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There is a definite need for replacement estrogen therapy in menopausal women exhibiting vasomotor symptoms or osteoporosis, particularly if the woman has had bilateral oophorectomy. There is a less clearly defined need in women complaining of emotional symptoms. Atrophic vaginitis and trigonitis is usually best treated with topical application of estrogen, which does not have systemic side effects if used weekly; more frequent use can lead to vascular absorption. Some of the problems associated with estrogen replacement are dose-related and can be eliminated by using smaller dosages. Uterine bleeding can usually be controlled by administering cyclically with progesterine. Hypertension, thrombosis, and adenocarcinoma are problems associated with administration of exogenous estrogens; use should be undertaken with great care in women exhibiting these conditions and patients should be followed closely to make sure such conditions are not developing. Other conditions which may worsen with estrogen therapy are diabetes mellitus, seizure disorders, migraine, multiple sclerosis, collagen diseases, cholelithiasis, and hyperlipidemia. None except hyperlipidemia is an absolute contraindication but risk/benefit ratios must be considered carefully in these cases.
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PMID:Estrogens for the menopause. Maximizing benefits, minimizing risks. 19 9

Case reports since 1957 implicate corticosteroids in excess of physiologic requirements as a cause of nontraumatic osteonecrosis. Both laboratory and clinical studies demonstrate marked alterations in lipid metabolism with hyperlipemia, fatty liver and systemic fat embolism. Intra-arterial infusion of fat produces embolic vascular obstruction, focal marrow necrosis and osteocytic death in the femoral head of the rabbit. Induced hypercortisonism in rabbits produces severe hyperlipemia, fatty liver, systemic fat emboli, terminal vascular obstruction in bone and associated areas of osteocytic death representing avascular necrosis. Osteoporosis develops without fracture. Histologic evidence of vasculitis, thrombosis, or microfracture is lacking. The specific biochemical pathway of corticosteroid lipid alterations is unknown.
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PMID:The role of fat embolism in the etiology of corticosteroid-induced avascular necrosis: clinical and experimental results. 63 8

Nutrient requirements do not change markedly with advancing age, but life style, socioeconomic status, psychologic changes, and the presence of chronic disease alter nutrient intake in the elderly. It is important to recognize and deal with these factors in attempting to correct malnutrition and in prescribing dietary treatment. Malnutrition includes a variety of disorders: undernutrition, nutrient deficiencies and imbalances, and obesity. Frequent small feedings, with nutritional supplements for patients with profound weight loss, are the initial treatment for undernutrition. Iron supplements and a diet of foods rich in iron and in promoting iron absorption are required in treating iron deficiency anemia. Management of macrocytic anemia should include specific nutrient therapy plus improvement of diet to include leafy vegetables and animal foodstuffs. Diet is an important adjunct in treating chronic diseases. Maturity-onset diabetes mellitus often can be managed by diet alone, with attention to correct proportions of fat, carbohydrate, and protein and to the decreased caloric requirements of elderly patients. The importance of continuing dietary modifications in hyperlipidemia and hypertension is well known. Although dietary manipulation in osteoporosis is not curative, a diet high in calcium and containing adequate floride and vitamin D affords maximum dietary protection against progress of the disease.
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PMID:Guidelines for maintaining adequate nutrition in old age. 64 78

In a retrospective study of 632 patients with pituitary disease we diagnosed pituitary insufficiency without hypersecretion of any pituitary hormone in 122 patients. Patients were substituted with sex hormones (76%), hydrocortisone (74%) and/or L-thyroxine (77%). 76% had additional growth hormone deficiency, as shown by an increase of growth hormone of less than 5 ng/ml after i.v. administration of L-arginine. In 17% of all patients the diagnosis of osteoporosis was proven or suspected radiologically. 57% had low bone mass of lumbar spine (dualphotonabsorptiometry) and 73% had low bone mass of the proximal forearm (singlephotonabsorptiometry). BMD values of pituitary insufficient patients were in the same range as those of patients with established osteoporosis. More than half of all patients (53%) complained of tiredness, exhaustion and muscle weakness. 40% suffered from adipositas. 77% had hyperlipidemia (68% hypertriglyceridemia and 42% hypercholesterinemia), 18% had hypertension. 14% of the patients had arteriosclerotic events in their history (myocardial infarction or stroke). These figures are higher than incidences shown in the German PROCAM-study. These data show an increased prevalence of osteoporosis and vascular diseases. This is in contrast to the general opinion, that patients with pituitary insufficiency are adequately treated by substitution with adrenal, thyroid and sex hormones. Whether other factors such as the additional growth hormone deficiency are responsible for these diseases has to be examined in prospective studies.
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PMID:[Increased prevalence of osteoporosis and arteriosclerosis in conventionally substituted anterior pituitary insufficiency: need for additional growth hormone substitution?]. 176 81

The analysed clinico-biological manifestations, evolutive course and treatment of 30 patients with GCA are presented. The most frequent symptoms were fever and headache. 33% of patients had FOD criteria. 26% had various visual alterations. All patients were initially treated with steroids. Of the 26 patients followed up, 21 (81.7%) experienced some sort of complication: Cushing iatrogenic, osteoporosis, vertebrae collapse, aseptic necrosis of the femur head, arterial hypertension, diabetes mellitus, hyperlipidemia, steroid myopathy. 6 patients were treated with cyclophosphamide, following severe complications secondary to steroid therapy, and all of them had a good clinical evolution.
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PMID:[Giant-cell arteritis: the clinico-biological manifestations and the complications secondary to steroid treatment]. 191 67

