Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Copper deficiency (normal serum copper level: 78-136 micrograms/dl) has been reported in patients with long-term enteral nutrition, caused by a copper deficit in enteral nutrition. Occasionally, this leads to anemia and leukopenia. We used Hershey's pure cocoa that is rich in copper (content 3.8 mg/cocoa 100 g) for copper deficiency. A total of 86 (40 men and 46 women, mean age 69 years) patients on enteral nutrition were studied. The primary diseases were cerebral vascular disease in 71 patients, neurological disease in 5 and others in 10. Those who showed serum copper levels of 20 micrograms/dl or less (N = 8) were given 30-45 g of cocoa (copper content 1.14-1.71 mg) per day for about 40 days. Among them, two patients could not continue because of vomiting and diarrhea and were excluded from this study. Mean serum copper levels increased from 8.7 +/- 6.2 to 99.0 +/- 25.4 micrograms/dl (N = 6). Those who showed serum copper levels 20-77 mg/dl (N = 31) were given 10 g of cocoa (copper content 0.38 mg) per day for about 40 days. When mean serum copper levels increased from 50.5 +/- 19.3 to 89.0 +/- 12.9 micrograms/dl with cocoa administration, anemia and neutropenia caused by copper deficiency showed a tendency to improve. After completing the study period, cocoa was reduced to 5 g (copper content 0.19 mg) per day in 23 patients. The mean serum copper levels increased from 90.7 +/- 10.4 to 100.6 +/- 17.1 micrograms/dl for about 100 days. Recently, the amount of daily copper requirement for adults has been reported to be 1.28-2.5 mg per day. We showed that 10 g of cocoa (0.6 mg total copper: 0.38 mg in cocoa and 0.22 mg in other nutrients) is sufficient to treat copper deficiency, and 5 g of cocoa (0.37 mg total copper: 0.19 mg in cocoa and 0.18 mg in other nutrients) is enough to maintain the normal level of serum copper in patients with long-term enteral nutrition.
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PMID:[Copper supplement with cocoa for copper deficiency in patients with long-term enteral nutrition]. 1091 28

Brucellosis is a disease that may lead to changes in hematologic parameters such as anemia, neutropenia, and thrombocytopenia; however, thrombotic microangiopathy (TMA) is a rare finding. Severe TMA may be associated with life-threatening hematologic, renal, and neurologic disorders. To prevent this mortality caused by brucellosis, prompt recognition of this complication and prompt therapy are essential. A patient with TMA associated with Brucella melitensis is presented who initially presented with fever, skin purpura, epistaxis, confusion, microangiopathic hemolytic anemia, and thrombocytopenia. TMA was treated with plasmapheresis with cryosupernatant plasma replacement, energetically. A rapid improvement in platelet count, lactate dehydrogenase level, hemolytic anemia, and neurologic symptoms was observed with this treatment. For cases with infection-induced thrombotic microangiopathy, short-term plasmapheresis may be applied as an urgent therapy in addition to antimicrobial therapy.
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PMID:Severe thrombotic microangiopathy associated with brucellosis: successful treatment with plasmapheresis. 1567 81

Granulocyte colony-stimulating factor (G-CSF) has been used in the treatment of neutropenia in hematologic disorders. The neuroprotective and anti-inflammatory effects of G-CSF were reported in various neurological disease models. In this study, we examined whether G-CSF induces functional recovery after intracerebral hemorrhage (ICH). ICH was induced using collagenase injection in adult rats. Either G-CSF (50 microg/kg, i.p.) or saline was given from 2 h after ICH and every 24 h for 3 days. 72 h after ICH induction, the rats were sacrificed for histological analysis and measurement of brain edema. Behavioral tests were performed before and 1, 7, 14, 21, 28, and 35 days after ICH. We also measured the blood-brain barrier (BBB) permeability using Evans blue dye injection method. G-CSF-treated rats recovered better on rotarod and limb placing tests, starting from 14 days throughout 5 weeks after ICH. The brain water content and BBB permeability of G-CSF-treated group decreased in the lesioned hemispheres compared with those of ICH-only group. In G-CSF-treated group, the number of TUNEL+, myeloperoxidase+, and OX42+ cells was smaller than that of ICH-only group in the periphery of hematoma. These findings suggest that G-CSF induces long-term sensorimotor recovery after ICH with reduction of brain edema, inflammation, and perihematomal cell death.
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PMID:Granulocyte colony-stimulating factor induces sensorimotor recovery in intracerebral hemorrhage. 1582 21

