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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathology of the parathyroid glands in two cases in which hyperparathyroidism was associated with chronic renal disease and 10 in which the association was with the malabsorption syndrome is described. It is concluded that whereas in chronic renal disease the development of an autonomous adenoma may be preceded by anatomical secondary diffuse hyperplasia such a stage is not proven when the adenomas develop against a background of the malabsorption syndrome. The importance of this latter association is stressed.
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PMID:Parathyroid adenomas associated with the malabsorption syndrome and chronic renal disease. 543 Apr 25

In our first 200 cases of primary hyperparathyroidism confirmed by operation 12 were also shown to have a long history either of a malabsorption syndrome or of chronic renal-glomerular failure. We consider that they first went through a phase of secondary hyperparathyroidism, during which one or more of the glands became autonomous adenamata. This then produced the biochemical changes of "primary" hyperparathyroidism, necessitating excision of the adenoma. This condition is best described as "tertiary" hyperparathyroidism. The transition from secondary to tertiary hyperparathyroidism occurred in four of the 12 patients while under our observation. We think the same process can be traced retrospectively in the other eight cases. The concept of tertiary hyperparathyroidism may help to explain the high incidence of other diseases in association with primary hyperparathyroidism.The behaviour of the parathyroid glands provides a valuable model for the investigation of tumour formation in man. All states occurred in our patients with primary hyperparathyroidism, from normal through hyperplasia to adenoma formation and finally to parathyroid carcinoma.
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PMID:Tertiary hyperparathyroidism. 569 Dec

In the present case a primary hyperparathyroidism was aggravated by postgastrectomy bone disease and led to a spontaneous fracture of the left femur and to a pseudofracture of the right femur. Renal symptoms like concrements or nephrocalcinosis were based on the intestinal conditioned malabsorption of vitamin-D and calcium not evident. Radiologically there was a mixed pattern of ostitis fibrosa cystica generalisata von Recklinghausen and osteomalacia respectively osteoporosis based on postgastrectomy bone disease. Treatment was fully effective consisting of exstirpation of the adenoma and substitution of calcium and vitamin-D and ingestion of digestive enzymes and many little meals corresponding to the prescriptions of nutrition for partially gastrectomised patients.
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PMID:[Left spontaneous femoral fracture in primary hyperparathyroidism and postgastrectomy bone disease following a Billroth II stomach resection]. 662 60

Primary hyperparathyroidism is seldom associated with other autoimmune disorders. The presence of normocalcemia in primary hyperparathyroidism should prompt the physician to look for vitamin D deficiency. This observation concerns a 34-year-old vegetarian woman with combined primary hyperparathyroidism, Graves' disease, and celiac disease. The patient presented with severe bone deformities; she was unable to walk, and had severe muscular weakness and weight loss. Biochemical findings revealed severe hyperparathyroidism with normocalcemia, hypophosphatemia, very low urinary calcium, and low 25-hydroxy vitamin D level. Thyroid tests showed hyperthyroidism with positive thyroid receptor antibodies, confirming the presence of Graves' disease. Positive antigliadin and antireticulin antibodies and complete villous atrophy on duodenal biopsy established the presence of celiac disease. The patient underwent a near-total thyroidectomy, with the removal of a parathyroid adenoma. To our knowledge, this observation is the first finding of an association between celiac disease, Graves' disease, and primary hyperparathyroidism. It emphasizes the need to rule out intestinal malabsorption in the case of normocalcemic hyperparathyroidism.
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PMID:Osteomalacia secondary to celiac disease, primary hyperparathyroidism, and Graves' disease. 947 14

In South African blacks colorectal cancers are uncommon and adenomatous polyps are rare, despite major changes in diet and lifestyle in the large urbanized community of Soweto (population over 3 million). Factors favouring adenomas formation are changes in bowel function. Thus, stool weights, defaecation frequencies, oro-caecal transit times and whole-gut transit times in Sowetans approximate those of western populations. Moreover a measure of westernization of diet has occurred, the salient feature being a greatly reduced fibre intake (14 g daily). Factors thought to inhibit adenoma formation are physiological malabsorption of maize, lactose and fructose. Sucrose activity is significantly lowered compared with whites. With regard to diet, fat consumption is well below that of western societies. There are differences in colon cell proliferation, faecal short chain fatty acids, faecal pH and colonic microflora compared with white groups. Equivocal factors that may be involved in adenoma formation are time trends and genetic background. In the context of the above it is apparent that in South African blacks inhibiting factors outweigh promotive factors in adenoma formation.
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PMID:Rarity of colorectal adenomas in the African black population. 988 82

