Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a case report of a twenty-five years old man who developed, due to lead intoxication, a severe axonal peripheral predominantly motor neuropathy, after a shotgun injury. The projectile was retained in the right hip. Before this diagnosis had been done he was treated with corticosteroids in immunosuppressive doses and showed an improvement, but he had worsened at each attempt to interrupt the drug. Because he had also other signs of lead intoxication, such as abdominal cramps, severe anemia and seizures it was search for the blood levels of lead that was 101.2 micrograms/dl. The patient was treated with calcium disodium edetate and surgical removal of lead fragments. After that he had a good outcome with no need of corticosteroids. It is emphasized the possible relevance of the immune system on the mechanism of plumbic intoxication and the importance of the withdrawal of the lead material retained in joints.
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PMID:[Possible role of the immune system in lead peripheral polyneuropathy. Case report]. 933 73

The authors, by means of documental research, study the possibility that the physical and psychic symptoms of Vincent van Gogh may have been due to chronic lead poisoning. The technique and materials used by Van Gogh are analysed as the cause of repeated exposure to lead as well as the possible means of penetration of the metal. Through historical-biographical analysis, the progressive symptoms of the illness are compared with those of lead poisoning. The authors conclude that the excessive and continuous use by Van Gogh of pigments which were highly toxic due to their high lead content, such as white lead (lead carbonate) and yellow chrome (lead chromium), could have penetrated his organism by digestive system (primarily) in minimal daily amounts, giving rise to a clinical condition of chronic lead poisoning. This type of poisoning coincides with the clinical symptoms Van Gogh describes in his autographed letters: initial debilitation, stomatitis with loss of teeth, recurring abdominal pains, anaemia (with a "plumbic" skin tone), neuropathy of the radial and saturnine encephalopathy including epileptic crises, progressive character changes and periods of delirium. The clinical symptoms shown by Van Gogh meet present criteria for diagnosis of Organic Mental Disorder due to cerebral lesion or somatic illness (F.06; CIE-10) (DSM-IV-R), and Organic Character Disorder (F.07; CIE-10) (DSM-IV-R).
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PMID:[Implication of lead poisoning in psychopathology of Vincent van Gogh]. 942 66

The objective of this study was to demonstrate the effects of prolonged exposure to 6-ANA at low dose-levels in dogs. A male and a female Beagle dog received daily oral repetitive doses of 1 mg/kg or less for 20 weeks. Both dogs showed lacrimation, conjunctivitis, reduced motility and anemia since the second week of treatment. The female dog was more affected than the male and at the end of treatment period it had tremor, hanging lower jaw, stepping gait of the hind limbs, hunched posture, and general debilitation. Post-mortem examination of the female dog revealed prominent brain edema with pressure atrophy of the dorsal cranial bones. Microscopic examination of the nervous system revealed spongiform neuropathy in both animals mainly affecting the telencephalic cortex and hippocampal fascia dentata, the substantia gelatinosa in the spinal cord and the dorsal root and autonomic ganglia. The changes were produced by vacuolation of astrocytes in the central nervous system and perineuronal satellite cells in the ganglia. Examination of the other organs revealed thymic atrophy and high hematopoietic activity of the bone marrow in both dogs. The male had severe interstitial edema and vacuolar degeneration of the testicular seminiferous tubules and the female had marked chronic pyelonephritis. This chemically induced spongiform neuropathy in dogs obviously represents a subchronic form of the "energy deprivation syndrome" induced by impaired glucose utilization. Vacuolar degeneration of the testicular seminiferous epithelium may have the same pathogenesis.
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PMID:Spongiform neuropathy induced in dogs by prolonged, low-level administration of 6-aminonicotinamide (6-ANA). 978 99

Fifteen patients with chronic inflammatory demyelinating neuropathy (CIDP) were treated with pulse intravenous cyclophosphamide (IVCY) monthly for up to 6 months. Eleven patients reached a complete remission; only one patient worsened. Complications included nausea, vomiting, anemia, and hair loss. This case series suggests that monthly IVCY is beneficial in the treatment of CIDP and warrants a controlled study.
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PMID:Pulse cyclophosphamide therapy in chronic inflammatory demyelinating polyneuropathy. 1048 72

