantial progress was achieved in the ultrastructural identification and biochemical characterization of HIV, its mode of action in the causation of AIDS is not yet fully understood. This article explores the main processes involved in the HIV infection and in its role in the origin of AIDS. It describes the phases of HIV infection, investigates the effects of HIV on the various components of the immune system, and analyzes the pathogenesis of the HIV-induced lymphadenopathies and encephalopathy, as well as the causes and mechanisms of AIDS-associated opportunistic infections and opportunistic neoplasias. The total failure of immune surveillance against a host of infectious and oncogenic agents, unprecedented in human pathology, is thus traced to the initial event of specific HIV infection of the CD4 T-lymphocytes.
Cancer Res 1990 Sep 01
PMID:Immunopathogenesis of human immunodeficiency virus infection. 197 24

Ifosfamide-associated central nervous system toxicity has been reported in 5% to 30% of patients treated with ifosfamide. Its pattern is characterized by metabolic encephalopathy with confusion, blurred vision, mutism, auditory or visual paranoid hallucinations, seizures, and rarely coma. The biochemical cause of the neurotoxicity is not understood completely, but it is thought to result from an accumulation of drug metabolites with direct central nervous system effects. A case of ifosfamide neurotoxicity is reported that had unusual extrapyramidal features in a patient treated with a 5-day course of infused ifosfamide. Although usually spontaneously reversible with cessation of drug administration, ifosfamide neurotoxicity occasionally has been associated with prolonged psychopathologic sequelae. Death from irreversible encephalopathy has also been reported rarely. The authors believe that classic extrapyramidal symptoms should be considered to be a part of the neurotoxic profile of ifosfamide.
Cancer 1991 Jul 01
PMID:Ifosfamide extrapyramidal neurotoxicity. 142 8

We undertook this phase II study to evaluate the efficacy and toxicity of epidoxorubicin and ifosfamide in the treatment of locally advanced and/or metastatic soft-tissue sarcomas. We used escalating doses of epidoxorubicin (from 60 to 75 mg/m2) on day 1 and 1.2 g/m2 ifosfamide on days 1-5. Chemotherapy courses were repeated every 3-4 weeks. A total of 16 patients--13 who had not previously been treated and 3 who had undergone prior therapy with anthracyclines--entered the study. In all, 15 patients were evaluable for response and 16, for toxicity. At least two courses of chemotherapy were given. A complete remission (CR) was seen in 1 patient, a partial remission (PR) in 5, and a minor response (MR) in 1, for an objective response rate (CR + PR) of 40% (6/15); this value reached 50% in non-pretreated patients (6/12). Stable disease (SD) was observed in 40% (6/15) of patients. The relative dose intensity of epidoxorubicin ranged from 10 to 23.3 mg/m2 (median, 16.6 mg/m2). The time to objective response ranged from 4 to 12 weeks (median, 8.5 weeks). The duration of response was 4 months for the single CR, and that for the five PRs was 6+ months (range, 4-18 months). Toxicity was evaluated according to WHO criteria in 16 patients; it was mild and consisted mainly of alopecia, nausea and vomiting, and leucopenia. In only three patients did we observe grade 3 leucopenia. In one case an ifosfamide-associated encephalopathy occurred, but it regressed after 24 h. Neither chronic nor acute cardiac toxicity was reported. In this preliminary analysis, the response rate obtained with the combination of epidoxorubicin and ifosfamide was encouraging and the toxicity was acceptable.
Cancer Chemother Pharmacol 1990
PMID:Epidoxorubicin plus ifosfamide in advanced and/or metastatic soft-tissue sarcomas. 212 78


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