Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although osteoma of the paranasal sinus is comparatively common, involvement of the sphenoidal sinus region is extremely rare. Lame reported that a total of twelve cases had been described in the European literature since 1800. Mikaelin, Kulczynski and Dolan, since then, described three cases. This paper deals with two surgical cases of sphenoidal sinus osteoma, reviewing literature on paranasal sinus osteoma and differential diagnosis in the sphenoidal sinus lesion. Case 1. A 20-year-old man was referred to us by an ophthalmologist, complaining of left visual disturbance (visual acuity: 0.02). He had a past history of chronic sinusitis. Neurological examination revealed papilledema on the left. Plain skull X-ray film showed marked destruction of the sphenoidal sinus and tomography demonstrated thinning and expanding of the sella floor with cloudiness in the sphenoidal sinus. CT scan showed an irregular high density mass in the sphenoidal sinus. Sublabial-nasoseptal sphenoidotomy was performed. The sinus was occupied by homogeneous osseous tissue surrounded by thin fibrous tissue. The osseous part was removed as much as possible by a high speed air drill. Histopathologic examination confirmed mature osteoma. Postoperative course was uneventful and left visual acuity was improved up to 0.06. He is now doing well without recurrence for six months. Case 2. A 59-year-old woman was admitted to our hospital, complaining of acromegaly for ten years. She had a past history of chronic sinusitis, hypertension, diabetes mellitus and left putaminal hemorrhage which was evacuated five months before. She had typical acromegalic features and serum levels of growth hormone was 65.8 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Osteoma of the sphenoid sinus--report of two cases]. 380 13

We evaluated the pathogenesis of skin thickening in three patients with acromegaly. Growth hormone levels were normal in one patient and were elevated in two patients. Skin biopsy specimens were obtained from the forearm. Hematoxylineosin staining showed slight epidermal thinning and, in two of the patients, a small increase in the number of fibroblasts. Selective stains for collagen, elastic, and reticular fibers disclosed normal connective tissue. The most striking abnormality was increased glycosaminoglycan deposition on the slides stained with colloidal iron. Glycosaminoglycan infiltration occurred mostly in the papillary and upper reticular dermis and was not directly related to the simultaneous growth hormone levels. Tissue digestion with specific enzymes identified hyaluronic acid, chondroitin-4- and 6-sulfate, and dermatan sulfate as the most prominent glycosaminoglycans in the dermis. The skin ultrastructure appeared to be preserved on electron microscopy. We conclude that cutaneous mucinoses is the main cause for the thickening of the skin in acromegaly.
 ...
PMID:Histochemical characterization of the cutaneous involvement of acromegaly. 621 6

Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The age-specific incidence of hip fractures is increasing so that the public health burden will increase out of proportion to the burden imposed by the increase in the numbers of elderly men in the community. Vertebral fractures are a public health problem of lesser magnitude in terms of morbidity, mortality, and cost, but they are debilitating and are seen commonly in clinical practice. (Forearm fractures should probably not be regarded as a public health problem.) The pattern of earlier gain/later loss of bone during ageing in healthy men is well documented. Peak bone mass is higher in men than women because men have bigger bones. Peak bone density is the same. The absolute amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men. It is less because endocortical resorption is less, and periosteal formation is greater, in men. Bone loss may accelerate in elderly men and women (rather than decelerate), perhaps because endocortical resorption and increasing cortical porosity increase the effective surface available for resorption in cortical bone. Thus, bone fragility is less in men because (a) the cross-sectional surface of the vertebral body is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced bone density in men with fractures may be due to reduced peak bone density and bone loss. As found in women with spine fractures, men with fractures have smaller bone size. Bone loss occurs by reduced bone formation and increased bone resorption. Loss of connectivity appears to predominate in men with vertebral fractures; trabecular thinning appears to predominate in men with hip fractures. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may be concomitants of ageing or may contribute to reduced bone-formation and bone loss. Men with vertebral fractures may be more deficient in growth hormone and insulin-like growth factor 1. Thy often have illness, hypogonadism, or illnesses associated with hypogonadism that should be sought with a high index of suspicion.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:The dilemma of osteoporosis in men. 770 40

