Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 9 beta-methyl carbacyclin, a chemically stable analogue of epoprostenol (prostacyclin, PGI2) were studied, in comparison with epoprostenol, both in vitro and in vivo in man. In vitro 9 beta-methyl carbacyclin and epoprostenol inhibited platelet aggregation induced by ADP, collagen, the endoperoxide analogue U46619 and arachidonic acid. The potency of 9 beta-methyl carbacyclin relative to epoprostenol was comparable in ADP and collagen-aggregated platelet rich plasma (PRP), 9 beta-methyl carbacyclin being 0.01 times as active as epoprostenol. The anti-aggregatory potencies of the two compounds were comparable in PRP and whole blood. The phosphodiesterase inhibitor isobutyl methyl xanthine enhanced the anti-aggregatory activity of both compounds in vitro. 9 beta-methyl carbacyclin and epoprostenol elevated platelet cyclic AMP, 9 beta-methyl carbacyclin being 0.04 times as active as epoprostenol. In a placebo controlled trial both drugs produces significant headache and facial flushing when compared with placebo. Nasal stuffiness, abdominal discomfort and nausea were reported on all three treatments. Both drugs caused significant and comparable increase in heart rate and decrease in pre-ejection (PEP) and PEP/left ventricular ejection time (LVET) ratio compared with placebo. Systolic and diastolic blood pressure, LVET and QS2 index were unchanged. Platelet aggregation responses to ADP were significantly inhibited by all three doses of both drugs compared with placebo. Bleeding time was significantly longer during epoprostenol infusion than either placebo or 9 beta-methyl carbacyclin infusion. Neither drug had significant effect, compared with placebo, on kaolin activated clotting time in PPP, PRP or in PRP in the presence of heparin, prothrombin time, partial thromboplastin time, thrombin clotting time, fibrinogen, fibrinogen degradation products or euglobulin clot lysis time. The pharmacodynamic effects and duration of action of 9 beta-methyl carbacyclin and of epoprostenol are similar; 9 beta-methyl carbacyclin is approximately 100 times less potent than epoprostenol in man.
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PMID:A chemically stable analogue, 9 beta-methyl carbacyclin, with similar effects to epoprostenol (prostacyclin, PGI2) in man. 608 4

A rare case of spontaneous bilateral extradural hematomas probably due to hypofibrinogenemia is reported. On April 17, 1983, a 21-year-old woman was referred to our hospital because of her comatose state. She has complained of her longer duration of menstrual bleeding lasting 10 days to 2 weeks, but has had no history of hemorrhagic diseases. At the last night, she complained of headache and vomited several times, after drinking some beer but she went to bed without therapy. We cannot see a history of her head injury several days before admission. On admission, she was comatose with bilateral dilated pupils and flexed her upper extremities against painful stimuli. There was a tendency for subcutaneous hematomas to form immediately in places where the stimuli were applied. Skull fracture was not found on craniogram and CT scan showed bilateral extradural hematomas (60 ml on the right side and 130 ml on the left side). Laboratory data showed leukocytosis (14800), longer prothrombin time (15.2 seconds with a control of 11.9 seconds), markedly elongated activated partial thromboplastin time (90 seconds with a control of 15-45 seconds) and decreased fibrinogen concentration (114 mg/dl with a control of 200-400 mg/dl). At the bilateral decompressive craniectomies with infusion of 5 gram of fibrinogen and 300 ml of fresh blood, we found neither scalp hemorrhage nor skull fracture and after removal of coagulated hematomas no dural anomaly was found. After operation she improved gradually and laboratory re-examination was normal including bone marrow puncture. Now, 5 months after operation she is clear with slight tetraparesis on her rehabilitating course.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spontaneous bilateral extradural hematomas: a case report]. 652 41

Orally administered dipyridamole in combination with naproxen was compared with subcutaneously administered low-dose heparin in prevention of deep venous thrombosis after abdominal hysterectomy. The radioactive fibrinogen test was used to diagnose thrombosis. Only one patient in the total series of 65 developed thrombosis. She belonged to the dipyridamole-naproxen group; the oral intake of the agents was disturbed by postoperative gastrointestinal side-effects. Vomiting and headache were more common in the dipyridamole-naproxen group, but wound complications (haematomas, ruptures and infections) were more common in the low-dose heparin group.
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PMID:Prevention of venous thrombosis by dipyridamole-naproxen and low-dose heparin in patients undergoing hysterectomy. 675 6

