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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two horses with red maple (Acer rubrum) toxicity responded to treatment with high doses of vitamin C (ascorbic acid), in addition to blood transfusions, and intravenous fluid therapy. The clinical course included Heinz body anemia, marked methemoglobinemia, depression, and evidence of severe tissue anoxia. Clinical recovery was dramatic with stabilization achieved 36 hours following the initiation of ascorbic acid therapy.
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PMID:The use of ascorbic acid in the treatment of 2 cases of red maple (Acer rubrum)-poisoned horses. 164 80

Substances that are inhaled for the purpose of recreational self-intoxication include aliphatic hydrocarbons, alkyl halides, alkyl nitrites, aromatic hydrocarbons, ethers, and ketones. All have the ability to cause asphyxia, arrhythmias, cardiovascular depression, neurologic dysfunction, and mucosal, pulmonary, and skin irritation following acute exposure and permanent neurologic damage with chronic exposure. The acute effects of alkyl halides and alkyl nitrites also include carbon monoxide poisoning and hepatorenal toxicity, and methemoglobinemia, respectively. Chronic exposure to aromatic hydrocarbons and ketones can result in liver, kidney, and bone marrow injury; myopathy, rhabdomyolysis, metabolic acidosis, and electrolyte abnormalities are further complications of chronic aromatic hydrocarbon inhalation.
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PMID:Volatile substances of abuse. 220 21

A 30-month-old female infant had a cardiopulmonary arrest due to viscous lidocaine. The protective airway mechanisms were blunted by this drug, resulting in aspiration, hypoxia, seizures, and death. Lidocaine has also been associated with respiratory depression, psychosis, methemoglobinemia, and toxic cardiovascular reactions. We do not recommend the use of viscous lidocaine for minor oral irritation in infants and young children.
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PMID:Cardiopulmonary arrest due to misuse of viscous lidocaine. 405 69

Subacute and chronic oral toxicities of trinotroglycerin (TNG) were studied in beagle dogs, CD rats, and CD-1 mice. No adverse effects were seen in dogs given up to 1 mg/kd/day of TNG for 4 weeks, then 5 mg/kg/day for 9 more weeks. Dogs given 25 to 200 mg/kg/day for 5 days had transient and dose-related severe methemoglobinemia, while 200 mg/kg/day produced depression; dogs given 1, 5, or 25 mg/kg/day for 12 months had transient and dose-related mild methemoglobinemia. Rats fed 0.1% TNG for 5 weeks, then 0.5% (230-234 mg/kd/day) for 8 more weeks had decreases in feed consumption and weight gain after the increase in dosage; rats fed 2.5% TNG (1406 or 1416 mg/kg/day for males and females, respectively) for 13 weeks suffered adverse effects, including weight loss, compensated anemia, and testicular degeneration, but they resumed gaining weight as feeding continued. Rats fed 1% TNG (363 or 434 mg/kg/day for males and females, respectively) for 2 years had decreased weight gain, decreased grooming, methemoglobinemia and its sequelae, cholangiofibrosis , hepatocellular carcinoma, and interstitial cell tumors of the testis. A decrease in the naturally occurring pituitary chromophobe adenoma and mammary tumors increased the life span of the females. Some rats fed 0.1% TNG (31.5 or 38.1 mg/kg/day for males and females, respectively) had mild hepatic lesions similar to those seen in rats fed the larger doses. No adverse effects were seen in mice fed up to 0.1% TNG for 3 weeks, then 0.5% for 10 more weeks. Mice fed 1% TNG (1022 or 1058 mg/kg/day for males and females, respectively) for 2 years had decreased weight gain, decreased grooming, and methemoglobinemia and its sequelae, but no obvious cellular changes as found in the rats.
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PMID:Subacute and chronic toxicity studies of trinitroglycerin in dogs, rats, and mice. 642 46

Signs of acute hemolytic anemia developed in 4 adult horses from 2 Georgia farms 3 to 4 days after the ingestion of wilted leaves from cut red maple trees (Acer rubrum). Clinical findings included weakness, polypnea, tachycardia, depression, icterus, cyanosis, and brownish discoloration of the blood and urine. Blood changes included methemoglobinemia, free plasma hemoglobin, decreased pcv, and Heinz bodies in erythrocytes. These findings plus hemoglobinuria suggested intravascular hemolysis. Three of the 4 horses diet 5 to 7 days after ingestion of the leaves. Gross pathologic changes included generalized icterus, splenomegaly and swollen, black kidneys. Microscopic changes including tubular nephrosis with hemoglobin casts, vacuolization of centrilobular hepatocytes, and sequestration of erythrocytes in splenic sinusoids. A disease indistinguishable from the field cases was induced in a pony by the oral administration of dried, ground red maple leaves at a dosage of 1.5 g/kg. The findings of methemoglobinemia, hemolysis, and Heinz bodies suggested that the toxic principle of the red maple leaf was an oxidant.
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PMID:Hemolytic anemia in horses after the ingestion of red maple leaves. 705 81

Acute acetaminophen intoxication in the cat was studied to characterize the antidotal profile of acetylcysteine. Toxicosis was associated with cyanosis, hyperventilation, depression, and facial edema. Abnormal laboratory findings were methemoglobinemia and elevated serum glutamic-pyruvic transaminase activity. In one trial, each of ten cats was given a 325-mg tablet of acetaminophen, then another after 4 hours. Five of the cats were given antidotal treatment with acetylcysteine (140 mg/kg, per os) at the time of the second dosing with acetaminophen and at 8-hour intervals thereafter for a total of three treatments. All treated cats survived. Two of the untreated cats died. In another trial, doubling each dose of acetaminophen (650 mg) proved fatal in all of four untreated cats. When antidotal therapy was initiated at the time of the second dosing with acetaminophen and repeated at 8- or 4-hour intervals for three treatments, two of four cats in each treatment group survived. Although antidotal therapy was associated with a return of serum glutamic-pyruvic transaminase and methemoglobinemia values toward normal, only the methemoglobin value was a reliable prognostic indicator.
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PMID:Acetylcysteine for treatment of acetaminophen toxicosis in the cat. 740 22

