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

Rickets is a common and paradoxical feature of infantile malignant osteopetrosis and results from the inability of osteoclasts to maintain a normal calcium-phosphorus balance in the extracellular fluid. Despite a markedly positive total body calcium balance, rickets arises when the serum calcium x phosphorus product is insufficient to mineralize newly formed chondroid and osteoid. In five children with malignant infantile osteopetrosis, there were clinical, radiographic, biochemical, and histologic findings of rickets. Characteristic biochemical abnormalities included hypocalcemia, hypophosphatemia, and elevated levels of serum acid phosphatase, alkaline phosphatase, c-terminal parathyroid hormone, and 1,25-dihydroxyvitamin D. The urinary calcium/creatinine ratio was markedly depressed. The serum calcium x phosphorus product was below 30 in all children at the time the rickets was diagnosed, and above 40 by the time the rickets had resolved. Baseline bone density measurements were markedly elevated in all children (> 5 standard deviation above normal) and showed even significant increases (> 7 SD) when the rickets was treated with vitamin D and calcium. The children showed marked clinical improvement, decreased lethargy, increase in mobility and activity, and stimulation of appetite, without any additional adverse hematologic or neurologic effects. The rickets was reversible in all children: in one by HLA-identical sibling bone marrow transplantation and in four by physiologic doses of vitamin D and calcium. The parathyroid and renal responses to hypocalcemia were appropriate, but glucocorticoids, used in treating the hematologic complications of the disease, may have blunted the intestinal response to maximal vitamin D stimulation. This latter blockade can be overcome by increasing dietary calcium. By liberalizing rather than by restricting calcium and phosphorus intake, hypocalcemia can be minimized, phosphorus metabolism can be improved, and rickets can be cured.
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PMID:Osteopetrorickets. The paradox of plenty. Pathophysiology and treatment. 839 71

Two polar bear (Ursus maritimus) cubs born at the Denver Zoological Gardens were abandoned by a primiparous mother. Lethargic and extremely chilled, the cubs were transported to the zoo hospital for intensive care and hand rearing. Both cubs developed rickets. Dietary changes were instituted, and both cubs completely recovered with the exception of a bowed right femur (genu varum) in the female cub.
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PMID:Rickets in two hand-reared polar bear (Ursus maritimus) cubs. 1036 55

Vitamin D-dependent rickets type 2 in a four-month-old cat A 4-month-old male domestic shorthair cat was examined because of lethargy, vomiting, diarrhea, muscle tremors, and mydriasis. Laboratory evaluation revealed hypocalcemia, hyperphosphatemia, and high intact parathormone and calcitriol concentrations. Findings were compatible with a diagnosis of vitamin D-dependent rickets type 2. Treatment consisted of oral administration of calcium and calcitriol supplements. During the subsequent 18 months, the cat remained clinically normal. Treatment with oral calcium supplements was eventually discontinued, and the cat was able to maintain serum calcium concentrations within reference limits.
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PMID:Vitamin D-dependent rickets type 2 in a four-month-old cat. 1256 96

Prolonged vitamin D deficiency resulting in rickets is seen mainly during rapid growth. A distinct age distribution has been observed in the Copenhagen area where all registered hospital cases of rickets were either infants and toddlers or adolescents from immigrant families. Growth retardation was only present in the infant and toddler group. A state of deficiency occurs months before rickets is obvious on physical examination. Growth failure, lethargy and irritability may be early signs of vitamin D deficiency. Mothers with low vitamin D status give birth to children with low vitamin D status and increased risk of rickets. Reports showing increasing rates of rickets due to insufficient sunlight exposure and inadequate vitamin D intake are cause for serious concern. Many countries (including the USA from 2003) recommend vitamin D supplementation during infancy to avoid rickets resulting from the low vitamin D content of human milk. Without fortification only certain foods such as fatty fish contain more than low amounts of vitamin D, and many children will depend entirely on sun exposure to obtain sufficient vitamin D. The skin has a high capacity to synthesize vitamin D, but if sun exposure is low vitamin D production is insufficient, especially in dark-skinned infants. The use of serum 25-hydroxyvitamin D to evaluate vitamin D status before development of rickets would be helpful; however, there is no agreement on cut-off levels for deficiency and insufficiency. Furthermore, it is not known how marginal vitamin D insufficiency affects children's bones in the long term.
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PMID:Vitamin D and bone health in early life. 1501 81

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 commercially available, renal failure diet was used to manage suspected renal failure in a 10-week-old Shetland sheepdog puppy. Rickets subsequently developed, possibly from low phosphorous intake and an increased calcium to phosphorus ratio. Decreased dietary calcium in addition to decreased phosphorus may have played a role in decreasing bone mineral density. Lethargy, decreased long bone growth, angular limb deformity, and osteopenia occurred, but these signs resolved within 3 months with nutritional management.
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PMID:Dietary-related skeletal changes in a Shetland sheepdog puppy. 1639 96

Renal tubular acidosis is usually associated with chronic renal conditions and is rarely encountered in pregnancy. It may be inherited causing osteomalacia and rickets in children or acquired following autoimmune diseases or following exposure to nephrotoxic agents. It is known to worsen during pregnancy and if left untreated may cause maternal and foetal morbidity or death. We report a 28-year-old woman, gravida 3 para 2, who presented at 30 weeks gestation with lethargy, weakness and generalized myalgia. Investigation revealed severe hypokalaemia and a systemic metabolic acidosis due to proximal renal tubular acidosis. Her previous pregnancies were both complicated by foetal losses at term. Following prompt correction of her electrolyte disturbance and metabolic acidosis, she went on to deliver a healthy female infant at term. Regular evaluation up to 1 year post-partum revealed mild persistence of her hypokalaemia. At 1 year, the infant showed no signs of the disorder and is growing normally.
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PMID:Proximal renal tubular acidosis in pregnancy. A case report and literature review. 1690 7

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

Phosphorus is an essential substance in our body, and hypophosphataemia (HP) is well-described in rickets, refeeding syndrome, diabetic ketoacidosis (DKA), and in chronic alcohol-abuse. However, to our knowledge, HP among severely-malnourished children has not been studied in detail, and information on prevalence, severity, and treatment is scarce. Currently, there are only a few published case reports of HP. This case series describes three cases of HP that presented to Dhaka Hospital of the International Centre for Diarrhoeal Disease Research, Bangladesh (icddr,b). Our first case required mechanical ventilation for respiratory distress associated with severe hypokalaemia (K 1.1 mmol/L) and moderate hypophosphataemia (P 2.1 mg/dL). The second case presented with severe sepsis which was associated with symptomatic hypocalcaemia (Ca 1.68 mmol/L), hypokalaemia (K 1.82 mmol/L), and severe hypophosphataemia (P 0.9 mg/dL). The third case presented with pneumonia and sepsis which were complicated by hypokalaemia (K 2.05 mmol/L) and severe hypophosphataemia (P 1.1 mg/dL). Marked lethargy and severe hypotonia were associated with HP in all of these cases. Manifestations of HP are diverse and can occur in association with other electrolyte imbalances, especially among malnourished children. Malnutrition, combined with sepsis, is one of the major killers of children younger than 5 years of age, and both malnutrition and sepsis can cause HP. It is concluded that the underlying causes of morbidity, including HP, should be actively sought and treated to reduce the mortality of children aged below five years.
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PMID:Hypophosphataemia among severely-malnourished children: case series. 2330 16


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