Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 55-year-old female presented with sore throat and slight fever. The patient was admitted to our hospital on December 13, 1993. Full blood count showed hemoglobin 10.7 g/dl, white cell count 960/microliters (neutrophils 14%, lymphocytes 82%, blasts 2%) and platelets 13,000/microliters. Bone marrow examination showed hypocellularity with 4.5% of myeloblast positive for peroxidase. The bone marrow specimens on Dec. 20 showed 15.5% of myeloblasts, some of which had Auer rods. These findings led to the diagnosis of refractory anemia with excess myeloblast in transformation (RAEB-T) of French-American-British Cooperative Group. The patient was transfused and treated with cytarabine ocfosfate (SP-AC) (100 mg tid) and 6-mercaptopurine (50 mg tid) for 14 days. During chemotherapy she complained of nausea and anorexia, but they were managed easily with medication. On Feb. 7, 1994, forty-two days after the start of administration, peripheral blood and bone marrow aspirate were compatible with a complete remission. Although complete remission was sustained with courses of chemotherapy for 4 months, relapse occurred and the patient died of septicemia on August 29, 1994 after induction failure. Observation suggested that oral SPAC in combination with 6-mercaptopurine had a good antileukemic effect on the myelodysplastic syndrome. However, the duration response was short, and further improvement of the therapy is needed.
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PMID:[Refractory anemia with excess myeloblast in transformation induced remission by combined oral administration of cytarabine ocfosfate and 6-mercaptopurine]. 779 1

A 27-year-old pregnant woman was admitted to a local hospital because of headache, nausea, and general fatigue. Her blood examination showed leukocytosis, anemia, and thrombocytopenia. She was referred to our hospital in March 1998. Her bone marrow was normocellular with an excess of blasts (89.1%, peroxidase stain(-), PAS stain(-)) that displayed a positive immunophenotype for CD2, CD4, CD5, CD7, CD34, CD38, and CD71. Chromosome analysis revealed complex abnormal karyotypes. The patient was given a diagnosis of acute lymphoblastic leukemia associated with central nervous system and breast infiltration, and received induction chemotherapy during the second trimester of her pregnancy. After she achieved complete remission, a cesarean section was performed, and a healthy baby delivered. Our experience in this case demonstrated that combination chemotherapy during the second trimester of pregnancy is feasible.
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PMID:[Acute lymphoblastic leukemia with breast infiltration during the second trimester of pregnancy and followed by successful delivery]. 1049 40

Addison's disease is a rare disorder in patients with end-stage renal disease (ESRD). In patients, the diagnosis of Addison's disease is difficult in clinical practice because most of the clinical findings of this disease are similar to those of the renal failure. We present a 51-year-old male patient, who underwent hemodialysis therapy for 8 years, diagnosed with Addison's disease after having myalgia, skin hyperpigmentation, weight loss, sweating, and nausea for the past few weeks. The physical examination was completely normal except for muscle weakness, hyperpigmentation on labial mucosa and skin in a patient. The laboratory tests revealed anemia and hypoglycemia. Serum cortisol, adrenocorticotropic hormone (ACTH) levels, and ACTH stimulation test results were consistent with Addison's disease. Adrenal computerized tomography revealed bilateral atrophic glands. Additionally, it was found that elevated serum thyroid stimulating hormone levels and antithyroid peroxidase antibody titer were positive. Our purpose is to emphasize that physicians should be alert to the potential for additional different conditions particularly in terms of adrenal failure in patients with ESRD.
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PMID:Misdiagnosis of Addison's disease in a patient with end-stage renal disease. 2121 12

Migraine is a common painful neurovascular disorder usually associated with several symptoms, such as photophobia, phonophobia, nausea, vomiting and inflammation, and involves immune cells. Mast cells (MCs) are immune cells derived from hematopoietic pluripotent stem cells which migrate and mature close to epithelial, blood vessels, and nerves. In almost all vascularized tissues there are MCs that produce, contain and release biologically active products including cytokines, arachidonic acid compounds, and proteases. In addition, MCs participate in innate and adaptive immune responses. Innate responses in the central nervous system (CNS) occur during neuroinflammatory phenomena, including migraine. Antigens found in the environment have a crucial role in inflammatory response, causing a broad range of diseases including migraine. They can be recognized by several innate immune cells, such as macrophages, microglia, dendritic cells and MCs, which can be activated trough Toll-like receptor (TLR) signaling. MCs reside close to primary nociceptive neurons, associate with nerves, and are capable of triggering local inflammation. MCs are involved in the pathophysiology of various tissues and organs, especially where there is an increase of angiogenesis. Activated MCs release preformed mediators include histamine, heparin, proteases (tryptase, chimase), hydrolases, cathepsin, carboxypeptidases, and peroxidase, and they also generate pro-inflammatory cytokines/chemokines. In addition, activated macrophages, microglia and MCs in the CNS release pro-inflammatory cytokines which provoke an increase of arachidonic acid product levels and lead to migraine and other neurological manifestations including fatigue, nausea, headaches and brain fog. Innate immunity and pro-inflammatory interleukin (IL)-1 cytokine family members can be inhibited by IL-37, a relatively new member of the IL-1 family. In this article, we report that some pro-inflammatory cytokines inducing migraine may be inhibited by IL-37, a natural suppressor of inflammation, and innate and acquired immunity.
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PMID:Progression in migraine: Role of mast cells and pro-inflammatory and anti-inflammatory cytokines. 3052 70