Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of the pituitary-adrenal axis on epinephrine synthesis in the human adrenal medulla was examined by the estimation of the 24-h urinary epinephrine level after treatment with glucocorticoids in four patients with systemic lupus erythematodes (SLE), one patient with rheumatoid arthritis (RA) and one patient with adrenal pheochromocytoma. 24-h urinary catecholamines (CAs) were measured by HPLC before and after glucocorticoid treatment, dexamethasone or prednisolone was orally given for more than seven days to patients with SLE, RA or isolated ACTH deficiency and five days to a patient with adrenal pheochromocytoma. In patients with isolated ACTH deficiency, the 24-h urinary epinephrine level was significantly lower than the normal range. In patients with SLE or RA, the 24-h urinary epinephrine level was normal and it was significantly suppressed by therapeutic doses of prednisolone 30-40 mg/day. In a patient with adrenal pheochromocytoma, 24-h urinary epinephrine was extremely high and it was significantly increased after dexamethasone 0.5 mg/day. These results suggest that epinephrine synthesis in the human adrenal medulla may be dependent on the pituitary-adrenal axis. But the increase in epinephrine synthesis due to dexamethasone in a patient with pheochromocytoma may reflect the direct effect via the feeding artery to the tumor, as previously shown in an in vitro culture system.
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PMID:In vivo evidence of regulation by pituitary-adrenal axis of urinary epinephrine excretion in men. 379 75

A 58 year old woman had a long history of immunocompromised state. Since age 28 she had multiple endocrine neoplasm type 2A: her thyroid gland and bilateral adrenal glands were removed because of pheochromocytoma and thyroid medullary carcinoma. Corticosteroid and levothyroxine were supplemented. At age 57 she was afflicted with systemic lupus erythematodes and nephrotic syndrome. Prednisolone therapy was started. Two months later she developed fever, lethergy, headache and left hemiparesis. MRI revealed multiple ring-enhancing lesions in the right cerebrum. CSF was negative for microorganisms. Blood culture hemolysed after 24 hours. Direct gram staining of the blood culture sample revealed gram-positive short rods without spore, suggested listeria. This enabled prompt initiation of high dose penicillin therapy before the official report of listseria infection. Neurological abnormality including left hemiparesis disappeared completely within one month. Enhancement of abscess wall decreased every month, but it persisted for five months despite continuous intravenous penicillin therapy. Listeria monocytogenes is well-recognized as an opportunistic pathogen. It requires prolonged therapy with antibiotics, since it is the intracellular organism. Monitoring of the brain abscess wall by the enhanced MRI is useful to determine the completion of therapy. Since listerial contamination is common among raw meat and unpasteurized milk, immunocompromised patients should be alarmed not to eat uncooked food products.
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PMID:[Direct Gram staining of blood culture sample enabled the early diagnosis of brain abscess due to Listeria monocytogenes]. 1068 44

A malignant pheochromocytoma with multiple metastases was diagnosed in a 7-year-old male wolfdog that resulted from a cross between an eastern timber wolf (Canis lupus lycaon) and an Alaskan malamute. A yellowish white neoplastic mass approximately 10 cm diameter was found in the right adrenal gland. The neoplasm penetrated through the wall of the caudal vena cava. A diagnosis of pheochromocytoma was established by histopathologic and immunohistochemical procedures. Immunohistochemically, the neoplastic cells expressed chromogranin A, substance P, synaptophysin, Leu-7, protein gene product 9.5, methionine-enkephalin, S100 protein, and galanin. Multiple metastatic tumors were found in the kidneys, spleen, lungs, heart, and liver.
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PMID:Immunohistochemical evaluation of a malignant phecochromocytoma in a wolfdog. 1146 80

We describe a patient with positive antinuclear and anti-Smith antibodies, proteinuria, and thrombocytopenia suggesting systemic lupus erythematosus (SLE). During hospitalization, the patient developed labile hypertension, tachycardia, and intermittent fever. A computer tomography scan of the abdomen showed an extraadrenal mass, which was confirmed as a pheochromocytoma. After removal of the pheochromocytoma, the patient's symptoms resolved and her serology normalized. Previous case reports describe SLE patients with adrenal pheochromocytomas that presented many years after the diagnosis of lupus. This is a novel case of pheochromocytoma discovered at the onset of SLE, with resolution of SLE manifestations shortly after its removal.
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PMID:New onset systemic lupus erythematosus with pheochromocytoma. 1206 56

