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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of the effects of 4 milk preparations on the early growth of low birth-weight newborns in Ceylon is reported. The following parameters were studied: mortality; weight gain; tolerance, as indicated by the incidence of diarrhea and the presence of sugar in the stools; blood glucose levels; and blood urea and serum sodium levels. A powdered and partially skimmed cow's milk, Nestogen, was used as it is available in the government hospitals throughout the island. 2 strengths constituted Formulas 1 and 2, and by addition of sucrose to the latter, a 3rd of higher calorie value was prepared. The 4th formula was breast milk. The study population from 3 nurseries consisted of 112 babies between 1250 and 2057 grams birth-weight, those of lighter weight being excluded as many required intravenous therapy initially. Weights were checked daily, and as soon as babies were able to suck adequately, they were allowed home. Mean blood glucose levels were within the normal range in babies appropriate and small for gestational age on all 4 milks. There was a high incidence of diarrhea among babies on all 3 Nestogen formulas. On Formulas 1 and 2, diarrhea occurred between the 4th and 12th day, and, in all cases, preceded weight loss and dehydration. Babies with diarrhea on Formula 3 showed symptoms between the 3rd and 5th days, and in each case lethargy, weight loss, dehydration, and in some, fever, were followed by diarrhea. Blood urea nitrogen levels increased with the protein content of the diet and may have reflected a diminished extra cellular fluid volume due to extra renal fluid losses. Mortality rates were similar in the Nestogen fed babies; no breast fed babies died. In sum, the comparison showed breast milk to be overall superior for those who could suck. A higher protein feed was associated with more rapid weight gain but addition of sucrose produced intolerance. Higher strengths of Nestogen which obligate greater urinary fluid are probably unsafe in a hot climate which induces considerable insensible losses of water.
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PMID:Feeding studies in Ceylonese babies. 449 4

In the United States, the drugs most commonly used to treat peptic ulcer disease are antacids and the H2-receptor antagonists cimetidine and ranitidine. Other available agents include anticholinergics and the coating agent sucralfate. Investigational drugs such as colloidal bismuth, carbenoxolone, prostaglandins, the tricyclic compound pirenzepine, and substituted benzimidazoles are not available for use in the United States. Most of the commercially available and investigational compounds have similar efficacy; therefore the optimal drug may be the one associated with the fewest adverse effects and the most convenient dosing regimen. Cimetidine causes a small number of adverse effects, including neuropsychiatric disorders, gynecomastia, impotence, loss of libido, elevation of serum creatinine and serum transaminases concentrations, and drug interactions. Some of these reactions have been of clinical significance. Presently, there are rare reports of gynecomastia, bradycardia, inhibition of acetylcholinesterase, headache, lethargy, diarrhea, and rash in patients receiving ranitidine. Antacids can produce either diarrhea or constipation and have been associated with low serum phosphorus concentrations, and metabolic alkalosis. Anticholinergics, especially in elderly or debilitated patients, can cause central nervous system disorders, intestinal atony, or urinary retention. Sucralfate may cause constipation, diarrhea, nausea, and headache. The investigational agents have their own side effect profiles. The adverse effects of anticholinergics make them unattractive therapeutic choices, and antacids and sucralfate have inconvenient dosing requirements compared with some equally efficacious alternatives. In addition, clinical experience with sucralfate in the United States is limited. The safety record of cimetidine is admirable. As clinical experience with ranitidine increases, currently unrecognized adverse effects may be reported. However, based on current data, ranitidine is as effective as cimetidine and is associated with a lower incidence of side effects.
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PMID:Problems associated with medical treatment of peptic ulcer disease. 609 62

Intravenous injection into rabbits and cats of an aqueous extract of hornet venom sac, produced a significant reduction in the intraocular pressure. The mean reduction of the ocular pressure was between 7 and 15 mm Hg within one hour past injection and it lasted 6-12 h or in several instances even more than 24 h. The effect is produced by some thermolabile high-molecular-weight fraction(s), is dose-dependent and is reproducible by repetitive injections. Side effects may include diarrhea, micturition and lethargy, but usually there is no marked effect on the size of the pupil.
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PMID:Intraocular pressure reduction induced by hornet venom in the normal eye. 612 99

