Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 43-year-old man who presented parkinsonism due to pontine and extrapontine myelinolysis was reported. Late in February, 1990, the patient presented suffered from a flu-like illness and was seen at a community hospital. Physical finding showed the pigmentation on the whole body and hypotension, and laboratory examination revealed severe electrolyte imbalance (serum sodium 100 mEq/l, serum potassium 6.9 mEq/l, serum chloride 68 mEq/l) and hypoglycemia (postprandial serum glucose 78 mg/dl). Given these results, adrenal failure was strongly suspected. Prompt correction of electrocyte imbalance was performed by the infusion of sodium chloride, and four days later the serum sodium level reached 131 mEq/l. On the other hand, the patient was noticed lethargic and showed parkinsonism i.e., rest tremor, cog-wheel rigidity, and hypokinesia. Fourteen days after the onset of neurological abnormalities, the patient was referred to our hospital for further evaluation of parkinsonism. Additionally, neurological examination revealed dysphagia, mutism and positive pyramidal tract sign. On admission brain computed tomography was unremarkable, but on the 14th hospital day it showed low density area in the pons. Brain magnetic resonance imaging also showed a striking increase in T2-weighted signal from the pons, the midbrain, and the bilateral thalamus. Based on these findings, a diagnosis of parkinsonism due to pontine and extrapontine myelinolysis was made, and levodopa therapy was started. After the initiation of levodopa therapy, improvement of tremor, rigidity, and hypokinesia ensued with marked functional benefit, and the patient was discharged on the 49th hospital day. Levodopa was stopped three weeks after discharge but, all neurological abnormalities were not recurrent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of parkinsonism due to pontine and extrapontine myelinolysis]. 130 Feb 56

Arenaviruses are rodent-borne negative strand RNA viruses and infection of these viruses in humans may result in disease and hemorrhagic fever. To date, supportive care, ribavirin, and in some cases immune plasma remain the foremost treatment options for arenaviral hemorrhagic fever. Research with the hemorrhagic fever causing-arenaviruses usually requires a Biosafety level (BSL)-4 environment; however, surrogate animal model systems have been developed to preliminarily study and screen various vaccines and antivirals. The Syrian golden hamster-Pirital virus (PIRV) surrogate model of hemorrhagic fever provides an opportunity to test new antivirals in an ABSL-3 setting. Thus, we challenged hamsters, implanted with telemetry, with PIRV and observed viremia and tissue viral titers, and changes in core body temperature, hematology, clinical chemistry, and coagulation parameters. Physical signs of disease of the PIRV-infected hamsters included weight loss, lethargy, petechial rashes, epistaxis, ocular orbital and rectal hemorrhage, and visible signs of neurologic disorders. However, treating animals with genistein, a plant derived isoflavone and general kinase inhibitor, resulted in increased survival rates and led to an improved clinical profile. In all, the results from this study demonstrate the potential of a general kinase inhibitor genistein as an antiviral against arenaviral hemorrhagic fever.
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PMID:Genistein, a general kinase inhibitor, as a potential antiviral for arenaviral hemorrhagic fever as described in the Pirital virus-Syrian golden hamster model. 2060 Mar 33

Hyperosmolar hyperglycemic state is a life-threatening emergency manifested by marked elevation of blood glucose and hyperosmolarity with little or no ketosis. Although there are multiple precipitating causes, underlying infections are the most common. Other causes include certain medications, nonadherence to therapy, undiagnosed diabetes mellitus, substance abuse, and coexisting disease. In children and adolescents, hyperosmolar hyperglycemic state is often present when type 2 diabetes is diagnosed. Physical findings include profound dehydration and neurologic symptoms ranging from lethargy to coma. Treatment begins with intensive monitoring of the patient and laboratory values, especially glucose, sodium, and potassium levels. Vigorous correction of dehydration is critical, requiring an average of 9 L of 0.9% saline over 48 hours in adults. After urine output is established, potassium replacement should begin. Once dehydration is partially corrected, adults should receive an initial bolus of 0.1 units of intravenous insulin per kg of body weight, followed by a continuous infusion of 0.1 units per kg per hour (or a continuous infusion of 0.14 units per kg per hour without an initial bolus) until the blood glucose level decreases below 300 mg per dL. In children and adolescents, dehydration should be corrected at a rate of no more than 3 mOsm per hour to avoid cerebral edema. Identification and treatment of underlying and precipitating causes are necessary.
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PMID:Hyperosmolar Hyperglycemic State. 2943 5