3 conditions may be responsible for absence of menstruation in women taking the minipill: pregnancy, extrauterine pregnancy, or endometrial atrophy which is the most frequent cause but should be treated only after the other 2 possibilities are excluded. The most frequent cause of pregnancy while taking minipills is error in pill consumption due to forgetting, but malabsorption due to vomiting less than 2 hours after taking the pill or an interaction with some other medication may be responsible. The possibility of extrauterine pregnancy should be systematically considered, and the possibility that a micropill and not a minipill is involved should be ruled out. With a sequential minipill contraceptive efficacy does not reach 100% but iatrogenic amenorrhea is infrequent because of the strong dose of ethinyl estradiol. In the case of a preexisting amenorrhea that does not respond to the estrogen or progestin dose, a prolactin adenoma may be suspected. After 2 consecutive beta tests of pregnancy 8 days apart have been negative, it may be concluded that endometrial atrophy is the cause of the amenorrhea. Unprotected sexual relations should be avoided and the patient should be given a fast-acting combined oral contraceptive such as Lutestral to induce bleeding, after which the minipill can be resumed. If unprotected intercourse occurs there is a risk of pregnancy since amenorrhea and anovulation are not synonymous. A morning after pill can be used if the unprotected sexual relations occurred within the last 72 hours. If a pill was forgotten or probably forgotten before the emenorrhea, the most prudent attitude would be to consider the pill to have been ineffective during the preceding 21 days and to test for pregnancy. Unprotected intercourse should be avoided, a fast-acting combination pill should be prescribed to induce bleeding, and the minipill should then be resumed. Amenorrhea in the 1st month of use after an abortion is not significant. This secondary effect of the minipill should be explained to the patient to avoid unnecessary worry.
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PMID:[Do's and don'ts in treating amenorrhea in women taking the minipill]. 1226 2

Heat-stable enterotoxin (STa), elaborated by enterotoxigenic Echerichia coli, is a worldwide cause of secretory diarrhea in infants and travelers. Both STa and guanylin, a peptide structurally similar to STa, increase intracellular cGMP levels after binding to the same intestinal receptor, guanylate cyclase C (GC-C). Distinct from its role as an intestinal secretagogue, guanylin may also have a role in intestinal proliferation, as guanylin expression is lost in intestinal adenomas. To determine the function of guanylin in intestinal epithelia, guanylin null mice were generated using a Cre/loxP-based targeting vector. Guanylin null mice grew normally, were fertile and showed no signs of malabsorption. However, the levels of cGMP in colonic mucosa of guanylin null mice were significantly reduced. The colonic epithelial cell migration rate was increased and increased numbers of colonocytes expressing proliferating cell nuclear antigen (PCNA) were present in crypts of guanylin null mice as well. The apoptotic index was similar in guanylin null mice and littermate controls. We conclude from these studies that loss of guanylin results in increased proliferation of colonic epithelia. We speculate that the increase in colonocyte number is related to decreased levels of cGMP and that this increase in proliferation plays a role in susceptibility to intestinal adenoma formation and/or progression.
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PMID:Targeted inactivation of the mouse guanylin gene results in altered dynamics of colonic epithelial proliferation. 1246 32

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

Coeliac disease is a gluten-sensitive enteropathy of varying severity. Osteomalacia and hypocalcaemia can result from malabsorption of vitamin D and calcium, which, in turn, can lead to secondary hyperparathyroidism. If coeliac disease remains untreated for long, tertiary hyperparathyroidism can also develop through autonomy of the parathyroid glands via chronic stimulation. Primary hyperparathyroidism also has been reported in some cases of coeliac disease. We report the case of an adolescent with coeliac disease presenting with severe hypercalcaemia from a parathyroid adenoma. A 14 year-old girl was admitted to our department for delayed puberty and growth retardation. Laboratory examination revealed iron deficiency anaemia, low 25OH vitamin D level (7 ng/ml), high parathyroid hormone level (PTH) (955 pg/ml), and hypercalcaemia (13.4 mg/dl). Endoscopic biopsy was compatible with gluten enteropathy. Endomysium antibody was positive. A gluten-free diet was started. Her calcium returned to normal after excision of the parathyroid adenoma. After four months of the gluten-free diet, she began to mature, and puberty began with development of breasts and axillary-pubic hair growth. It has been suggested that autonomous four-gland hyperplasia or tertiary hyperparathyroidism may progress to adenoma formation, and that this should be termed "quaternary hyperparathyroidism". More studies are required to explain the relationship between coeliac disease and hyperparathyroidism.
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PMID:Parathyroid adenoma with coeliac disease: primary or quaternary hyperparathyroidism? 2237 99

Up to 25% of patients with primary hyperparathyroidism have ectopic parathyroid adenoma. A 45-year-old formerly obese woman underwent extended thymectomy for a parathyroid adenoma located in hyperplastic thymic tissue, associated with primary hyperparathyroidism and severe vitamin D deficiency, but normal bone mineral density. At nine months follow-up, all laboratory test results were within normal limits and she presented no symptoms and no recurrence of disease. In this case, autonomous growth of a parathyroid adenoma was reasonably secondary to chronic calcium and vitamin D malabsorption, which often occurs after bariatric surgery for pathologic obesity.
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PMID:Intrathymic ectopic parathyroid adenoma caused primary hyperparathyroidism with vitamin D deficiency several years after bariatric surgery. 2627 43


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