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)

Eighty-four patients have undergone surgical exploration following a clinical diagnosis of hyperpathyroidism over a 20-year period. Urinary tract calculi were the major indication for exploration, and 90% of these patients had recurrent calculi. Osteitis fibrosa was a rare presentation of hyperparathyroidism. Lethargy, sometimes profound, was an important symptom, in some instances the dominant feature. Persistent hypercalcaemia remains the chief diagnostic investigation, with helpful confirmation from estimation of the parathyroid hormone level. Little attempt was made in this series to utilize preoperative localization techniques, reliance being placed on meticulous bloodless surgery to find normal and abnormal parathyroid tissue. Eighty-five explorations were carried out in the 84 patients. Seventy-four of the explorations were successful, converting the patient to a normocalcaemic state. Of these, 63 had a single adenoma (86%).
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PMID:Twenty years' experience with parathyroid exploration. 28 Dec 16

In a consecutive series of 100 neck explorations for primary hyperparathyroidism, 42 patients were 60 years of age or older; in this group of elderly patients the surgical cure rate was 100%. These patients were reviewed retrospectively by means of a structure interview. Twenty-one patients had had preoperative neuromuscular symptoms that ranged from coma to subjective muscular weakness. These patients had significantly-higher preoperative serum calcium and parathyroid hormone levels than did 21 patients without neuromuscular symptoms (P = 0.003 and P = 0.046, respectively). Most of the neuromuscular symptoms improved in the postoperative period. In particular, 15 of 17 patients with muscle weakness reported a significant improvement, while 14 of 15 patients who suffered from fatigue and lethargy reported an improvement. An improvement also occurred in the level of day-to-day function in eight patients. While surgery for primary hyperparathyroidism generally is undertaken for a specific indication, such as severe hypercalcaemia or renal stones, it appears from this study that neuromuscular symptoms also may improve, particularly in elderly patients.
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PMID:Neuromuscular symptoms in elderly patients with hyperparathyroidism: improvement with parathyroid surgery. 339 14

Hyperparathyroid crisis is a rare disease but should be suspected in acutely ill patients complaining of weakness, lethargy, nausea, vomiting, confusion and abdominal pain. Despite the variety of clinical manifestations, the syndrome forms a distinctive pattern which, in the presence of a serum calcium level greater than 16 mg/100 ml, should be recognized. The most difficult problem in diagnosis is the differentiation of hyperparathyroid crisis from ectopic parathyroid hormone-producing tumors. The disease is an endocrine emergency which requires prompt surgery after rapid correction of dehydration and hypercalcemia. The best results are achieved by removing offending parathyroid tissue within 72 hours after the onset of symptoms.
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PMID:Primary hyperparathyroidism: hyperparathyroid crisis. 730 6

An 85-year-old man who presented with depression and lethargy was found to have hypercalcemia, normal phosphorous, and low-normal intact parathyroid hormone level. Work-up revealed no evidence of a malignant or inflammatory process. However, 24-hour urinary calcium excretion was increased, 1,25 dihydroxy (OH2) vitamin D3 level was elevated, and angiotensin-converting enzyme (ACE) level was twice normal. The patient responded to a trial of steroids and his 1,25-OH2 vitamin D3 and ACE levels decreased to within normal limits. The patient has remained eucalcemic on low-dose steroids.
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PMID:Hypercalcemia associated with an elevated 1,25 dihydroxy vitamin D3 level and an elevated angiotensin-converting enzyme level in a patient without evidence of sarcoidosis or malignancy. 805 95

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

Primary hyperparathyroidism (PHP) is an infrequently diagnosed disorder in cats. In this report the signs and symptoms of two cats with hypercalcaemia due to PHP are described, together with diagnostic approach, results of treatment, and immunohistochemical findings. A 9-year-old and a 13-year-old neutered male domestic shorthair cat were presented with signs of lethargy, anorexia, and vomiting. Both cats had persistent hypercalcaemia and normo- to hypophosphataemia. Cytological examination of a fine-needle aspiration biopsy sample of a palpable cervical mass revealed groups of benign glandular-epithelial cells in one cat. In the other cat no cervical mass was palpable. In this cat plasma parathyroid hormone (PTH) levels were measured repeatedly and these values exceeded the maximum reference value on two occasions. Following exclusion of other causes of hypercalcaemia both cats were subjected to neck surgery and in both a solitary parathyroid adenoma was removed. The adenomas contained an abundance of PTH, as demonstrated by immunohistochemical techniques. Plasma calcium and phosphate concentrations returned to within, reference ranges postoperatively. Recovery was uncomplicated and there were no signs of recurrence on follow-up examinations.
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PMID:Primary hyperparathyroidism in two cats. 922 38

A six-month-old, intact female Himalayan kitten was presented to the University of Tennessee Veterinary Medical Teaching Hospital for evaluation of chronic lethargy, inappetance, muscle tremors, and seizures. Upon physical examination, the kitten was very small for her age. Bilateral, incipient-to-immature cataracts were seen on ophthalmic examination. Severe hypocalcemia and concurrent hyperphosphatemia were identified on initial diagnostic evaluation. A diagnosis of primary hypoparathyroidism was made by identifying reduced concentrations of parathyroid hormone (PTH). The kitten responded well to treatment with calcium, vitamin D, and aluminum hydroxide and is clinically normal 17 months after initiation of treatment.
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PMID:Hypocalcemia and hyperphosphatemia due to primary hypoparathyroidism in a six-month-old kitten. 982 87

Primary hyperparathyroidism is diagnosed with increasing incidence. Many patients are misinterpreted as being asymptomatic, but they do indeed suffer from a broad variety of non-specific symptoms. Investigations show that patients with primary hyperparathyroidism may be lethargic, apathic, demented and depressed. Many suffer from bone and joint pain. Surgical treatment can be done with few complications and a high cure rate, resulting in reversal of symptoms. Since symptoms do not correlate with S-Ca++ or S-parathyroid hormone and since the symptoms can be attributed to many other causes, we need more research to find those patients, who will benefit from surgical treatment.
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PMID:[Non-specific symptoms and primary hyperparathyroidism]. 1100 37

Severe hypomagnesemia (0.8 mg/dl; reference range, 1.6 to 2.3 mg/dl), hypocalcemia, and protein-losing enteropathy were identified in a 5-year-old castrated male 3-kg (6.6 lb) Shih Tzu examined because of anorexia, lethargy, paresis, and abdominal distention. Histologic examination of intestinal biopsy specimens revealed lymphangiectasia and lymphocytic, plasmacytic, neutrophilic infiltrates. Initial treatment included administration of magnesium (0.80 mEq/kg [0.36 mEq/lb]) of body weight in a balanced electrolyte solution. This treatment resulted in normalization of the serum magnesium concentration (1.7 mg/dl); resolution of the lethargy, paresis, and tachycardia; and an increase in the serum parathyroid hormone and ionized calcium concentrations. Findings were consistent with secondary hypoparathyroidism attributable to hypomagnesemia. Magnesium concentration should be monitored in all dogs with gastrointestinal tract disease, especially those with protein-losing enteropathy, anorexia, and weakness.
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PMID:Secondary hypoparathyroidism attributed to hypomagnesemia in a dog with protein-losing enteropathy. 1176 24

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


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