Systematic evaluations of anemia, thrombocytopenia, and coagulopathy are essential to identifying and managing their causes successfully. In all cases, clinicians should evaluate RBC measurements alongside WBC and platelet counts and WBC differentials. Multiple competing factors may coexist; certain factors affect RBCs independent of those that affect WBCs or platelets. Ideally, clinicians should examine the peripheral blood smear for morphologic features of RBCs, WBCs, and platelets that provide important clues to the cause of the patient's hematologic disorder. Thrombocytopenia arises from decreased platelet production, increased platelet destruction, or dilutional or distributional causes. Drug-induced thrombocytopenias present diagnostic challenges, because many medicines can cause thrombocytopenia and critically ill patients often receive multiple medications. If they suspect type II HIT, clinicians must promptly discontinue all heparin sources, including LMWHs, without awaiting laboratory confirmation, to avoid thrombotic sequelae. Because warfarin anticoagulation induces acquired protein C deficiency, thereby exacerbating the prothrombotic state of type II HIT, warfarin should be withheld until platelet counts increase to more than 100,000/microL and type II HIT is clearly resolving. The presence of a consumptive coagulopathy in the setting of thrombocytopenia supports a diagnosis of DIC, not TTP-HUS, and is demonstrated by decreasing serum fibrinogen levels, and increasing TTs, PTs, aPTTs, and fibrin degradation products. Increasing D-dimer, levels are the most specific DIC parameter and reflect fibrinolysis of cross-linked fibrin. Elevated PTs or a PTTs can result from the absence of factors or the presence of inhibitors. Clinicians should suspect factor inhibitors when the prolonged PT or aPTT does not correct or only partially corrects following an immediate assay of a 1:1 mix of patient and normal plasma. In addition to factor inhibitors, antiphospholipid antibodies (e.g., lupus anticoagulant) can produce a prolonged aPTT that does not correct with normal plasma but is overcome by adding excess phospholipid or platelets. Paradoxically, a tendency to thrombosis, not bleeding, accompanies lupus anticoagulants and the antiphospholipid antibody syndrome. Transfusion of red blood cells, platelets, or plasma products is sometimes warranted, but clinicians must carefully weigh potential benefits against known risks. In critically ill patients, administering RBCs can enhance oxygen delivery to tissues. Among euvolemic patients who do not have ischemic heart disease, guidelines recommend a transfusion threshold of HGB levels in the range of 6.0 to 8.0 g/dL; patients who have HGB that is at least 10.0 g/dL are unlikely to benefit from blood transfusion. The use of rHuEPO to increase erythropoiesis offers an alternative to RBC transfusion, assuming normal, responsive progenitor cells and adequate iron, folate, and cobalamin stores. Future research should examine whether clinical outcomes from rHuEPO use in critically ill patients are important and cost-effective. Because platelets play an instrumental role in primary hemostasis, platelet transfusions are often important in managing patients who are bleeding or at risk of bleeding with thrombocytopenia or impaired platelet function. Platelet transfusions carry risks, and decisions to transfuse platelets must consider clinical circumstances. Most important, platelet transfusions are generally contraindicated if the underlying disorder is TTP or type II HIT, because platelet transfusion in these settings may fuel thrombosis and worsen clinical signs and symptoms. Plasma products can correct hemostasis when bleeding arises from malfunction, consumption, or underproduction of plasma coagulation proteins. Choice of plasma product for transfusion depends on clinical circumstances. FFP is the most commonly used plasma product to correct clotting factor deficiencies, particularly coagulopathies that are attributable to multiple clotting factor deficiency states as in liver disease, DIC, or warfarin anticoagulation. PCC or rFVIIa that is administered in small volumes may provide advantages over FFP when coagulopathies require quick reversal without risk of volume overload. Factor concentrates can replace specific factor deficiencies. Recombinant FVIIa bypasses inhibitors to factors VIII and IX and vWF. Use of rFVIIa in managing hemostatic abnormalities from severe liver dysfunction; extensive surgery, trauma, or bleeding; excessive warfarin anticoagulation; and certain platelet disorders requires further study to determine optimal and cost-effective dosing regimens. Recombinant activated protein C reduces mortality from severe sepsis that is associated with organ dysfunction in adults who are at high risk for death (APACHE scores of at least 25). In severe sepsis, levels of protein C decrease, as do fibrinogen and platelet levels. Because of its anticoagulant effect, however, drotrecogin alfa may induce bleeding. Guidelines for drotrecogin alfa use must take into account bleeding risks.
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PMID:Critical issues in hematology: anemia, thrombocytopenia, coagulopathy, and blood product transfusions in critically ill patients. 1471 Jun 93

