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 case of central pontine myelinolysis (CPM) following rapid correction of hyponatremia is reported and a review of the literature is made. The patient was a 63-year-old non-alcoholic female who had no liver or kidney diseases in her past history. She was found unconscious after a series of convulsions and was admitted to the hospital. Eighteen months prior to admission, she had a surgery for a ruptured anterior communicating artery aneurysm. Her postoperative course was uneventful except for an urinary incontinence and mild disorientation. She was initially lethargic with conjugate deviation toward right. Nine days after admission, she still remained lethargic, and laboratory studies showed a serum sodium value of 93 mEq/l, serum osmolarity 206 mOsm/l and urine osmolarity 270 mOsm/l when she was clinically diagnosed as having SIADH. She was treated by a strict elimination of water, and administration of sodium, dexamethasone and demeclocycline. In three days, serum sodium was corrected and returned to 137 mEq/l. However, she deteriorated in consciousness and became comatose and developed quadriplegia. CT scans and cerebral angiograms were normal. One month later, another CT scans demonstrated a well-defined hypodensity area in the pons. Brain stem auditory response (BSAR) showed a prolongation of III-V interpeak latency, especially IV-V interval. Her neurological state was essentially unchanged thereafter and she died of septic shock after 12 months' hospitalization. No permission for autopsy was obtained. The clinical course, CT scans and BSAR reported here are indicative of the diagnosis of CPM.
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PMID:[A case of central pontine myelinolysis]. 374 96

While SSRIs have been reported to cause SIADH, the actual incidence remains unclear. From the published case reports, the elderly may appear to be at higher risk of developing SIADH. Symptomatic and laboratory presentation in these patients includes lethargy, hyponatremia, elevated urinary sodium excretion, and hyperosmolar urine. However, evaluation of SSRI-induced SIADH has been incomplete. Normalization of serum sodium concentrations occurred after discontinuation of the SSRI and/or fluid restriction. Of the published reports, only three convincingly demonstrated a causative role of SSRI-induced SIADH by rechallenge. As a result, the published case reports cannot definitely established a causal relationship. Pharmacists can play an important role in the care of patients with suspected SSRI-induced SIADH. Pharmacists should be familiar with the clinical and biochemical presentation of SIADH as well as the limitations of published case reports implicating SSRIs as a cause of SIADH. A complete medication history, including when these agents were initiated or discontinued, should be taken. Pharmacists must understand, recognize, and ensure the proper monitoring parameters, namely daily fluid intake, patient weight, and serum sodium concentrations.
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PMID:Association of SIADH with selective serotonin reuptake inhibitors. 899 75

A 56 year old man was admitted cause he had increasing symptoms as weakness, lethargy, disorientation. The total eosinophil count was 3000/mm3, the serum sodium concentration was 120 mmol per litre. In spite of severe hyponatriemia, urinary sodium excretion was not suppressed and serum osmolality (240 mOsm/Kg was lower than urine osmolality (488 mOsm/Kg). SIADH and Idiopathic Hypereosinophilic Syndrome was diagnosed because we found systemic failure signs due to hypereosinophilia (hepatitis, gastritis, pulmonary hypertension, and encefalopathy). Cortisonic treatment was started with symptoms improving, natriemia, eosynophil count and hepatitis signs normalization. After treatment stopping, reappeared asymptomatic hypereosinophilia, than we choosed Idrossiurea but, non-standing hypereosinophilia disappeared, appeared signs of preexisting adrenal insufficiency, emphasized by stopping cortisone therapy. A RMN showed an hypofiseal adenoma. Many cases of SIADH and Hypereosinophilia hiding adrenocortical insufficiency are reported with severe and unusual hypereosinophilia.
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PMID:[Association of hyponatremia and eosinophilia: correlated idiopathic hypereosinophilic syndrome and SIADH or adrenal insufficiency with secondary eosinophilia]. 1285 64

A 3-month-old intact male Prague ratter was presented to the emergency service for evaluation of progressive lethargy, weakness, coughing and labour breathing after an episode of resistance to oral deworming. The patient exhibited depression, increased respiratory effort and cyanosis at initial presentation. Results of first diagnostic work-up (complete blood cell count, biochemistry panel and thoracic x-rays) were all consistent with aspiration pneumonia. The puppy was initially treated with balanced isotonic crystalloids, broad spectrum antibiotics, nebulization with thoracic coupage and was transferred to an infant incubator with a sustained FiO2 of 40-50%. Twenty-four hours after ICU admission the patient's condition suffered a worsening and the dog was orthopneic, severely depressed with episodes of intermittent dysphoria and seizuring. New thoracic radiographs and several samples of blood and urine were collected to go further in the diagnostic workup revealing severe hyponatremia, severe plasma hypotonicity, high natriuresis and metabolic acidosis with a worsening of the radiological pulmonary pattern. Based on these new clinical findings a diagnosis of SIADH was established. Emergency treatment with hypertonic 3% saline solution and loop diuretics was started like a sodium supplement and to inhibit water resorption in renal tubules, thus reducing the volume overload. The goal of this treatment was to achieve a progressive and controlled increase of plasma sodium concentration and promoting the excretion of positive body water imbalance. The patient's condition improved clinically over the following days, treatment was progressively discontinued and the dog was discharged 7 days after admission. To the author's knowledge this is the first report of a puppy younger than 12 weeks with respiratory distress developing SIADH associated to aspiration pneumonia.
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PMID:Syndrome of Inappropriate Antidiuretic Hormone Secretion in a Mini-Breed Puppy Associated With Aspiration Pneumonia. 2952 34