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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Though tetany is not among the reported side effects of oral contraceptive usage, specifically of the use of estrogen, a case study is reported which links the development of tetany to administration of estrogen-containing oral contraceptives. The case was a 35-year-old woman, who presented with muscular cramps and hypocalcemia of unknown origen. 4 years earlier, shortly after taking an oral contraceptive preparation, she had experienced the same symptoms; now, she was reacting apparently to treatment with chorionic gonadotropins for mild obesity. Clinically, she evinced persistent hypocalcemia, hyperphosphatemia, normal renal function, and low plasma parathyroid hormone (PTH); such characteristics are consistent with hypoparathyroidism. With the former, no PTH response was measured, whereas with the latter antiserum, normal response of PTH was found; hence, it was concluded that the patient's PTH was immunologically abnormal and biologically ineffective. These data support the hypothesis that estrogens have a PTH-independent effect on bone; i.e., oral administration of estogens (in this case ethinylestradiol) caused hypocalcemia with tetanic symptoms resulting from estrogenic inhibition of bone resorption by specific action on the bone, not by antagonizing PTH action in vivo.
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PMID:Estrogen-induced tetany in idiopathic hypoparathyroidism. 82 Jun 24

A 36-year-old patient developed tetany manifested only by a positive Trousseau's sign and with a negative Chvostek's sign 8 weeks after gastric bypass surgery for obesity. The usual causes of tetany (hypocalcemia, hypomagnesemia and alkalosis) were absent. The only possible etiology found was hypokalemia. Previous cases of hypokalemia induced tetany reported were always accompanied by alkalosis. Its absence in our patient makes this case unique and determines that hypokalemia per se in the absence of alkalosis may be a cause of tetany. It is suggested that the Trousseau's sign should be investigated in patients with severe potassium deficiency.
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PMID:Tetany induced by hypokalemia in the absence of alkalosis. 370 94

Obesity, a well-known phenomenon in Western society, is frequently associated with cardiovascular and endocrine disease. Strokes, myocardial infarction, diabetes and hyperlipidemia are classical reasons for the high mortality and morbidity of overweight people. For this reason, intensive weight-reduction programs have been proposed: low-calorie diets, total starvation, drugs and even surgery. Total starvation and some low-calorie diets are, however, also associated with sudden death, most probably of cardiac origin. Experimental data from our laboratory show that total starvation is accompanied by a severe depletion of magnesium in myocardial tissue. Protein-sparing modified low-calorie diets, however, can protect against this mineral loss even if magnesium supplementation alone cannot obtain this goal. Applying these principles in overweight man show weight reduction without mineral loss or cardiac disturbance. Surgery with 'ileal bypass' procedures gives rise to severe hypomagnesemia and hypocalcemia with tetany and spasmophilia. New procedures, derived from experimental surgery, are 'gastric bypass' and 'gastroplasty'. These methods, only applied in very obese patients (body mass index greater than 40, normal 23-27) show no change in mineral concentrations of calcium and magnesium and no clinical symptoms suggestive for mineral loss. A good, controlled weight-reduction program under strict medical surveillance can, in this way, offer new perspectives in the treatment of one of our most frequent 'culture-induced' diseases.
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PMID:Magnesium and obesity: effects of treatment on magnesium and other parameters. 382 Nov 74

Leptin is a small protein produced mainly by adipocytes. Recently, its relationship to obesity has been studied extensively. It was proved that obese individuals have either relative or absolute leptin deficiency. Several years ago, leptin was found to be produced also by the placenta. This stimulated us to study relationship between leptinemia and placental hormones in 85 women in the second gravidity trimester. Within the prenatal screening, these pregnant women were subjected to analysis of AFP, hCG, SP-1 glycoprotein and leptin and the results obtained were processed statistically. The control group consisted of 20 nonpregnant women with tetany. Women in the second gravidity trimester were found to have a significantly higher leptinemia than nongravid women (even with respect to body weight). This may be due to a larger amount of adipose tissue during gravidity and also leptin-resistance. Moreover, we recorded a negative correlation between leptinemia related to body weight and concentration of SP-1 glycoprotein. This finding supports the presumption that mother's leptinemia correlated negatively in the second gravidity trimester with quality and quantity of the placental syncytiotrophoblast. Our findings can be explained as follows: the biological effect of leptin is metabolically unfavourable for the growth of the foetus and the placenta. An increased leptinemia with advancing gravidity can be caused by a larger fatty mass and an increased activity of adipocytes when leptin presence increases in system circulation but the organism begins to be leptin-resistant and an "unfavourable" metabolic effect fort the gravid woman and the foetus is not distinct. These findings thus support the hypothesis postulating the nonsignificance of leptin production in human placenta and on the contrary the necessity of leptin-resistance for foetus development from the metabolic point of view. Thus, a decreased leptinemia immediately before and after the delivery could be caused by the still unclear regulators of leptin sensitivity. This is again a metabolically highly favourable state (reduced appetite, decreased body weight, increased energy output and others).
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PMID:[Serum leptin in women during the third trimester of pregnancy]. 1042 93