The ability of polyriboinosionic acid [poly(rI)].polyribocytidylic acid [poly(rC)], mismatched analog poly (rI).poly[r(C12Uracil)n], and poly(rI).poly(rC) complexed with poly L-lysine and carboxymethylcellulose [poly(ICLc)] to induce interferon and the comparative toxicity of each in cats were evaluated. Each induced high levels of circulating interferon, although poly(ICLC) injected intravenously at 1 to 4 mg/kg induced up to 10 times more interferon than the other compounds. Each compound was pyrogenic and caused a transient decrease in leukocyte numbers. Poly(rI).poly(rC) and the mismatched analog caused severe diarrhea and nausea at the highest drug concentrations (1 to 4 mg/kg), but poly (ICLC) did not. Each compound also caused depression and lethargy and impaired coordination.
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PMID:Interferon induction by and toxicity of polyriboinosinic acid [poly(rI)].polyribocytidylic acid [poly (rC)], mismatched analog poly (rI).poly[r(C12Uracil)n], and poly(rI).poly(rC) L-lysine complexed with carboxymethylcellulose. 615 63

A 17 year old high school boy experienced fever and diarrhea, which subsided within 4 days by appropriate medications. Six days later, however, he developed unsteadiness and limb spasm. On the morning of admission, he was found to have drowsiness, dysarthria, gait disturbance and involuntary jerks. When he was brought to the hospital, he was lethargic but could follow simple verbal commands. Frequent involuntary movements manifested by facial grimacings, limb spasms and twitchings with dystonic features were seen. Decorticate posturing was readily elicited by painful stimuli. There was no meningeal irritation sign or gross sensory impairment. The deep tendon reflexes were symmetrically exaggerated with bilateral Babinski signs. Bilateral lateral rectus muscle weakness was found together with mild ptosis and upward gaze limitation. Nystagmus was not present and the funduscopic examination was normal. Immediately he was placed on anticonvulsants, steroid hormone, gamma-globulin and antibiotics as well. A brain CT scan and a CSF examination revealed no abnormality. Meanwhile he continued to show a progressive deterioration associated with fever and status epilepticus, and within 24 hours he lapsed into coma in decorticate posture. An EEG obtained at the 3rd hospital day was compatible with spindle coma. In spite of aggressive treatment he remained febrile and comatous. Therefore, vidarabine (adenine arabinoside) was initiated from the 3rd hospital day for 5 days. Then he began to groan and show frequent choreic movements. For the subsequent 2 weeks he made a slow recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of brain stem encephalitis with complete recovery (Bickerstaff's encephalitis)]. 620 73

During the past two decades, the essentiality of zinc for man has been established. Deficiency of zinc in man due to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in a population subsisting mainly on cereal proteins. Alcoholism is known to cause hyperzincuria and thus may play a role in producing zinc deficiency in man. Malabsorption, cirrhosis of the liver, chronic renal disease and other chronically debilitating diseases may similarly induce zinc deficiency in human subjects. A severe deficiency of zinc has recently been recognized to occur in patients with sickle cell anemia and a beneficial effect of zinc therapy in such patients has been reported. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. Taste abnormalities, correctable with zinc supplementation, have been observed in uremic subjects. Recently, abnormal dark adaptation related to zinc deficiency in patients with cirrhosis of the liver and sickle cell disease has been reported. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances and intercurrent infections predominate and if untreated the condition becomes fatal. Zinc deficiency is known to affect testicular functions adversely in man and animals. This effect of zinc is at the end organ level and it appears that zinc is essential for spermatogenesis and testosterone steroidogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. Thymidine kinase, RNA polymerase, DNA-polymerase from various sources and RNA-dependent DNA polymerase from viruses have been shown to be zinc-dependent enzymes. Zinc also regulates the activity of RNase; thus the catabolism of RNA appears to be zinc-dependent. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues. Three enzymes, alkaline phosphatase, carboxypeptidase and thymidine kinase, appear to be most sensitive to zinc restriction in that their activities are affected adversely within three to six days of institution of a zinc-deficient diet to experimental animals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Zinc deficiency in human subjects. 636 78