Granulocyte colony-stimulating factor (G-CSF) has been used for the treatment of neutropenia in hematologic disorders. The neuroprotective effects of G-CSF were reported in neurological disease models. In the present study, we examined whether G-CSF can protect dopaminergic neurons against MPTP-induced cell death in a mouse model of Parkinson's disease. Mice of one group were injected intraperitoneally with MPTP for five consecutive days, those of another group with MPTP and intraperitoneal G-CSF at 2 days and 1 day before the first MPTP injection, and 30 min before each MPTP injection, while control mice received saline injections. Immunohistochemistry, western blotting analysis, and HPLC were performed to evaluate damage of substantia nigra dopaminergic neurons and expression of Bcl-2 and Bax protein. MPTP induced dopaminergic cell death in the substantia nigra. G-CSF significantly prevented MPTP-induced loss of tyrosine hydroxylase-positive neurons (p < 0.05), increased Bcl-2 protein and decreased Bax protein expression. Our findings indicate that G-CSF provides neuroprotection against MPTP-induced cell death and this effect is mediated by increasing Bcl-2 expression levels and decreasing Bax expression levels in C57BL/6 mice.
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PMID:Recombinant human granulocyte colony-stimulating factor protects against MPTP-induced dopaminergic cell death in mice by altering Bcl-2/Bax expression levels. 1707 57

Although Parkinson's disease (PD) is considered mainly a movement disorder, robust information accumulated during the last 30 years has shown that about 30% of PD patients may also suffer from psychosis, which deeply affects their quality of life and eventually brings them to permanent hospitalization in nursing homes. PD psychosis (PDPsy) mainly occurs after 10 or more years of treatment. The main features of PDPsy include recurrent and continuous hallucinations and delusions for at least 1 month. In addition, a recent consensus of the National Institute of Neurological Disorders and Stroke and National Institute of Mental Health Working Group also included illusions and a false sense of presence as "minor symptoms" supporting the diagnosis. In addition, accumulated clinical data have shown that "minor symptoms" and benign hallucinations also imply a bad prognosis with time. In the diagnostic criteria for PDPsy, it is considered that patients suffer from PD for at least more than 1 year before psychosis develops. If this is not the case, there is an unsolved problem of an overlapping diagnosis with Dementia with Lewy Bodies. Most clinicians consider that the main cause of psychosis is chronic exposure to dopaminergic medication. However, from an operational point of view there remain difficulties in defining a specific time of exposure and dose of treatment and the occurrence of PDPsy. Specific rating scales have been developed for the evaluation of PDPsy, such as the Parkinson Psychosis Rating Scale. The Scale for the Assessment of Positive Symptoms usually applied in schizophrenic patients has also proved useful for scoring psychotic symptomatology in PD. Clozapine in low doses has been proven to be the most effective antipsychotic medication for PDPsy. However, its use may cause neutropenia. Therefore, new atypical antipsychotic drugs with serotonin 5-HT2A receptor inverse agonist properties have been developed. Recently, pimavanserin--a 5-HT2A inverse agonist--has been studied. We hope that soon we will have the possibility to include new agents for the management of PDPsy.
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PMID:Hallucinations and psychosis in Parkinson's disease. 2012 47

Celiac disease has been associated with several neurologic disorders which may result from micronutrient deficiencies, coexisting autoimmune conditions, or gluten sensitivity. Copper deficiency can produce multiple neurologic manifestations. Myeloneuropathy is the most common neurologic syndrome and it is often irreversible, despite copper replacement. We report the case of a 55-year-old man who presented with progressive proximal limb weakness and weight loss in the setting of untreated celiac disease without gastrointestinal symptoms. He had anemia, neutropenia, and severe hypocupremia. The pattern of weakness raised the suspicion that there was an underlying myopathy, although this was not confirmed by electrodiagnostic studies. Weakness and hematologic abnormalities resolved completely within 1 month of total parenteral nutrition with copper supplementation and a gluten-free diet. Myopathy can rarely occur in patients with celiac disease, but the mechanism is unclear. Pure proximal limb weakness has not been previously reported in copper deficiency. We propose that this may represent a novel manifestation of hypocupremia and recommend considering copper deficiency and gluten sensitivity in patients presenting with proximal limb weakness.
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PMID:Proximal Limb Weakness in a Patient with Celiac Disease: Copper Deficiency, Gluten Sensitivity, or Both as the Underlying Cause? 2799 96