Sudden cerebrovascular insults occurred during or immediately following remission induction therapy in 4 children with acute lymphoblastic leukemia. In 3, cerebral infarction was due to thrombosis. In the fourth, an intracerebral hematoma developed representing either frank hemorrhaging or a hemorrhagic infarction. None of the patients had central nervous system leukemia or extreme leukocytosis at the time of diagnosis. Symptoms were obtundation, hemiparesis, seizures, and headache. The induction chemotherapy included L-asparaginase which causes deficiencies of antithrombin, plasminogen, fibrinogen, and factors IX and XI. These hemostatic abnormalities may explain the thromboses and bleeding observed in these children.
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PMID:Thrombotic and hemorrhagic strokes complicating early therapy for childhood acute lymphoblastic leukemia. 693 53

L-Asparaginase therapy for childhood acute lymphoblastic leukemia causes deficiencies of plasma hemostatic proteins, especially antithrombin, plasminogen, and fibrinogen. Severe thromboses and hemorrhages occurred in 18 children receiving vincristine, prednisone, and asparaginase therapy for ALL. Thirteen children had intracranial thrombosis or hemorrhage, four had extremity thrombosis, and one had both an intracranial hemorrhage and an extremity thrombosis. These events occur characteristically in the third and fourth weeks of therapy during or just after a three-week course of L-asparaginase. Symptoms of headache, obtundation, hemiparesis, and seizure were common for the intracranial events: local pain, swelling, and discoloration were common for the extremity thromboses. These complications have been recognized in 1 to 2% of children undergoing induction therapy which includes asparaginase.
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PMID:A syndrome of thrombosis and hemorrhage complicating L-asparaginase therapy for childhood acute lymphoblastic leukemia. 695 21

Five cases of intracranial hematoma secondary to chronic disseminated intravascular coagulation syndrome (DIC) were reported. Intracranial hematomas included a case of acute subdural hematoma combined with intracerebral hematoma and 4 cases of acute or subacute hematoma. Primary diseases which caused DIC were cancer; a case of carcinoma of choledochus and 4 cases of gastric carcinoma. All cases were in the advanced stage of carcinoma or at least, had metastasis to other organs. They showed coagulation disorders, such as, the reduction of platelets and the hemorrhagic diastasis, which were referred as chronic DIC, before the onset of intracranial hematoma. After the onset of intracranial hematoma, their coagulation disorders got worse and were diagnosed as acute DIC. They showed the rising of FDP, reduction of the serum fibrinogen and platelets and others. The blood transfusion and the trivial head injury were considered a triggers of exacervation from chronic DIC to acute DIC, that is, from compensated DIC to decompensated DIC. The long-term administration of anticancer drugs might play a part of the role as triggers. Initial symptoms of intracranial hematoma were headache in 4 case and dullness in a case. Three cases immediately lapsed into coma after 1 to 2 hours from the onset. Two cases turned out coma state after 4 to 5 days from the onset. Evacuations of hematoma were performed in 3 cases but they gave rise to rebleeding of intracranial hematomas later. All of 5 cases including surgically and non-surgically treated cases died at last. It is certain that DIC is rather common in the advanced stage of cancer. Matsuda reported that DIC existed in 20% of died patients with cancer. Though the incidence of intracranial hematoma secondary to DIC were less than that of cerebral infarct, it is no reasonable to assume that the actual number of the intracranial hematoma secondary to chronic DIC is rare.
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PMID:[Intracranial hematoma secondary to chronic DIC (author's transl)]. 709 72

A case of a young women with paroxysmal nocturnal hemoglobin (PNH) who developed thrombosis of the cerebral veins after beginning a regimen of oral contraceptives is presented. She was 24 years old and presented with a 3-week history of frontal headache, neck stiffness, paraesthesiae of both arms, and weakness of the left leg. She had begun use of Microgynon 2 months before presentation, but had discontinued use when symptoms began. Hematological studies showed a shortened partial thromboplastin time, high fibrinogen and factor VIII levels, and prlonged euglobulin clot lysis time. Though this patient had a history of coagulation difficulties, it was not until after taking the estrogen-containing contraceptive preparation that PNH developed. The mechanism of thrombosis may be related to the liberation of thromboplastic material from hemolysed erythrocytes and to interaction between complement-sensitive platelets and complement components in plasma. It is suggested that the estrogen augmented the previously existing thrombotic condition in this patient, and that administration of estrogen-containing preparations should not occur in women with thrombotic disorders.
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PMID:Cerebral vein thrombosis and the contraceptive pill in paroxysmal nocturnal haemoglobinuria. 744 35