Basic fibroblast growth factor (FGF) promotes branching neuritogenesis and survival in rat hippocampal neurons in vitro. Basic FGF is a broad spectrum mitogen which does not normally circulate, but increases in serum from a variety of cancers. In prior work, we described spontaneously-occurring fibroblast growth factor-like autoantibodies in serum from a subset of breast cancer patients with neurological complications. The FGF-like autoantibodies mimicked the potent endothelial cell growth-promoting activity of bFGF yet had remarkably increased stability (activity survived storage at 0-4 degrees C for up to 5 years). In the present study we tested whether FGF-like autoantibodies from breast cancer sera is neurotrophic or neuroprotective. We now report that FGF-like autoantibodies (2-3 microg/mL) from breast cancer sera promoted neuritogenesis in DIV 12 embryonic day 18 rat hippocampal neurons and neurite extension in undifferentiated rat pheochromocytoma PC12 cells. The FGF-like autoantibodies from a breast cancer patient with lupus were unique in protecting rat hippocampal neurons from glutamate-induced cell loss and promoting long-lasting neurite extension and survival in PC-12 cells (up to 25 days in vitro). Breast cancer sera FGF-like autoantibodies induced large sustained increases in inward cationic current associated with depolarization in hippocampal neurons that exceeded the electrophysiological effects of substantial concentrations of basic FGF. These results suggest that differences in potency or other unknown factors contribute to whether subsets of FGF-like autoantibodies from breast cancer sera exhibit long-lasting neurotrophic and neuroprotective effects or an early neurotrophic effect followed by accelerated late neuron death.
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PMID:Neurotrophic effects of fibroblast growth factor-like autoantibodies in serum from three patients with breast cancer. 1905 21

The present review examines the types of hypertension that women may suffer throughout life, their physiopathological characteristics and management. In early life, the currently used low-dose oral contraceptives seldom cause hypertension. Pregnancy provokes preeclampsia, its main medical complication, secondary to inadequate transformation of the spiral arteries and the subsequent multisystem endothelial damage caused by deportation of placental factors and microparticles. Hypertension in preeclampsia is an epiphenomenon which needs to be controlled at levels that reduce maternal risk without impairing placental perfusion. The hemodynamic changes of pregnancy may unmask a hypertensive phenotype, may exacerbate a chronic hypertension, or may complicate hypertension secondary to lupus, renovascular lesions, and pheochromocytoma. On the other hand a primary aldosteronism may benefit from the effect of progesterone and present as a postpartum hypertension. A hypertensive pregnancy, especially preeclampsia, represents a risk for cardiac, vascular and renal disease in later life. Menopause may mimic a pheochromocytoma, and is associated to endothelial dysfunction and salt-sensitivity. Among women, non-pharmacological treatment should be forcefully advocated, except for sodium restriction during pregnancy. The blockade of the renin-angiotensin system should be avoided in women at risk of pregnancy; betablockers could be used with precautions during pregnancy; diuretics, ACE inhibitors and angiotensin receptor antagonists should not be used during breast feeding. Collateral effects of antihypertensives, such as hyponatremia, cough and edema are more common in women. Thus, hypertension in women should be managed according to the different life stages.
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PMID:[Hypertension in women]. 2373 98