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)

Hyperparathyroidism is a disease characterized by hypercalcemia with hypophosphoremia resulting from increased secretion of parathyroid hormone (PTH). The disease may be divided into 3 forms: a) primary, b) secondary, c) tertiary (secondary refractory form). Primary hyperparathyroidism is rare in children; hyperplasia is more frequent during the early years of life (neonates and infants) and is difficult to distinguish from adenoma in children. The disease may be asymptomatic; elevated calcemia levels (>12 <13.5 mg/dl) are accompanied by anorexia, asthenia and persistent stipsis; severely elevated concentrations (>13.5 mg/dl) are accompanied by nausea, vomiting, polyuria due to osmosis, with dehydration and progressive onset of lethargy, stupor and coma. Osteopenia or osteitis fibrosa cystica may be present due to augmented bone resorption. Height and weight increases are altered due to anorexia and dehydration. Differential diagnosis includes iatrogenic causes of hypercalcemia (excessive vitamin D intake, prolonged immobilization, etc.) and idiopathic familial hypercalcemia. Emergency treatment is required in cases of extremely elevated hypercalcemia (Ca >13.5-14 mg/dl), due to risk of injury to the heart, the central nervous system, the gastrointestinal tract and the kidneys. The 4 cardinal points of treatment are: hydration, calciuresis, inhibition of bone calcium resorption, treatment of the cause underlying hyperparathyroidism. Secondary hyperparathyroidism is found in cases where chronic hypocalcemia is present, particularly in chronic renal failure, untreated deficiency rickets, chronic intestinal malabsorption, hepatobiliary disease, types I and II vitamin D-dependent rickets, tubular acidosis or Fanconi's syndrome. The tertiary form is distinguished by the autonomous nature of the parathyroid glands which have become hypertrophic/hyperplastic due to uncontrollable, chronic severe renal failure. It can also be of iatrogenic origin due to excessive intake of inorganic phosphates in familial hypophosphatemic rickets or chronic vitamin D deficiency.
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PMID:Hyperparathyroidism. 1524 24

A three-month-old male Bull Terrier was referred to the Animal Medical Centre, Nihon University with chief complaints of subacute emesis and lethargy. Severe leukocytosis, high CRP, hypercalcemia and hypochloremia were detected. Moreover, severe calcification of gingival mucosa and abdominal skin, and abnormalities of the skeletal system were discerned. Abdominal X-ray and endoscopic examination revealed ulcer and hemorrhage on the mucosal membrane of the stomach. This might have been due to injections of high dose vitamin D at 3 and 2 weeks ago by another practioner, according to the detailed history of medication. After two months, a gastrointestinal and skin disorder disappeared, although calcification of the stomach membranes remained and abnormality of the skeletal system had worsened. Therefore, vitamin D should be carefully administrated to a puppy.
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PMID:Severe calcification of mucocutaneous and gastrointestinal tissues induced by high dose administration of vitamin D in a puppy. 1547 80

A three-year-old Border collie was presented with a two-week history of lethargy, stiff gait, polydipsia and polyuria. Biochemical analysis revealed hypercalcaemia. Serum concentrations of 25-hydroxyvitamin D (25[OH]D) and 1,25-dihydroxyvitamin D (1,25[OH]2D) were markedly elevated and parathyroid hormone was undetectable. Subsequent analysis of the dog's diet revealed that the food contained excessive amounts of vitamin D. The hypercalcaemia resolved following treatment with bisphosphonates and dietary change. Hypervitaminosis D was diagnosed in a second unrelated dog, which had been fed the same brand of dog food as case 1. The dog was also hypercalcaemic and had markedly elevated serum concentrations of 25(OH)D and 1,25(OH)2D. Hypervitaminosis D in dogs has been reported to occur secondarily to ingestion of either rodenticides containing cholecalciferol or antipsoriatic ointments that contain vitamin D analogues. Hypervitaminosis D has also been reported following the treatment of hypoparathyroidism. To the authors' knowledge, this is the first report of hypervitaminosis D in dogs following the accidental over supplementation of a commercial diet with vitamin D. While the benefits of adequate dietary vitamin D are well established in dogs, the potential deleterious effects of over supplementation of vitamin D should also be acknowledged.
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PMID:Hypercalcaemia in two dogs caused by excessive dietary supplementation of vitamin D. 1603 50