Malnutrition is a common problem of patients undergoing liver transplantation. To treat malnutrition, it must first be identified through a nutritional assessment. Because many objective nutritional assessment parameters have limitations in end-stage liver disease, subjective nutritional indicators may be used as an alternative. Nutritional needs following transplantation are categorized as short and long term. The short-term nutritional goal, anabolism, can be complicated by the nutritional status of the patient, surgical procedures, and necessary medications. The increased nutrient needs during the early posttransplant phase require particular nutritional support. Nutrition-related problems following transplantation may include obesity, hyperlipidemia, hypertension, diabetes mellitus, hyperkalemia, edema, or osteoporosis. Dietetic advice relative to the nutritional needs of the liver transplant recipient can improve both the short- and long-term outcomes.
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PMID:Nutritional implications of liver transplantation. 208 51

Heel pain is most commonly the result of mechanical abnormality in foot structure or function. Systemic disease, however, may also affect the heel, resulting in pain, deformity, or both of the rearfoot. This article discusses and reviews notable systemic conditions, exclusive of the seronegative spondyloarthropathies, which may produce subjective or objective heel findings. Specific conditions discussed are rheumatoid arthritis, crystal deposition arthropathies, osteoporosis, diffuse idiopathic skeletal hyperostosis, diabetes mellitus, hypertrophic osteoarthropathy, Paget's disease, hyperlipidemia, sarcoidosis, sickle cell anemia, and acromegaly and their effects on the heel.
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PMID:The heel in systemic disease. 218 35

The Agricultural Revolution was almost certainly associated with a substantial decrease in human calcium intake. Calcium intakes typical of contemporary humans may well be inadequate for many individuals. Various slowly developing chronic disorders such as osteoporosis, hypertension, hyperlipidemia, and colon cancer may be induced or exaggerated by the current low level of dietary calcium intake in Western societies. We propose two hypotheses relating calcium intake to diverse diseases: first, the adaptation required to adjust to low intakes is inadequate to maintain critical components of cellular calcium regulation; second, the constant, forced adaptive response to low intake itself produces untoward consequences.
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PMID:Dietary calcium and chronic diseases. 219 36

Little notice has been paid in the surgical literature to problems with psychoeffective lithium, which by interfering with adenylate cyclase affects thyroid and parathyroid function, causing hypercalcemia, hyperparathyroidism, and hypothyroidism. Seven patients with lithiumogenic hyperparathyroidism occurring after years of lithium therapy underwent treatment and manifested osteoporosis (n = 2), hypertension (n = 2), nephrolithiasis (n = 1), coma (n = 1), rising hypercalcemia (n = 1), goitrous myxedema (n = 4), nephrogenic diabetes insipidus (n = 2), renal failure (n = 2), and hyperlipidemia (n = 1). Disease-directed parathyroidectomy (without morbidity) was curative. Unique laboratory findings included normal serum phosphorus and reduced urinary calcium and cyclic adenosine monophosphate values. Three separate cases of thyroid carcinoma after long-term lithium therapy were also treated, being preceded by myxedema (n = 2) and concurrent with hyperparathyroidism (n = 1). There has been only one previous report of lithium-associated thyroid carcinoma. All patients taking lithium should undergo surveillance for thyroid and parathyroid dysfunction and neoplasia, and appropriate surgical and medical treatment should be considered in each situation. Although hyperparathyroidism may be reversible with lithium discontinuance, such therapy may be obligatory for patient well-being, thus dictating parathyroidectomy.
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PMID:Lithiumogenic disorders of the thyroid and parathyroid glands as surgical disease. 224 24

Bone and ligament lesions induced by systemic retinoids (premature epiphyseal closure, osteophytes, calcification of ligaments, osteoporosis, etc.) are radiologically nonspecific. We assessed the incidence of "possibly retinoid-induced bone and ligament lesions" (MRKBV) in 46 patients (aged 24-82 years) who had been treated with various systemic retinoids for a variety of chronic dermatoses for an average of 4.5 years and compared the data with observations in a similarly structured group of control patients. All types of MRKBV were found more frequently in the retinoid group (41.3% vs 30.2%) and were more severe. Differences were only slight, however, being statistically significant only for moderate and severe MRKBV and for calcification of ligaments. Within the retinoid group, MRKBV were strikingly correlated with age, whereas no correlation was found with duration of treatment, mean daily and cumulative retinoid dose, underlying dermatosis, type of retinoid used or presence of other retinoid side-effects. Within the control group, MRKBV were also correlated with age, although to a lesser degree. We conclude that retinoids amplify and accelerate physiological and pathophysiological remodelling of the bones, thereby producing a varied range of lesions, which are characteristic for the age and the individual constitution of the patient treated. Retinoid-induced bone and ligament lesions, as a rule, do not cause subjective symptoms and are not associated with predictive or accompanying laboratory values. Also, MRKBV are not paralleled by other retinoid-induced side-effects (hyperlipidaemia, elevation of liver transaminases). In 16 cases in which bone X-ray had been performed prior to retinoid treatment, no indication of reversibility of MRKBV was found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Retinoid-induced changes of the bones and ligaments]. 225 96


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