Copper, zinc, selenium, and molybdenum are involved in many biochemical processes supporting life. The most important of these processes are cellular respiration, cellular utilization of oxygen, DNA and RNA reproduction, maintenance of cell membrane integrity, and sequestration of free radicals. Copper, zinc, and selenium are involved in destruction of free radicals through cascading enzyme systems. Superoxide radicals are reduced to hydrogen peroxide by superoxide dismutases in the presence of copper and zinc cofactors. Hydrogen peroxide is then reduced to water by the selenium-glutathione peroxidase couple. Efficient removal of these superoxide free radicals maintains the integrity of membranes, reduces the risk of cancer, and slows the aging process. On the other hand, excess intake of these trace elements leads to disease and toxicity; therefore, a fine balance is essential for health. Trace element--deficient patients usually present with common symptoms such as malaise, loss of appetite, anemia, infection, skin lesions, and low-grade neuropathy, thus complicating the diagnosis. Symptoms for intoxication by trace elements are general, for example, flu-like and CNS symptoms, fever, coughing, nausea, vomiting, diarrhea, anemia, and neuropathy. A combination of observation, medical and dietary history, and analyses for multiple trace elements is needed to pinpoint the trace element(s) involved. Serum, plasma, and erythrocytes may be used for the evaluation of copper and zinc status, whereas only serum or plasma is recommended for selenium. Whole blood is preferred for molybdenum. When trace element levels are inconsistent with medical evaluations, a test for activity of the suspected enzyme(s) would support the differential diagnosis. Furthermore, it is important to differentiate whether trace element deficiency or toxicity is the primary cause of the disorder, or is secondary to other underlying diseases. Only successful treatment of the primary disorder will lead to complete recovery. In the event of sample contamination during collection or analysis, the physician may be misled by falsely elevated results. Royal blue top evacuated tubes containing negligibly low concentrations of the trace element or acid-washed plastic sterilized syringes should be used for blood, serum, or plasma collection. Powdered gloves must be avoided. When possible, mineral supplements are not to be administered to the patient for a minimum of 3 days prior to sample collection. Serum and plasma specimens are to be transported in acid-washed polypropylene and polyethylene tubes. Analysis is performed in a controlled environment to minimize or eliminate contamination. During analysis, all laboratory wares should be acid-washed for decontamination. A detailed description of these precautions may be found in reviews by Aitio and Jarvisalo and by Chan and Gerson. Copper and zinc analysis on serum and plasma are commonly performed by flame atomic absorption spectrometry, inductively coupled plasma-atomic emission spectrometry, and inductively coupled plasma-mass spectrometry. Serum and plasma selenium levels are determined by graphite furnace atomic absorption with Zeeman background correction and neutron activation analysis. Molybdenum levels are best determined by neutron activation and highly sensitive inductively coupled plasma-mass spectrometry. The reader is referred to reviews by Tsalev and Jarvis.
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PMID:The role of copper, molybdenum, selenium, and zinc in nutrition and health. 989 6

Cryoglobulins are a group of proteins with the common property of precipitating from cooled serum. Cooled cryoglobulinemia is a classic disease caused by immune complexes which subside on vessel walls and produce a clinical picture represented by recurrent purpura, asthenia, arthralgias, Raynaud's phenomenon, glomerulonephritis and sensorimotor neuropathy. The authors describe a case of a patient C.M., 37 years old, with cryoglobulinemia, chronic hepatitis C and gravidic cholestasis at 28 weeks' gestation. The clinical picture worsened with the appearance of mild hypertension with proteinuria and hypochromic anaemia. At 31 weeks' the arthralgic symptomatology and pruritus revealed degeneration with an alteration of glycemic profile values and treatment with rapid human insuline was started. The cardiotocography began to be pathologic and a cesarean section was performed; the newborn weighted 1570 g. Cooled cryoglobulinemia is a pathology which worsens in a gravidic state and can impair the outcome of pregnancy.
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PMID:Essential mixed type II cryoglobulinemia in a HCV positive pregnant woman: case report. 998 69

Most dialysis patients experience prolonged periods of physical inactivity and often bedrest. The physiological consequences of bed rest and inactivity are many and detrimentally affect the functioning of many bodily systems, several of which affect physical functioning. Reductions in plasma volume reduce cardiac filling, stroke volume, and cardiac output. Skeletal muscle fiber size, diameter, and capillarity are reduced, as is bone density. These changes result in profound reductions in physical work capacity. The effects of bed rest and inactivity in patients with chronic renal failure may have more serious consequences, in that they may exacerbate the pathophysiology of renal failure such as cardiac dysfunction, anemia, muscle wasting, muscle weakness, neuropathy, glucose intolerance, and reduced bone density.
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PMID:The physiological consequences of bed rest and inactivity. 1023 Aug 79