Eleven academic institutions were selected to study mitoxantrone administered on a schedule of 10 mg/m2/d for five days initially and later at 12 mg/m2/d for five days, each given as a 30 minute intravenous (IV) infusion each day. Patients with acute or chronic leukemia were stratified by leukemic type and clinical status and included one group of patients considered to be in relapse after complete remission from previous chemotherapy and another group of patients considered refractory to standard induction and/or salvage chemotherapy. During the initial treatment schedule, complete remissions were obtained in two of seven patients with acute nonlymphoblastic leukemia, in one of three patients with acute lymphoblastic leukemia, but in none of the patients with chronic granulocytic leukemia in blast crisis. The durations of remission for these three patients were 22, 57, and 78 days, respectively. An increase in mitoxantrone dose to 12 mg/m2/d produced complete remissions in 8 of 19 evaluable patients with acute nonlymphoblastic leukemia, in one of ten patients with refractory acute nonlymphoblastic leukemia, and in one of four patients with chronic granulocytic leukemia in blast crisis. Each of these patients required only a single course of mitoxantrone to achieve remission; the median time to remission was 37 days (range 18 to 64 days). Remission duration ranged from 35 days (chronic granulocytic leukemia) to 186 days, with the median duration for those patients with acute nonlymphoblastic leukemia achieving remission being 135 days. Of the six patients with acute lymphoblastic leukemia, none achieved remission at the higher dose level. Drug-related gastrointestinal toxicity included mucositis (25%), diarrhea (21%), and nausea and vomiting (61%). Systemic infection (nonfatal) was experienced by 21% of patients and alopecia by 17%. Other side effects that occurred occasionally were hepatic dysfunction, decreased renal function, confusion, lethargy, anxiety, and fever. Possible drug-related phlebitis developed in one patient, and a single episode of minor epistaxis was reported in another. Cardiovascular toxicity was low. At a mitoxantrone dose of 10 mg/m2/d for five days, one patient developed hypotension, and one episode of congestive heart failure was reported in another. At the higher dose of 12 mg/m2/d, no drug-related hypotension, congestive heart failure, tachycardia, or chest pain were reported. These data indicate that mitoxantrone is a promising single drug for the treatment of acute nonlymphoblastic leukemia and possibly for acute lymphoblastic leukemia.
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PMID:Mitoxantrone in the treatment of relapsed and refractory acute leukemia. 638 65

Two cases of infantile dumping syndrome which developed following Nissen fundoplication for gastroesophageal reflux are described. Both infants were fed postoperatively via a gastrostomy and showed the typical clinical picture of dumping with failure to thrive, intermittent diarrhea, lethargy and pallor postprandially. Several glucose tolerance tests were highly pathological with marked hyperglycemia immediately after a gastrostomy meal followed by hypoglycemia two hours later. In one case HbA1c was significantly elevated which is thought to be an expression of recurrent hyperglycemia. In both infants the first and most impressive clinical sign was absolute refusal or oral feeds. Normal oral food intake was slowly re-established after normalization of blood glucose homeostasis.
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PMID:Dumping syndrome following Nissen's fundoplication: a cause for refusal to feed. 642 40

Groups of 8 male crossbreed domestic goats were given 3 dosage levels of aflatoxin B1 [(AFB1) mg/kg of body weight/day] orally: 0.1 for 34 days; 0.2 for 18 days; or 0.4 for 10 days. Clinical condition, feed consumption, and selected blood values were determined. Clinical signs of toxicosis included decreased feed consumption, slight-to-moderate loss of body weight, mucopurulent nasal discharge, dyspnea, coughing, lethargy, icterus, diarrhea (4 goats), and subnormal body temperature 24 to 48 hours before death. Clinicopathologic changes included increases in total RBC count, PCV, hemoglobin concentration, serum bilirubin concentration, and serum activities of aspartate aminotransferase, isocitric dehydrogenase, and ornithine carbamyl transferase. Goats given the 2 smaller dosage levels of AFB1 had slight increases of serum total protein (TP) concentration compared with control goats, but goats given the larger dosage levels of AFB1 initially had a slight decrease in TP. Aflatoxin had little effect on total WBC count. Serum alanine aminotransferase (ALT) activities in goats given the 2 larger dosage levels of AFB1 were similar to those of control goats, but goats given the smallest dosage level of AFB1 had increased serum ALT activities. Aflatoxin did not produce consistent dose-related changes in serum alkaline phosphatase activities. Seemingly, goats are susceptible to aflatoxin. Onset of clinical signs was dose-related. Onset and magnitude of increases in PCV, hemoglobin concentration, serum bilirubin concentration, and activities of serum aspartate aminotransferase, ornithine carbamyl transferase, and isocitric dehydrogenase were dose-related. Changes in TP and activities of serum ALT and alkaline phosphatase were neither dose-related nor were they potentially useful indicators of toxicosis.
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PMID:Caprine aflatoxicosis: experimental disease and clinical pathologic changes. 643 Jan 34

Thalicarpine, a plant alkaloid of novel structure, was evaluated in a phase II clinical trial. Fourteen previously treated patients with advanced malignant disease were given thalicarpine at a dose of 1100 mg/m2 weekly as a constant 2-hour iv infusion. Common toxic effects included nausea, ECG changes, arm pain, and lethargy; less frequent effects included vomiting, tachycardia, hypotension, pain distant from infusion site, urticaria, chills, diarrhea, and mydriasis. There was no hematologic, hepatic, or renal toxicity. There were no complete or partial objective responses. Although the drug's true response rate in any given tumor type cannot be determined, its absence of activity in man, to date, and the recent closing of its IND, make further clinical investigation with thalicarpine unlikely.
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PMID:An abbreviated phase II trial of thalicarpine. 645 Dec 89


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