Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case in which prescription medications induced heat intolerance which led to heat stroke is presented. A subject who suffered from depression and was treated with fluoxetine HCL (prozac) and lithium carbonate was engaged in mild intermittent work for 4 hours under hot/dry climatic conditions (Ta = 37 degrees C, rh = 15%). The subject lost consciousness, was hyperthermic and suffered from disseminated intravascular coagulation. A year later residual cerebellar symptoms were still evident and severe atrophy of the cerebellar tissue was demonstrated in a CT scan. It is suggested that drug-induced heat intolerance was the predisposing factor that reduced the patient ability to sustain exercise-heat stress, and under the favorable environmental circumstances led to excessive heat accumulation which ultimately caused heat stroke. This is the first description, to our knowledge, of heat intolerance of a patient treated by a combination of fluoxetine and lithium carbonate.
 ...
PMID:Heat intolerance induced by antidepressants. 910 Sep 34

Acetazolamide (Diamox) is a carbonic anhydrase inhibitor commonly used in patients with glaucoma in order to reduce intraocular pressure. Acetazolamide (AZ) is mostly excreted in the urine, therefore, the blood levels of AZ often tend to increase in patients with chronic renal failure. We experienced a case of chronic renal failure in a patient suffering from acute hemorrhagic gastritis associated with AZ intoxication. A 66-year-old female with chronic renal failure was referred to our hospital because of drowsiness and an acute deterioration of renal function. She had been treated with AZ, 500 mg per every day for eleven days for the treatment of glaucoma. Laboratory studies showed leukocyturia, thrombocytopenia, severe anemia, and tarry stools. The serum concentration of AZ was elevated to a maximum of 76.5 mg/ml. She was thus diagnosed as having AZ intoxication. On further examination, acute extensive hemorrhagic gastritis was also found by gastroscopy. Despite of the administration of intensive therapies, she died of disseminated intravascular coagulation (DIC) and septic shock due to bone marrow depression 6 days after admission. It is generally known that excessive blood levels of AZ inhibit not only the gastric juices but also prostaglandin levels and HCO3- excretion in the gastric mucosal barrier. We thus concluded that an excessive dose of AZ had probably destroyed the gastric mucosal barrier or thrombocytopenia due to bone marrow disorder and thus eventually led to the development of hemorrhagic gastritis. As far as we know, this is the first case report of acute hemorrhagic gastritis associated with AZ intoxication. Even though AZ tends to strongly bind to plasma protein and its clearance is generally poor by hemodialysis (HD), in our patient, HD was observed to be rather effective since the clearance of AZ was 45.8 ml/min on HD and 66 ml/min on direct hemoperfusion (DHP). DHP often reduces the number of platelets, also DHP needs a lot of heparin, therefore, we should have performed HD alone instead of DHP. In patients with an impaired renal function, AZ should therefore be administered very carefully in order to avoid an accumulation of the drug. In addition, HD alone should be used to remove any excessive amounts of AZ from the blood.
 ...
PMID:Acute hemorrhagic gastritis associated with acetazolamide intoxication in a patient with chronic renal failure. 935 64

Clinical signs and haematological abnormalities of haemophagocytic syndrome of unknown origin are described for a male, nine-year-old rottweiler referred because of weakness, depression, mild weight loss and relapsing fever. Mucous membranes were pale and the spleen was enlarged. Ultrasonography revealed diffuse irregular structures in the enlarged spleen, and cytological examination of multiple fine needle aspirates of the spleen demonstrated extramedullary haematopoiesis. Haematological examination revealed pancytopenia and disseminated intravascular coagulation. A bone marrow smear contained numerous marrow macrophages with a cytologically benign appearance, containing phagocytosed haematopoietic cells. The dog died one week after referral. The differential diagnosis is discussed.
 ...
PMID:Haemophagocytic syndrome with disseminated intravascular coagulation in a dog. 957 64

Disseminated intravascular coagulation (DIC) can be caused by a variety of diseases. Experimental models of DIC have provided substantial insight into the pathogenesis of this disorder, which may ultimately result in improved treatment. Disseminated coagulation is the result of a complex imbalance of coagulation and fibrinolysis. Simultaneously occurring tissue factor-dependent activation of coagulation, depression of natural anticoagulant pathways and shutdown of endogenous fibrinolysis all contribute to the clinical picture of widespread thrombotic deposition in the microvasculature and subsequent multiple organ failure. Cornerstone for the treatment of DIC is the optimal management of the underlying disorder. At present, specific treatment of the coagulation disorders themselves is not based on firm evidence from controlled clinical trials. Plasma and platelet transfusion are used in patients with bleeding or at risk for bleeding and low levels of coagulation factors or thrombocytopenia. The role of heparin and low molecular weight heparin is controversial, but their use may be justified in patients with active DIC and clinical signs of extensive fibrin deposition such as those with meningococcal sepsis. There is some evidence to indicate that low molecular weight heparin is as effective as unfractionated heparin but may be associated with a decreased bleeding risk. Antithrombin III (AT III) replacement appears to be effective in decreasing the signs of DIC if high doses are administered, but effects on survival or other clinically significant parameters are at best uncertain. If AT III supplementation is used, the dosage should be selected to achieve normal or supranormal plasma levels of 100% or higher. Results of studies on protein C concentrate, thrombomodulin or inhibitors of tissue factor are promising, but the efficacy and safety of these novel strategies remains to be established in appropriate clinical trials.
 ...
PMID:Current drug treatment strategies for disseminated intravascular coagulation. 961 92