Nineteen patients with recurrent or refractory ovarian carcinoma after a first-line platinum-based chemotherapy were treated with a 3-hour i.v. infusion of paclitaxel 175 mg/m2 every 3 weeks from November 1992 to October 1996. The major hematologic toxicity was neutropenia (63.2%). No febrile neutropenia was observed. Other hematologic effects were leukopenia (47.4%) and anemia (47.4%). The main non-hematologic toxicities were as follows: neuropathy (52.6%), nausea and vomiting (36.8%), myalgia (36.8%), cardiac toxicity (15.8%) and mucositis (10.5%). Alopecia was observed in the majority of cases. The overall response rate was 47.4%, with 5 (26.3%) complete responses (CRs) and 4 (21.1%) partial responses (PRs). The median duration of response was 7 months (range: 3-19), with a median follow-up of 17 months (range: 3-61). Quality of life of responding patients was good. Our results confirm that paclitaxel as second-line therapy in relapsed and refractory ovarian cancer patients is an acceptable treatment with a good safety profile, and can be safely administered at the dose of 175 mg/m2. In our study paclitaxel was more active in relapsed than in refractory patients. Consequently, further studies are needed to identify more effective drugs for the refractory subset.
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PMID:Paclitaxel efficacy and tolerability in second-line treatment of refractory and relapsed ovarian cancer patients. 1046 33

The folates are made up of a pterdine ring attached to a p-aminobenzoate and a polyglutamyl chain. The active form is tetrahydrofolate which can have C1 units enzymically attached. These C1 units (as a formly group) are passed on to enzymes in the purine pathway that insert the C-2 and C-8 into the purine ring. A methylene group (-CH2-) attached to tetrahydrofolate is used to convert the uracil-type pyrimidine base found in RNA into the thymine base found in DNA. A further folate cofactor, i.e. 5-methyltetrahydrofolate, is involved in the remethylation of the homocysteine produced in the methylation cycle back to methionine. After activation to S-adenosylmethionine this acts as a methyl donor for the dozens of different methyltransferases present in all cells. Folate deficiency results in reduction of purine and pyrimidine biosynthesis and consequently DNA biosynthesis and cell division. This process is most easily seen in a reduction of erythrocytes causing anaemia. Reduction in the methylation cycle has multiple effects less easy to identify. One such effect is certainly on the nerve cells, because interruption of the methylation cycle causing neuropathy can also happen in vitamin B12 deficiency due to reduced activity of the vitamin B12-dependent enzyme methionine synthase (EC 2.1.1.13). In vitamin B12 deficiency, blocking of the methylation cycle causes the folate cofactors in the cell to become trapped as 5-methyltetrahydrofolate. This process in turn produces a pseudo folate deficiency in such cells, preventing cell division and giving rise to an anaemia identical to that seen in folate deficiency.
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PMID:Folate and vitamin B12. 1046 89

Lentinan is a beta 1-->3 glucan isolated from Lentinus edodes (Shiitake mushroom) which has immune modulating properties. We have conducted two phase I/II placebo-controlled trials on a total of 98 patients. In one study at the San Francisco General Hospital (SFGH), ten patients each were administered 2, 5, or 10 mg of lentinan or placebo i.v. once a week for eight weeks. In the second study at the Community Research Initiative in New York (CRI), two groups of 20 patients each were administered 1 or 5 mg of lentinan i.v. twice a week for 12 weeks, and ten patients were administered placebo (vehicle containing mannitol plus dextran 40) i.v. twice a week. Entry criteria were an HIV positive test, CD4 levels of 200-500 cells, age 18-60 years, and without current opportunistic infections. This study confirms, in Caucasian subjects also, the good tolerability of lentinan observed in Japanese cancer patients. Side effects were mainly mild, especially when infusion was carried out over a 30-minute period. In the SFGH study, where administration was over a ten minute period, there were nine side effects severe enough to be reported to the FDA (one case each of anaphylactoid reaction, back pain, leg pain, depression, rigor, fever, chills, granulocytopenia and elevated liver enzymes) and there were four patients who discontinued therapy because of side effects. In the CRI study, where infusion was over a 30-minute period, there were no side effects reportable to the FDA and there were four dropouts due to side effects or personal preference. Most side effects resolved promptly after the discontinuation of medication, and all of them were relieved within 24 hours. Patients in the study have shown a trend toward increases in CD4 cells and in some patients neutrophil activity. Because of the small numbers, these values do not have statistical significance. Inasmuch as no side effects such as anemia, leukopenia, pancreatitis or neuropathy were seen, and in view of the positive effects of lentinan on certain surrogate markers (recognizing that these were small studies), we recommended a long-term clinical trial of lentinan in combination with didanosine (ddI) or zidovudine in HIV positive patients. Most patients in these trials did not have measurable p24 levels. In the CRI trials of ten patients with elevated p24 levels, eight on lentinan and two on placebo had decreased p24 levels. Of these decreases, those with lentinan and one with placebo were marked. These results were provocative and needed confirmation. Subsequent to this study, a trial of lentinan in combination with didanosine (ddI) showed a mean increase of 142 CD4 cells/mm3 over a twelve month period, in contrast to a decrease in CD4 cells in patients on ddI alone (Gordon et al. 1995).
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PMID:A placebo-controlled trial of the immune modulator, lentinan, in HIV-positive patients: a phase I/II trial. 1050 66


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