The dose of vitamin D that some researchers recommend as optimally therapeutic exceeds that officially recognized as safe by a factor of two; it is therefore important to determine the precise mechanism by which excessive doses of vitamin D exert toxicity so that physicians and other health care practitioners may understand how to use optimally therapeutic doses of this vitamin without the risk of adverse effects. Although the toxicity of vitamin D has conventionally been attributed to its induction of hypercalcemia, animal studies show that the toxic endpoints observed in response to hypervitaminosis D such as anorexia, lethargy, growth retardation, bone resorption, soft tissue calcification, and death can be dissociated from the hypercalcemia that usually accompanies them, demanding that an alternative explanation for the mechanism of vitamin D toxicity be developed. The hypothesis presented in this paper proposes the novel understanding that vitamin D exerts toxicity by inducing a deficiency of vitamin K. According to this model, vitamin D increases the expression of proteins whose activation depends on vitamin K-mediated carboxylation; as the demand for carboxylation increases, the pool of vitamin K is depleted. Since vitamin K is essential to the nervous system and plays important roles in protecting against bone loss and calcification of the peripheral soft tissues, its deficiency results in the symptoms associated with hypervitaminosis D. This hypothesis is circumstantially supported by the observation that animals deficient in vitamin K or vitamin K-dependent proteins exhibit remarkable similarities to animals fed toxic doses of vitamin D, and the observation that vitamin D and the vitamin K-inhibitor Warfarin have similar toxicity profiles and exert toxicity synergistically when combined. The hypothesis further proposes that vitamin A protects against the toxicity of vitamin D by decreasing the expression of vitamin K-dependent proteins and thereby exerting a vitamin K-sparing effect. If animal experiments can confirm this hypothesis, the models by which the maximum safe dose is determined would need to be revised. Physicians and other health care practitioners would be able to treat patients with doses of vitamin D that possess greater therapeutic value than those currently being used while avoiding the risk of adverse effects by administering vitamin D together with vitamins A and K.
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PMID:Vitamin D toxicity redefined: vitamin K and the molecular mechanism. 1714 39

We retrospectively studied seven children (six girls, one boy) aged from 7.5 to 25 months who presented to our institution after taking large doses of vitamin D (900 000-4 000 000 U) prescribed by medical practitioners for wrong indications like failure to thrive, etc. The clinical manifestations were constipation, decreased appetite, lethargy, polyuria, dehydration and failure to thrive. All patients had hypercalcemia (serum calcium ranging from 12 to 16.8 mg/dl), high 25[OH]D levels (ranging from 96 to >150 ng/ml), suppressed intact parathyroid hormone (ranging from <3 to 8.1 pg/ml). Hypercalciuria (urinary calcium/creatinine ranging from 1 to 2.45) was found in all patients, while nephrocalcinosis was present in five patients. All were treated with intravenous fluids, oral prednisolone, restriction of calcium in diet, while four patients received pamidronate infusion for reducing hypercalcemia.
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PMID:Hypercalcemia due to hypervitaminosis D: report of seven patients. 1933 14

Most common causes of hypercalcemia are hyperparathyroidism, malignancy, vitamin D-mediated conditions such as sarcoidosis, and vitamin D toxicity. Less commonly, hypercalcemia can be caused by drugs such as thiazide diuretics and lithium. Mild hypercalcemia is usually asymptomatic but severe hypercalcemia is associated with nausea, vomiting, abdominal pain, excessive thirst, muscle weakness, lethargy, confusion, and fatigue. We are reporting a case of abdominal pain and altered mental status caused by thiazide-induced severe hypercalcemia of 19.8 mg/dL. This is the most severe case of thiazide-induced hypercalcemia that we have seen reported. Patients on thiazide diuretics should have their electrolytes frequently checked, especially patients on calcium supplements. Management usually includes hydration and discontinuation of drugs causing hypercalcemia.
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PMID:Thiazide-induced severe hypercalcemia: a case report and review of literature. 2006 44

Sprague-Dawley rats were made chronically vitamin D deficient (VDD) and hypocalcemic, or VDD and normocalcemic. Rickets, severely reduced body weight, hair shedding, lethargy, muscular paralysis and a high mortality rate are characteristic features of the male VDD/hypocalcemic animals. An assessment was made of the neurotransmitter status of the VDD-hypocalcemic and VDD/normocalcemic animals. In nine out of eleven regions of the CNS studied, the increase in GABA induced by the GABA-T inhibitor ethanolamine sulphate (EOS) was significantly higher (P < 0.05 or P < 0.01) in the VDD/hypocalcemic group vs the normal controls. However, the EOS-mediated increase in GABA was similar in the VDD/normocalcemic and normal control groups suggesting that hypocalcemia is the likely cause of the increased GABA turnover in the VDD/hypocalcemic rats. Glutamate, dopamine, dihydroxyphenylacetic acid, homovanillic acid and norepinephrine, were also analysed in representative regions of the CNS. Their concentrations were not affected in any consistent way in either the VDD/hypocalcemic group or VDD/normocalcemic groups vs the normal controls. Therefore, despite the chronic, severe pathology induced by vitamin D deficiency and hypocalcemia, the neurotransmitters studied appeared to be normal in the CNS of these animals.
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PMID:Neurotransmitters in the CNS of the vitamin D deficient, hypocalcemic rat. 2050