Strontium-89 is effective in the palliation of bone pain caused by skeletal metastases. Its primary side effect is mild thrombocytopenia that typically recovers in 3 or 4 months. Subclinical disseminated intravascular coagulation is reported to be present in approximately 10% to 20% of patients with advanced prostate cancer. These patients may be at increased risk for severe marrow depression after radionuclide therapy for bone pain palliation. This report describes a patient with painful bony metastases resulting from prostate carcinoma. He had a normal platelet count and no clinical evidence of a coagulation disorder at the time of strontium-89 therapy, and a severe disseminated intravascular coagulation developed and lead to death after treatment. A normal platelet count before strontium-89 therapy does not preclude subsequent disseminated intravascular coagulation, and we support the Society of Nuclear Medicine's bone pain treatment procedure guideline that patients referred for bone palliation should be screened for disseminated intravascular coagulation before therapy.
 ...
PMID:Disseminated intravascular coagulation in a patient treated with strontium-89 for metastatic carcinoma of the prostate. 1055 66

Disseminated intravascular coagulation is characterised by systemic activation of blood coagulation, resulting in formation of intravascular thrombi and impaired organ perfusion. Simultaneously, the ongoing consumption of platelets and coagulation factors may lead to bleeding. Disseminated intravascular coagulation is seen in septicaemic infections, trauma, malignancies, obstetrical complications, vascular diseases, toxic and immunological reactions. In summary, the systemic deposition of fibrin is caused by enhanced thrombin generation, simultaneous depression of physiological anticoagulant mechanisms and diminished fibrin degradation due to inhibition of fibrinolysis. The increased insight into the pathogenesis of disseminated intravascular coagulation provides a solid basis for development of improved management strategies for patients with this complication. Therapy may include anticoagulants, platelet and plasma transfusion, concentrates of coagulation inhibitors and antifibrinolytic agents.
 ...
PMID:[Disseminated intravascular coagulation]. 1072 56

A 27-year-old woman (38 week pregnant) was admitted to an obstetric hospital with an acute severe abdominal pain. At that time, the fetal heart sound was not audible. The diagnosis of placental abruption was made and she underwent an emergency cesarean section (C/S) under general anesthesia. She had anemia which became worse in the first few hours after C/S, requiring blood transfusion. ST depression was also present in the ECG during this period. Subsequently, we found an increase in myocin light chain, but not in troponin-T. On the 2nd postoperative day, pulmonary edema appeared and DIC was suspected. We treated her with nitrates, diuretics, protease inhibitors and oxygen by mask. She was discharged on 14th postoperative day with no other complications. Cardiac echogram showed no abnormalities, but a borderline change was seen in her exercise ECG. Depression of the ST segment has been reported in C/S patients, but this does not indicate myocardial ischemia (MI) nor treatment is necessary in most cases. In our case, the diagnosis was not conclusive, but in view of the risks associated with MI, patients with placental abruption should be managed strictly as if they have MI.
 ...
PMID:[Myocardial ischemia during cesarean section in a patient with placental abruption]. 1088 50

A peri-parturient fifteen-month-old female Maine Coon cat was presented with extreme weakness and depression, profound hypovolaemia and hypothermia. Severe hyperkalaemia, hyponatraemia and anaemia were detected. Disseminated intravascular coagulation was suspected due to marked prolongation of activated partial thromboplastin time. Uterine torsion was diagnosed at exploratory laparotomy. The cat made a full recovery following ovariohysterectomy and intensive supportive therapy.
 ...
PMID:Successful treatment of uterine torsion in a cat with severe metabolic and haemostatic complications. 1171 4

"Club drugs" have become alarmingly popular. The use of 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) and gamma-hydroxybutyrate (GHB), in particular, has increased dramatically from 1997-1999. The pharmacokinetics of MDMA and GHB appear to be nonlinear, making it difficult to estimate a dose-response relationship. The drug MDMA is an amphetamine analog with sympathomimetic properties, whereas GHB is a gamma-aminobutyric acid analog with sedative properties. Symptoms of an MDMA toxic reaction include tachycardia, sweating, and hyperthermia. Occasional severe sequelae include disseminated intravascular coagulation, rhabdomyolysis, and acute renal failure. Treatment includes lowering the body temperature and maintaining adequate hydration. Symptoms of GHB intoxication include coma, respiratory depression, unusual movements, confusion, amnesia, and vomiting. Treatment includes cardiac and respiratory support. Because of the popularity of these agents and their potentially dangerous effects, health care professionals must be familiar with these substances and the treatment options for patients who present with symptoms of a toxic reaction.
 ...
PMID:A comprehensive review of MDMA and GHB: two common club drugs. 1206 74

HIT type II is one of the severe complications of heparin therapy. The antibody for the heparin-PF 4 complex, which causes thrombocytopenia of less than 100 x 10(3).microliter-1, thrombosis and DIC-like symptoms, is produced. We managed the patient with HIT type II, who underwent off-pump CABG using argatroban, a direct thrombin inhibitor, as an anticoagulant. Intraoperative activated coagulation time (ACT) was maintained above 250 sec with 5.0 micrograms.kg-1.min-1 of argatroban infusion and all the procedures were successful. We also investigated the platelet count in the 100 patients with heparin therapy in CCU. The incidence of the platelet depression after heparin administration was as high as 59%, and in 12% of the patients the platelet count dropped below 100 x 10(3).microliter-1. In conclusion, thrombocytopenia by heparin therapy is not rare, and argatroban as an anticoagulant during off-pump CABG is thought to be useful.
 ...
PMID:[Intraoperative management for a patient with heparin-induced thrombocytopenia (HIT) undergoing off-pump coronary bypass surgery using argatroban, a direct thrombin inhibitor]. 1184 Jun 59


<< Previous 1 2 3 4 5 6 7 8 Next >>