We evaluated the radiological, biochemical and growth hormone (GH)/insulin-like growth factor-I (IGF-I) changes in 10 children with severe protein-energy malnutrition (PEM) who had rachitic manifestations (group 1), 10 children with severe PEM without clinical signs of rickets (group 2), and 10 children with normal body weight-for-length and -age, suffering from vitamin-D-deficiency with signs of florid rickets (group 3) and 10 normal age-matched children (group 4). Serum calcium (Ca2+), phosphorus (PO4), and albumin concentrations were markedly decreased in the two groups with PEM. Malnourished children with rickets had significantly higher serum alkaline phosphatase (ALP) concentrations compared to the malnourished group without rachitic manifestations. Radiological evaluation of the two groups who had rachitic manifestations revealed demineralization of long bones, thinning of the bony cortex, increased formation of osteoid tissue, and metaphyseal changes including cupping, fraying, and flaring. The incidence of these radiological findings did not differ among the well-nourished and the malnourished groups with clinical signs of rickets. However, the incidence of fracture of the shaft was higher (40 per cent) in the malnourished group compared to the well-nourished group (10 per cent) with rickets. In the malnourished group without clinical evidence of rickets, demineralization and cortical thinning was detected in 40 per cent without significant metaphyseal changes. Basal concentrations of GH and peak GH response to clonidine were significantly elevated and IGF-I concentrations were significantly depressed in the malnourished groups v. the other two groups. There were no significant differences in the fasting and the clonidine provoked GH levels or IGF-I concentrations between the rachitic children (group 3) and the normal children. These data suggest that in rachitic children there is not a major role for circulating GH (and by implication IGF-I) on bone mineralization. However, during malnutrition decreased IGF-I production can slow or stop epiphyseal growth and might contribute to the demineralization of the cortex of long bones.
 ...
PMID:Radiological, biochemical, and hormonal changes in malnourished children with rachitic manifestations. 882 Jun 18

Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20-30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocortical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.
 ...
PMID:Osteoporosis in men. 936 40

There is now little doubt that growth hormone (GH) and insulin-like growth factor-1 (IGF-1) play a role in cardiac development and in cardiovascular physiology in adult life. Congenital lack of GH is associated with defective cardiac growth, ventricular wall thinning, and impaired systolic function. These abnormalities limit exercise capacity and contribute to the poor quality of life in patients with GH deficiency. In addition, studies with in vitro muscle preparations have shown that IGF-1 affects myocardial contractility by a direct mechanism. These findings suggested that GH would benefit patients affected by heart failure. Indeed, GH and/or IGF-1 have proven beneficial in various models of experimental heart failure. Tested in patients with classes II-IV heart failure, they improved cardiac performance and clinical status. These effects were associated with improved myocardial energetics and de-activation of the neurohormonal system. Because of the uncontrolled nature of the studies and the small number of cases examined, conclusions as to the effectiveness of GH and IGF-1 must await the results from larger trials.
 ...
PMID:Growth hormone: a new therapy for heart failure? 1008 93

Growth retardation in children with thalassaemia major is multifactorial. We studied the growth hormone (GH) response to provocation by clonidine and glucagon, measured the circulating concentrations of insulin, insulin-like growth factor-I (IGF-I), IGF-binding protein-3 (IGFBP3), and ferritin, and evaluated the spontaneous nocturnal (12 h) GH secretion in prepubertal patients with thalassaemia and age-matched children with constitutional short stature (CSS) (height SDS < -2, but normal GH response to provocation). The anatomy of the hypothalamic pituitary area was studied in patients with abnormal GH secretion using MRI scanning. Children with thalassaemia had significantly lower peak GH response to provocation by clonidine and glucagon (8.8 +/- 2.3 micrograms/l and 8.2 +/- 3.1 micrograms/l respectively) than did controls (17.6 +/- 2.7 micrograms/l and 15.7 +/- 3.7 micrograms/l respectively). They had significantly decreased circulating concentrations of IGF-I and IGFBP3 (68.5 +/- 19 ng/ml and 1.22 +/- 0.27 mg/l respectively) compared to controls (153 +/- 42 ng/ml and 2.16 +/- 0.37 mg/l respectively). Seven of the thalassaemic children had a GH peak response of < 7 micrograms/l after provocation. Those with a normal GH response after provocation also had significantly lower IGF-I and IGFBP3 concentrations than controls. Analysis of their spontaneous nocturnal GH secretion revealed lower mean (2.9 +/- 1.77 micrograms/l) and integrated (2.53 +/- 1.6 micrograms/l) concentrations compared to controls (4.9 +/- 0.29 micrograms/l and 5.6 +/- 0.52 micrograms/l respectively). Five of them had mean nocturnal GH concentration < 2 micrograms/l and four had maximum nocturnal peak below 10 micrograms/l. These data denoted defective spontaneous GH secretion in some of these patients. MRI studies revealed complete empty sella (n = 2), marked diminution of the pituitary size (n = 4), thinning of the pituitary stalk (n = 3) with its posterior displacement (n = 2), and evidence of iron deposition in the pituitary gland and midbrain (n = 7) in those patients with defective GH secretion (n = 9). Serum ferritin concentration was correlated significantly with the circulating IGF-I (r = -0.47, p < 0.01) and IGFBP3 (r = -0.43, p < 0.01) concentrations. These data prove a high prevalence of defective GH secretion in thalassaemic children associated with structural abnormality of their pituitary gland.
 ...
PMID:Spontaneous and provoked growth hormone (GH) secretion and insulin-like growth factor I (IGF-I) concentration in patients with beta thalassaemia and delayed growth. 1066 1