This article describes the case of a 16-month-old Hispanic male toddler with cow's milk allergy living in northern California who was admitted to a children's hospital for weight loss and markedly elevated levels of serum alkaline phosphatase and parathyroid hormone. At a routine outpatient well-child visit, his mother expressed concern about a decrease in his appetite and activity level. A detailed diet history revealed that breast milk was his primary source of nutrition during his first year of life and he had not been given supplemental vitamins. With attempts to introduce cow's milk formula, he had developed a rash and swelling around the mouth. Shortly after his first birthday, his mother weaned him from breast milk and introduced unfortified rice milk as a palatable milk substitute. Upon admission he was pale and lethargic; his laboratory studies were remarkable for elevated serum alkaline phosphatase and parathyroid hormone and low levels of phosphorus, 25-hydroxy-vitamin D, and ferritin. Lower extremity radiographic studies were consistent with rickets. After 5 weeks of therapy with vitamin D(3) and iron, his serum 25-hydroxy-vitamin D level normalized. Within 12 weeks following therapy, the child demonstrated significant clinical improvement, with resolution of growth failure and bone reossification. His activity level had returned to normal. This case emphasizes the importance of adequate vitamin D intake for children with special attention to those who might have nutrition deficiencies attributable to milk allergy.
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PMID:Vitamin D--deficient rickets in a child with cow's milk allergy. 2809 94

A 67-year-old female was admitted to the hospital with a history of lethargy, memory impairment, confusion, anorexia and gait imbalance for 2 weeks duration. She did not have any history of fall or head injury. She had total hip replacement 1 year back and was on orthopedic follow-up. Magnetic resonance imaging (MRI) on admission revealed no focal abnormalities. Routine biochemistry detected hypercalcemia, and she was treated with I/V fluid, diuretics and glucocorticoids. She was screened thoroughly to exclude occult malignancy. After 7 days of admission, a follow-up orthopedic prescription revealed that she was getting inj. Arachitol 6 lac units every week for last 3 months. On the 9(th) day of admission, she was detected to have very high serum 25(OH) vitamin D level (254.70 ng/ml). Patient was discharged after 2 weeks after her serum calcium came down to normal range with the advice of no dietary calcium and vitamin D intake. Her 25(OH) vitamin D level remained high for the next 6 months. Now she is completely asymptomatic and her serum 25(OH) D is normal.
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PMID:Vitamin D toxicity. 2247 Aug 72

Phenytoin is indicated for tonic clonic seizures and status epilepticus. Phenytoin is known to deplete vital nutrients such as calcium, folic acid, vitamin D, vitamin K, biotin, carnitine, copper, selenium and zinc. Depletion of nutrients is known to cause adverse effects such as ataxia, nystagmus, lethargy, slurred speech and hematological disturbances. Spirulina is a rich source of vital nutrients including iron. It is proposed to study the effect of spirulina on the hematological disturbances induced by phenytoin. Seven groups of male albino rats weighing 130-150g were used. Each group consisted of six animals. Phenytoin at a dose of 20mg/kg/day dissolved in water, spirulina 50, 100, 200 mg/kg/day suspended in 1% tween 80 alone or in combination with phenytoin was administered for 30 days. Hemoglobin content, total leucocyte and erythrocyte count were determined on 30(th) day. Phenytoin significantly decreased the hemoglobin content, total erythrocyte and leukocyte count. Spirulina did not show any effect at the lower dose of 50 and 100mg/kg and higher dose of 200mg/ kg significantly elevated hemoglobin content. Spirulina at a dose of 200mg/kg/day in combination with phenytoin reversed the phenytoin induced decrease in hemoglobin content, total erythrocyte and leukocyte count. The results of this study indicates that supplementation of phenytoin with spirulina may reverse the hematological disturbances induced by phenytoin.
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PMID:Influence of spirulina on the phenytoin induced haematological changes. 2255 35


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