In normal erythrocytes, small quantities of methaemoglobin are formed constantly and are continuously reduced, almost entirely by the reduced nicotine adenine dinucleotide (NADH) diaphorase system, rather than the reduced nicotine adenine dinucleotide phosphate (NADPH) diaphorase system. Methaemoglobinaemias are usually the result of xenobiotics, either those that may directly oxidise haemoglobin or those that require metabolic activation to an oxidising species. The most clinically relevant direct methaemoglobin formers include local anaesthetics (such as benzocaine and, to a much lesser extent, prilocaine) as well as amyl nitrite and isobutyl nitrite, which have become drugs of abuse. Indirect, or metabolically activated, methaemoglobin formation by dapsone and primaquine may cause adverse reactions. The clinical consequences of methaemoglobinaemia are related to the blood level of methaemoglobin; dyspnoea, nausea and tachycardia occur at methaemoglobin levels of > or = 30%, while lethargy, stupor and deteriorating consciousness occur as methaemoglobin levels approach 55%. Higher levels may cause cardiac arrhythmias, circulatory failure and neurological depression, while levels of 70% are usually fatal. Cyanosis accompanied by a lack of responsiveness to 100% oxygen indicates a diagnosis of methaemoglobinaemia, which should be confirmed using a CO-oximeter. Pulse oximeters do not detect methaemoglobin and may give a misleading impression of patient oxygenation. Methaemoglobinaemia is treated with intravenous methylene blue (methyl-thioninium chloride; ;1 to 2 mg/kg of a 1% solution). If the patient does not respond, perhaps because of glucose-6-phosphate dehydrogenase (G6PD) deficiency or continued presence of toxin, admission to an intensive care unit and exchange transfusion may be required. Dapsone-mediated chronic methaemoglobin formation can be reduced by coadministration of cimetidine to aid patient tolerance. Increasing knowledge and awareness of drug-mediated acute methaemoglobinaemia among physicians should lead to prompt diagnosis and treatment of this potentially life-threatening condition.
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PMID:Drug-induced methaemoglobinaemia. Treatment issues. 882 17

Lisa Capaldini, a physician who treats patients with HIV-related fatigue, discusses symptoms, diagnosis techniques, and treatments of depression, anemia, and various other roots of fatigue in HIV-positive patients. Biochemical depression, caused by abnormal levels of serotonin and norepinephrine in the brain, is easily misdiagnosed or overlooked. Physical and emotional symptoms of depression mirror common effects of HIV such as exhaustion, anger, and irritability. Knowing the history of depression prior to HIV infection, including previous drug abuse and family history of depression, will help to diagnose fatigue. Dr. Capaldini recommends antidepressants provided the condition is properly diagnosed and the side effects are not harmful to the patient. Selective serotonin reuptake inhibitors (SSRI), the most frequently prescribed antidepressants, can cause short term sexual dysfunction. Bupropion and Wellbutrin can be prescribed to avoid this side effect. Psychotherapy can be effective if therapists are familiar with HIV disease and can distinguish between symptoms brought on by behavior, addictive habits, or pre-existing depression. Consideration also must be given to drug interactions, particularly with the antiretrovirals ritonavir and delavirdine, which can cause seizures or disturb cardiac rhythm. Anemia is most noticeable after physical exertion, and symptoms are more evident based on the increased rate that red blood cells move out of the normal range. To determine the course of treatment, physicians need to clarify the cause of anemia. Anemia can be caused by drugs, vitamin deficiencies, or other nutritional problems. Adrenal insufficiency, methemoglobinemia, and malnutrition are also causes of fatigue. Diagnosing fatigue due to hepatitis B or C, rather than HIV, can be achieved by measuring hepatitis levels and observing T cell counts and viral load. Dr. Capaldini suggests that proper diet and exercise prevent fatigue from getting worse.
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PMID:Fatigue and HIV: interview with Lisa Capaldini, M.D. Part II. Interview by John S. James. 1136 84

We studied an erythron response to acute nitrite intoxication in 30 white mature female rats. Sodium nitrite was subcutaneously injected into rats (10 and 50 mg/kg). One hour after the injection we observed development of hemolytic anemia followed by urgent reticulocyte withdrawal out of the bone marrow, methemoglobinemia, leucocytolysis and macrophages function depression. Thus, sodium nitrite action in acute intoxication is dose-dependent and involves both erythron and white blood cells system. The results confirm an important role of blood as the buffer-system in toxic effects compensation.
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PMID:[The response of erythrocytic system of mature rats to acute nitrite intoxication]. 1520 22

A seven month old domestic shorthaired male cat was presented with a known history of acetaminophen ingestion. Clinical findings included icterus, depression, hypothermia, tachypnea and pronounced edema of the head and neck. Treatment was aimed at providing substrate to assist in conjugation of the drug and reversing methemoglobinemia. Administration of oral acetylcysteine, ascorbic acid and IV fluids was insufficient in this case due to a delay in initiation of treatment. The salient postmortem findings were icterus, subcutaneous and pulmonary edema and evidence of hemolysis in the liver, spleen and urinary tract.The pathophysiology of the toxicosis and the current recommendations for treatment are reviewed.
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PMID:Acetaminophen toxicosis in a cat. 1742 85


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