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

Records of 11 patients undergoing biliary reconstruction after laparoscopic cholecystectomy are reviewed. Ductal injuries resulted from failure to define the anatomy of Calot's triangle. Risk factors include scarring, acute cholecystitis, and obesity. Presenting findings included anorexia, ileus, failure to thrive, pain, ascites, and jaundice. All patients required hepaticojejunostomies, which were multiple and above the hepatic bifurcation in four patients. Given the extensive nature of these injuries and the frequent need for intrahepatic anastomosis and early stenosis of repairs by referring physicians, we recommend reconstruction be undertaken by an experienced hepatobiliary surgeon. To avoid injuries, a greater appreciation of risk factors and anatomic distortion and variance and strict adherence to principles of dissection and identification of anatomic structures are suggested. The use of cholangiography and a low threshold for conversion to the open procedure are advised.
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PMID:Laparoscopic bile duct injuries. Risk factors, recognition, and repair. 153 9

A retrospective study was conducted to determine which types of children might have polysomnographic findings that are most compatible with obstructive sleep apnea (OSA). The charts of 93 patients who were aged 18 months to 12 years were examined. All 93 patients had symptoms that were initially suggestive of OSA, and they underwent polysomnography. The types of presenting symptoms and associated illnesses were noted. Physical findings, including height, weight, and tonsil size, were examined. Of 93 patients with symptoms that were suggestive of OSA, 34 met sleep study criteria for OSA. In 44 patients, OSA was not demonstrated, and 15 patients had other results. On the basis of age, sex, and symptoms, no significant differences could be found between the group with OSA and the group with normal polysomnographic findings. Cor pulmonale, tonsil hypertrophy, and failure to thrive were associated with OSA. Surprisingly, obesity was not significantly associated with OSA.
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PMID:Polysomnographic and clinical findings in children with obstructive sleep apnea. 162 96

The Prader-Willi syndrome consists of infantile hypotonia, failure to thrive, hypogonadism and developmental delay. It was first described in 1956. Later in life hypotonia improves. Between the age of two and four obesity becomes noticeable and between six and ten there is uncontrollable behaviour. A survey has been carried out of the 36 known cases in New Zealand and the pattern of the disease is similar to that elsewhere. In most cases the diagnosis was not established until between the ages of six and 10 when the obesity was marked and uncontrolled behaviour a problem. Early control of the obesity is helpful.
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PMID:Prader-Willi syndrome in New Zealand: a survey of 36 affected people. 231 43

Recommendations for weaning have been based on empiric practices and observations of physiologic development. Estimates of nutritional requirements mimic those of the preweaning infant, adjusted for a slower growth rate. Concern for the onset of deficiency states (e.g., obesity, failure to thrive, atherosclerosis, hypertension) may provide scientific bases for nutritional recommendations during weaning.
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PMID:Bases of weaning recommendations. 238 Aug 52

People with Prader-Willi syndrome exhibit infantile hypotonia and failure to thrive, genital hypoplasia, childhood-onset obesity, mental deficiency and behavioral abnormalities, hypogonadism, short stature, and characteristic dysmorphology. In over half the affected individuals, prometaphase chromosome analysis reveals a small interstitial deletion of chromosome 15q, del 15(q11-q12); with most of the remaining patients showing apparently normal chromosomes. Molecular genetic technology is currently being applied to the relevant region of chromosome 15 to determine if there is etiologic heterogeneity and to seek a consistent diagnostic marker. Diagnosis at this time is primarily based upon clinical criteria.
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PMID:Prader-Willi syndrome. 264 21

A 15 month old boy with an interstitial deletion 15q derived from a paternal insertion (5;15)(q31.3;q21.1q22.1) is described and compared with one other reported case. A beak like nose with hypoplastic nasal alae, a thin upper lip, failure to thrive in infancy with later onset of obesity, and severe mental retardation are features common to both.
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PMID:Deletion 15q21.1----q22.1 resulting from a paternal insertion into chromosome 5. 343 May 49

