Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 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

In dialysis patients, deficiency of calcitriol down regulates vitamin D receptor (VDR) and decreases density of Ca sensing receptor, resulting right shift of set point of extra cellular Ca concentrations to release of parathyroid hormone. And then, renal hyperparathyroidism occurs and progresses. The purpose of pulse therapy with calcitriol or its analogue is elevating extra cellular calcitriol level up to supra physiological level, which up regulates VDR and shift the set point to left. The extra cellular calcitriol level after injection of calcitriol cannot compare with the level after oral administration of calcitriol at the same dose. The left shift of set point is investigated 4 weeks after intravenous pulse therapy with calcitriol or maxacalcitol, and degree of shift to the left depends on the single dose of these medicines. There is another advantage of intravenous pulse therapy, which takes no account of drug compliance or existence of malabsorption of lipid soluble vitamins.
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PMID:[Advantage of intravenous pulse therapy with calcitriol or maxacalcitol in dialysis patients with renal hyperparathyroidism]. 1557 14

The somatostatin analogue lanreotide is effective in reducing growth hormone levels in patients with acromegaly. Acromegaly is characterized by calcium homeostasis alterations. The aim of our study was to evaluate the effects of lanreotide on bone turnover markers in a group of acromegalic patients and to verify a possible increase of intact parathormone (iPTH) levels in a transient or persistent way. Serum GH, IGF-I and serum and urinary markers of bone metabolism were measured before treatment and on months 3 and 24. In short-term treatment (3 months), lanreotide significantly decreased GH, IGF-I, serum calcium, osteocalcin and alkaline phosphatase levels, but increased iPTH level (49 +/- 16.7 vs pre-treatment 28.3 +/- 7.6 ng/L, p<0.001). During long-term study (24 months) GH and IGF-I were significantly still low; serum calcium and alkaline phosphatase levels returned to pre-treatment levels. iPTH level was significantly still higher compared with pre-treatment (46.4 +/- 9.2 vs 28.3 +/- 7.6 ng/L, p<0.05). No changes were seen in serum albumin, creatinine and vitamin D during short and long term treatment. The changes of most bone markers during lanreotide treatment can be explained by the decrease of GH and IGF-I. The increase of iPTH concentration suggests that lanreotide has ulterior and long-standing actions on calcium homeostasis: intestinal malabsorption of calcium due to the lanreotide could contribute to this "secondary" hyperparathyroidism. The clinical relevance of these long-standing effects needs to be further investigated.
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PMID:Long-term treatment of acromegaly with lanreotide: evidence of increased serum parathormone concentration. 1564 68

During growth, estrogen deficiency in females may produce increased bone size as a result of removal of inhibition of periosteal apposition, while failed endosteal apposition produces thin cortices and trabeculae in the smaller bone. In males, androgen deficiency produces reduced periosteal and endosteal apposition, reduced bone size, and cortical and trabecular thickness. At completion of longitudinal growth, advancing age is associated with emergence of a negative bone balance in each basic multicellular unit (BMU) because of reduced bone formation. Bone loss occurs, but slowly because the remodeling rate is slow. In midlife, in females, estrogen deficiency increases remodeling rate, increases the volume of bone resorbed, and decreases the volume of bone formed in each of the numerous BMUs remodeling bone on its endosteal (endocortical, trabecular, intracortical) surfaces so bone loss accelerates. In males, remodeling rate remains slow and is driven largely by reduced bone formation in the BMU. Hypogonadism in 20% to 30% of elderly men contributes to bone loss. In both sexes, calcium malabsorption and secondary hyperparathyroidism may partly be sex-hormone dependent and contributes to cortical bone loss. Concurrent periosteal apposition partly offsets endosteal bone loss, but less so in women than in men. More women than men fracture because their smaller skeleton incurs greater architectural damage and adapts less by periosteal apposition. Sex hormone deficiency during growth and aging is pivotal in the pathogenesis of bone fragility.
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PMID:Estrogen, androgen, and the pathogenesis of bone fragility in women and men. 1603 88

In order to illustrate a particular circumstance of diagnosis of celiac disease, we report the case of 54-year-old women with a history of thyroid enlargement with normal thyroid function and positive anti-peroxidase antibodies. Immediately after total thyroidectomy with preservation of the parathyroid glands, she developed tetany with total serum calcium level at 50mg/l. Intravenous calcium infusion increased the calcium level and led to resolution of hypocalcemia-induced signs but there was no result when calcium and vitamin D were taken orally. The diagnosis of malabsorption was very probable in light of the family history of celiac disease, the anemia and the hypoalbuminemia. The diagnosis was confirmed by antibodies assay and endoscopy. The PTH level was less than 1 pg/l and radiography showed signs of hyperparathyroidism. Gluten-free diet, calcium and vitamin D led to an improvement of serum calcium.
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PMID:[Celiac disease revealed by hypocalcemia complicating total thyroidectomy: a case report]. 1707 43