Fragility fractures in men are a public health problem. The increasing longevity in men is likely to increase the public health burden of fractures in men. This problem remains unrecognized by doctors, the public and governments. About one third of all hip fractures occur in men but the incidence and gender ratio varies from country to country for reasons that are not understood. The prevalence of spine fractures is about half that of women in most studies, but similar to that of women in several other studies. The incidence of spine fractures is uncertain but is likely to be about half that of women except in 80+ year olds, when it appears to be similar. The causes of the higher mortality in men than in women following hip or spine fracture are not well defined. Areal bone mineral density (aBMD) predicts fracture risk in men; the relative risk for spine and hip fracture conferred by a 1 SD lower aBMD, or by a prevalent fracture, is similar in men and women. The age-specific absolute risk (number of cases per 1,000 per year) conferred by a given hip aBMD is similar in men and women. The age-specific absolute risk conferred by aBMD at the calcaneus or radius for spine fracture is similar for men and women. If the absolute and relative risks are similar then the lower incidence of fractures in men than women may reflect the lower proportion of the male population distribution below a given structural determinant of bone fragility. That is, at any age, there may be fewer men than women with smaller bones, lower volumetric bone mineral density (vBMD), thinner trabeculae or cortices, architectural disruption, or higher remodeling rates. Higher mortality and fewer falls may also contribute to the lower incidence of fractures in men. This tail end of the male population distribution (for traits like bone size, vBMD, architecture, and remodeling rates) is the likely source of fracture cases in males. Hypogonadism is a risk factor for osteoporosis. However, the definition, prevalence, causes and structural consequence of hypogonadism are inadequately defined. At what level of testosterone is bone balance negative? What structural determinants of axial and appendicular strength are regulated by testosterone, estrogen, growth hormone (GH), insulin like growth factor 1 (IGF-1) (or their interactions)? Is reduced bone size in men with spine or hip fractures due to failed growth-related or age-related periosteal expansion? If reduced vBMD is due to reduced accrual, is this due to reduced cortical thickness? What factors regulate and coregulate the periosteal and endocortical modeling and remodeling? Are reduced trabecular numbers due to failed formation at the growth plate, excess resorption of primary trabeculae or reduced formation of secondary trabeculae? Is reduced trabecular thickness due to failed prepubertal or pubertal bone formation? Is reduced cortical and trabecular thickness during aging due to excessive endosteal resorption or reduced bone formation? If the former, is this due to increased remodeling sites or increased resorption depth? Most evidence favors reduced bone formation as the cause of bone loss with trabecular bone loss occurring by reduced formation and thinning more than by increased resorption and loss of connectivity. Cortical bone loss is less than in women because endocortical resorption is less and periosteal apposition is greater. If the reduced bone formation is most important, is this due to reduced osteoprogenitors, reduced osteoblast matrix synthesis or early osteoblast apoptosis? Anti-spine-fracture efficacy has been demonstrated in only one randomized heated with alendronate drug in men. The gaps in our knowledge remain large.
 ...
PMID:Unresolved issues in osteoporosis in men. 1170 79

The amount of human growth hormone (HGH) decreases significantly after the age of 30. This decrease has been implicated as one of the major causes in the signs of aging, such as thinning of the skin and bones, a decrease in lean muscle mass and an increase in adipose tissue. Supplementing the body's dwindling supply with recombinant human growth hormone (rHGH) has been shown to reverse the signs and symptoms of aging. However, drawbacks in rHGH replacement therapy include prohibitively high cost, the need for repeated injection and side effects such as carpel tunnel syndrome, gynecomastia and insulin resistance. The purpose of this study was to establish an in vitro model using genetically-engineered keratinocytes to screen natural compounds for the ability to stimulate HGH secretion. We now report that a combination of equal amounts of L-arginine and L-lysine, aged garlic extract (Kyolic), S-allyl cysteine and Pycnogenol significantly increased secretion of HGH in this in vitro model. The data indicate that this in vitro model may be used to screen for other secretagogues.
 ...
PMID:Kyolic and Pycnogenol increase human growth hormone secretion in genetically-engineered keratinocytes. 1212

Cockayne syndrome is a rare autosomal recessive condition characterized by growth failure and multisystem progressive degeneration. We report and describe this syndrome in a Jordanian brother and sister with Cockayne syndrome with first cousin parents. Clinical features included short stature, cachectic senile look, neurological deterioration, photosensitivity, mental retardation, hearing impairment and carious teeth. The phenotype is compatible with a mild variant of type I Cockayne syndrome. They showed an exaggerated response to growth hormone provocation test, with slightly elevated basal insulin-like growth factor 1 levels. The radiological findings of thinning of ribs and slender femora with narrow medullary canals have not previously been reported in this syndrome. We discuss the implications of these findings.
 ...
PMID:Cockayne syndrome in 2 siblings. 1595 89


1 2 Next >>