Eating is a sensitive barometer of emotional state and parent-child interaction. Psychosocial distortions often appear first to the health worker and are referred to the dietitian as distortions in eating. At times, the distortion is severe enough to be called an eating disorder. An eating disorder of childhood is the misuse of feeding in an attempt to solve or camouflage family problems of living that seem otherwise insoluble. The childhood eating disorder might take the form of failure to thrive, obesity, excessive finickiness, or, most commonly, vehement and protracted struggles between parent and child about eating. An eating disorder is a biopsychosocial problem. It is based on characteristics and distortions in physical, physiological, psychological, and social factors. The dietitian who is to be helpful with families referred to her for correction of eating difficulties must be able to detect the disordered situation and differentiate it from one that is simply problematic. If an eating disorder exists, it is unlikely that the situation will change without psychotherapeutic intervention into family functioning. An appropriately conducted symptom management approach to correct the eating distortion is a helpful and potentially successful adjunct to psychotherapy. Such a component should be constructed around the restoration of a positive feeding relationship.
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PMID:Childhood eating disorders. 345 87

A 16-year-old boy with Prader-Labhart-Willi syndrome (PLWS) had hypotonia, feeding difficulties, failure to thrive, strabismus and bilateral inguinal hernias with cryptorchidism during infancy followed by hyperphagia, marked early-onset obesity with insulin-dependent diabetes mellitus and necrobiosis lipoidica diabeticorum, short stature, hypogonadotropic hypogonadism and some of the facial characteristics of the individuals with the PLWS. IQ is estimated around 90. Cytogenetic studies showed mosaicism: 45,X, t(Y;15) with partial deletion 15 (15pter----15q12); 46,X, t(Y;15), dic (15)(15pter----15q12::15q12----15pter) and 47, X, t(Y;15), dic(15), dic(15). The dic(15) was bisatellited, NOR-positive on both arms and represented inv dup(15). Thus, the 2 lines with the dic(15) showed partial trisomy 15 (15pter----15q12) and partial pentasomy 15 (15pter----15q12), respectively. The cell line ratios were different in lymphocyte and fibroblast cultures. The unique cytogenetic findings in this patient, the reports of a variety of chromosome 15 aberrations in PLWS, as well as aberrations of other chromosomes, suggest that the condition is a contiguous gene syndrome rather than an aneuploidy syndrome.
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PMID:Unique mosaicism in Prader-Labhart-Willi syndrome--a contiguous gene or aneuploidy syndrome? 368 18

Seventy six children with documented Fanconi-type idiopathic infantile hypercalcaemia were studied and compared with 41 with the Williams-Beuren syndrome. Clinical comparison showed, as expected, very close similarities but also considerable differences, particularly in the severity of feeding problems and the degree of failure to thrive. The estimated incidence of idiopathic infantile hypercalcaemia alone has remained constant for the past 20 years, at approximately 18 cases per year in the United Kingdom (1 per 47 000 total live births). Long term morbidity in these children is mainly due to mental handicap and arteriopathy, but hypertension (29%), kyphoscoliosis (19%), hyperacusis (75%), and obesity (50%) may be added complications. In one child, hypercalcaemia recurred during adolescence but this seems to be excessively rare. More detailed investigation before treatment is required to discover the aetiology of hypercalcaemia in this condition.
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PMID:Idiopathic infantile hypercalcaemia--a continuing enigma. 646 28

Twenty nine (1.8%) of a national cohort of 1600 patients with growth hormone deficiency presented before the age of 2 years. Sixteen of the 29 presented before 6 months of age--11 with symptomatic hypoglycaemia, four with failure to thrive, and one with obesity. Hypoglycaemia was persistent and difficult to control until growth hormone treatment was started. Ten of the 11 hypoglycaemic patients had multiple pituitary hormone deficiencies compared with two of the remaining five. Thirteen children presented between 6 months and 2 years of age; 12 had failure to thrive and one had spontaneous hypoglycaemia. Twelve of the 29 were boys and all but one of these had microgenitalia . Growth hormone deficiency should be considered in the differential diagnosis of infants presenting with refractory hypoglycaemia and in boys with failure to thrive and microgenitalia .
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PMID:Growth hormone deficiency presenting under age 2 years. 674 76


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