Primary intestinal lymphangiectasis (PIL), also known as Waldmann's disease, is a rare protein-losing enteropathy characterized by abnormal enlargement of the lymphatic ducts in the bowel wall. The symptoms usually start in early infancy. We report a case of osteomalacia in a 63-year-old patient with delayed-onset of PIL, for which she was on dietary treatment. She presented with a 3-year history of mechanical pain in the back and pelvis. Mild ascites and edema with functional impairment of the lower limbs were noted. The neurological evaluation was normal. Blood tests showed hypocalcemia, hypophosphatemia, alkaline phosphatase elevation, and evidence of intestinal malabsorption. Radiographs of the pelvis disclosed a fracture, Looser's zones in the iliopubic rami and left femoral neck, and a washed-out appearance of the vertebras. Dual-energy X-ray absorptiometry showed bone loss with T-score values of -1.2SD at the lumbar spine and -2.5SD at the femoral necks. A diagnosis of osteomalacia related to vitamin D deficiency was given. Serum 25-OH-vitamin D was 18.2ng/ml (normal, 20-40ng/ml) and serum parathyroid hormone was 620pg/ml (normal, 15-65pg/ml), suggesting secondary hyperparathyroidism. Intramuscular vitamin D was given, together with oral calcium and an adequate diet. At follow-up 8 months later, small improvements were noted in the symptoms and absorptiometry findings.
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PMID:Osteomalacia in a patient with primary intestinal lymphangiectasis (Waldmann's disease). 1790 Sep 62

Chronic vitamin D deficiency, inadequate calcium intake, and secondary hyperparathyroidism are common in obese individuals, placing them at risk for low bone mass and metabolic bone disease. After bariatric surgery, they are at even higher risk, owing to malabsorption and decreased oral intake. Meticulous preoperative screening, judicious use of vitamin and mineral supplements, addressing modifiable risk factors, and monitoring the absorption of key nutrients postoperatively are essential in preventing metabolic bone disease in bariatric surgery patients.
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PMID:Perioperative management of bariatric surgery patients: focus on metabolic bone disease. 1855 75

Contrary to frequent claims, vitamin D insufficiency does not generally cause malabsorption of calcium because serum 1,25(OH)(2)D, which is the major determinant of calcium absorption, is maintained by secondary hyperparathyroidism. Nevertheless, because malabsorption of calcium has been described in osteomalacia, there must be a 25(OH)D level below which the serum 1,25(OH)(2)D can no longer be sustained, although it has never been defined. This paper seeks to define it. We examined the records of 3661 patients and found 319 with a serum 25(OH)D < or = 40 nM, in whom calcium absorption, serum calcium, PTH, bone markers, and vitamin D metabolites had been measured. They were grouped according to their serum 25(OH)D into four categories, 0-10, 11-20, 21-30, and 31-40 nM, and differences between the groups were tested by ANOVA. Correlations between the variables were also examined. Serum calcium, 1,25(OH)(2)D, and calcium absorption were significantly decreased and serum PTH and alkaline phosphatase (ALP) and urine hydroxyproline were increased in those with 25(OH)D < or = 10 nM. Serum ALP and urine hydroxyproline were more strongly related, inversely, to calcium absorption than to the vitamin D metabolites. We conclude that vitamin D deficiency does not reduce serum 1,25(OH)(2)D, and therefore calcium absorption, until the serum 25(OH)D falls to approximately 10 nM. At this level, the substrate concentration seems to be insufficient to maintain the level of the dihydroxy metabolite despite secondary hyperparathyroidism. Further studies are needed to see how these changes correlate with the histological changes of osteomalacia.
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PMID:Vitamin D metabolites and calcium absorption in severe vitamin D deficiency. 1859 33

A case of a brown tumor due to iatrogenic malabsorption following biliopancreatic diversion (BPD) is presented. A 52 year old women with a history of BPD 2 years before was referred to orthopedic surgery because of a painful lytic lesion of the left ankle. A bone biopsy revealed a giant cell tumor compatible with the diagnosis of a brown tumor. Subsequent metabolic evaluation showed severe 25-hydroxy vitamin D deficiency and secondary hyperparathyroidism (PTH 60 ng/L or twice the upper normal limit). Bone mineral density was decreased at the femoral neck (0.50 g/cm(2) ; T score of -3.92 or 66% of the expected value) and lumbar spine (T score of -1.75 or 93% of the expected value). A brown tumor can be the presenting symptom of iatrogenic malabsorption due to BPD. This case illustrates the severity of potential bone complications after BPD and the necessity of lifelong surveillance and vitamin supplements after BPD.
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PMID:A brown tumor after biliopancreatic diversion for severe obesity. 1912 47

We challenge the widespread assumption that malabsorption of calcium per se causes secondary hyperparathyroidism. Serum parathyroid hormone (PTH) does not rise at the menopause despite the fall in calcium absorption, nor is it raised in osteoporotic women with vertebral fractures despite their low calcium absorption. The age-related rise in serum PTH can be accounted for by the age-related fall in serum 25(OH)D and/or decline in renal function with consequent loss of the calcemic action of vitamin D on bone. The reference interval for serum PTH is established in the fasting state when it is at the top of its diurnal cycle and is maintaining serum ionized calcium at the expense of bone to meet the calcium being lost through skin, bowel, and kidneys. There is no evidence that the fasting PTH is influenced by the previous day's intake or absorption of calcium, although it can be lowered by a large evening calcium supplement. Malabsorption of calcium-like dietary calcium deficiency-is a risk factor for osteoporosis because it reduces or prevents the normal food-related daytime fall in PTH and bone resorption, not because it causes secondary hyperparathyroidism.
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PMID:Calcium malabsorption does not cause secondary hyperparathyroidism. 1948 68


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