We presented a case of a 22-year-old woman with pseudohypoparathyroidism type la. She was a typical congenital Albright syndrome patient with osteodystrophy including hands and feet, accompanied by obesity, strabismum, and retardation growth. Her calcium and phosphate levels were within the normal range which was stated during repeated hospitalisation due to infections. The diagnosis of PHPT was made at the age of 22 when the patient suffered twice from tetany seizure accompanied by numbness and tingling sensation in her hands and around the mouth as well as cramps in her legs. Typical phenotype were found: shortness in stature, obesity, rounded face, small hands and shortening of the third, the fourth and the fifth fingers in both hands and the third and the fourth toes in feet together with trophic disorders of nails and valgity of her knees. Somatic sings were accompanied by hypocalcaemia and hyperphosphatemia, hyperphosphatasia, lower calcium and phosphate urinary excretion and three-fold increased PTH serum level. Computerised tomography of the brain showed extensive evidence of cerebral calcification in basal ganglia as well as in dura mater and in skin covering the skull. X-ray and densitometry examinations revealed osteolytic foci in cranial, humeral and forearm bones as well as osteoporosis in palm and feet bones. The patient presented a typical case of PHPT with resistance of the kidney to PTH, what was confirmed by lower calcium and phosphate urinary excretion, with normal bone receptor sensibility to PTH. Elevated PTH levels resulted in osteoporosis and foci of osteolysis. Treatment with calcium and active form of vitamin D3 caused reversal of hypocalcemia symptoms and normalisation of biochemical features. We also found hormonal symptoms of latent hypothyreosis. No coexistence of PTH with thyroid receptor resistance was found. The case was described because it is rare disorder, difficult to diagnose. Early diagnosis and treatment is necessary to limit the irreversible changes as well as bone and central nervous system injury.
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PMID:[A case of pseudohypoparathyroidism]. 1080 May 89

Vitamin D, a secosteroid, is essential for the development and maintenance of healthy bone in both the adult and pediatric populations. Low level of 25-hydroxy vitamin D (25-(OH)-D) is highly prevalent in children worldwide and has been linked to various adverse health outcomes including rickets, osteomalacia, osteomalacic myopathy, sarcopenia, and weakness, growth retardation, hypocalcemia, seizure and tetany, autism, cardiovascular diseases, diabetes mellitus, cancers (prostate, colon, breast), infectious diseases (viral, tuberculosis), and autoimmune diseases, such as multiple sclerosis and Hashimoto's thyroiditis. Risk factors for hypovitaminosis D are people with darker skin pigmentation, use of sunscreen, insufficient ultraviolet B exposure, prematurity, living in northern latitudes, malnutrition, obesity, exclusive breastfeeding, low maternal vitamin D level, certain medications, drinking unfortified cow's milk, liver failure, chronic renal insufficiency, cystic fibrosis, asthma, and sickle cell hemoglobinopathy. This review highlights and summarizes the molecular perspectives of vitamin D deficiency and its potential adverse health outcomes in pediatric age groups. The recommended treatment regimen is beyond the scope of this review.
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PMID:Pediatric Hypovitaminosis D: Molecular Perspectives and Clinical Implications. 2822 97

Albright hereditary osteodystrophy (AHO) is a hereditary metabolic disorder that presents with seizure secondary to hypocalcaemia. A careful phenotypic assessment of patients presenting with seizure clues to the diagnosis of AHO. The characteristic features are short stature,obesity and brachydactyly.Pseudohypoparathyroidism (PHP) is observed in patients with AHO and is characterized by inability of the body to respond appropriately to parathormone, mainly characterized by hypocalcaemia, increased serum parathormone concentration, insensitivity to the biological activity of parathormone, and hyperphosphatemia. In this study, we report a 14-year-old boy with distinctive phenotype of AHO, oral manifestations, and signs of tetany with PHP presenting as recurrent generalized seizure.
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PMID:Hypocalcemic Recurrent Generalized Seizures with Bilateral Basal Ganglia and Frontal Calcification as the Initial Manifestation of Albright's Hereditary Osteodystrophy in a Child: A Pictorial and Video-graphic Representations. 3190 67