Recombinant human interleukin-6 (IL-6) has previously been shown to increase platelet counts in normal and sublethally irradiated mice, dogs, and primates. To assess its tolerance and efficacy in clinical use, we performed a randomized phase Ib study in patients with ovarian carcinoma. IL-6 was administered during an initial 7-day cycle before any chemotherapy. Beginning 7 days later, six cycles of chemotherapy containing carboplatin were administered every 3 weeks. During chemotherapy cycles 2 to 6, IL-6 was administered from day 4 through day 17 at escalating dose levels from 0.5 to 10 micrograms/kg/d. At each level, three patients received IL-6 and one patient received a placebo. During the prechemotherapy cycle of IL-6, a dose-dependent increase in platelet count was observed from day 12 to 15 and was maximal on day 15 (r = .77; P < .01). The median ploidy of bone marrow megakaryocytes shifted from 16 N to 32 N after 7 days of the initial prechemotherapy IL-6 administration. Dose-dependent increases in C-reactive protein (CRP) and fibrinogen levels were observed on day 8 (P < .0001 for both). A significant decrease in hemoglobin level occured rapidly after initiation of IL-6 therapy and was maximal on day 8 (P < .001). When given after chemotherapy, IL-6 accelerated platelet recovery after chemotherapy cycles 2 to 6. Postponements of scheduled chemotherapy due to thrombocytopenia were less frequent in patients treated with IL-6. No difference in either neutrophils or peripheral blood progenitor assays was observed during or after IL-6 treatment. Toxicity of IL-6 appeared mild and was not dose-limiting up to 10 micrograms/kg/d. Systemic symptoms such as fever, headache, and myalgia were the main side effects and were easily relieved by acetaminophen administration. No biologic toxicity was observed. The data indicate that IL-6 is a well-tolerated cytokine and capable of accelerating platelet recovery in patients receiving chemotherapy.
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PMID:Thrombopoietic effects and toxicity of interleukin-6 in patients with ovarian cancer before and after chemotherapy: a multicentric placebo-controlled, randomized phase Ib study. 753 10

The clinical experience with a combined oral contraceptive (COC) containing 150 micrograms desogestrel and 30 micrograms ethinylestradiol is reviewed. Fourteen clinical trials have been reported involving over 44,000 women for more than 190,000 cycles. None of the 17 pregnancies which occurred (overall Pearl Index 0.12) were due to method failure. The incidences of breakthrough bleeding and spotting after 6 treatment cycles varied from 0.1-6.0% and 2.8-11% of subjects, respectively, and at this time they were not significantly different from pretreatment in most trials. About 90% of subjects maintained regular cycles. The incidence of subjective side effects (approximately 5% for headache, 4% for breast tenderness, 2% for nausea) was low. No significant changes occurred in body weight or blood pressure. In all trials, the COC was well accepted and the rates of discontinuation were similar to those in other COC trials. Pharmacodynamic effects have been widely investigated. There were no significant changes in glucose metabolism or in haematological factors except for possibly minor increases in factors VII and X, fibrinogen and plasminogen. Over thirty studies of the effect of the COC on lipid metabolism have been published; significant increases occur in serum triglycerides, HDL-C and apoprotein A1. SHBG concentrations increase 2-3 fold with a consequent decrease in the levels of free testosterone. This effect can be particularly important therapeutically in women with hyperandrogenic skin disorders and 14 trials in women with these disorders have demonstrated significant clinical improvement with the COC. The findings from the various trials show the COC to be effective and acceptable with no adverse metabolic effects.
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PMID:Twelve years of clinical experience with an oral contraceptive containing 30 micrograms ethinyloestradiol and 150 micrograms desogestrel. 775 Feb 81

The clinical, laboratorial perimetric and fluorescein angiographic features of the arteritic type of the anterior ischemic optic neuropathy (A-AION) was studied in 25 patients (40 eyes) in order to characterize the profile of the disease and to allow the differential diagnosis with the non-arteritic anterior ischemic optic neuropathy (NA-AION) and other disorders of the optic nerve. The A-AION occurred in patients 60 to 88 years old (mean 74 years) and was highly predominant in females (64 per cent). Fifteen patients had both eyes involved, either simultaneously or usually within few days or weeks after the initial involvement. Headache and eye pain were the most commonly observed prodromic complaints whereas systemic symptoms of giant cell arteritis (GCA) were seen in all patients. The laboratorial abnormalities most commonly found were high values of reactive C protein, plasmatic fibrinogen and erythrocyte sedimentation rate. In the great majority of the patients visual acuity was severely affected. The optic disc was always abnormal, usually showing a pale edema. In addition to that retinal changes were commonly found. Goldmann perimetry disclosed a wide variety of visual fields abnormalities, the most common of them being inferior altitudinal defects. Fluorescein fundus angiography revealed delayed or absent disc fluorescence, or sectorial or diffuse hypofluorescence or hyperfluorescence of the optic disc. Choroidal filling delay was the most characteristic and frequent angiographic finding in the arteritc type of the disease.
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PMID:[The arteritic type of anterior ischemic optic neuropathy. Study of 25 cases]. 789 8


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