Cases reported "Obesity"

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1/112. Lower dosages of phentermine-fenfluramine given in the afternoon: five cases with significant weight loss.

    phentermine and fenfluramine are widely used in the treatment of obesity. Despite the fact that primary pulmonary hypertension and mitral valve insufficiency have been associated with fenfluramine use, many of these patients need medication to achieve weight loss. Small degrees of weight loss have been shown to significantly improve obesity-related medical conditions such as hypertension, hypercholesterolemia, and noninsulin-dependent diabetes mellitus. Current practice is to give phentermine and fenfluramine in the morning and afternoon. Doses for phentermine have ranged from 15 to 37.5 mg and for fenfluramine from 20 to 120 mg per day. We report five cases of severely obese women with medical complications who were treated with phentermine 8 mg twice per day (at 1:00 p.m. and 4:00 p.m.) and fenfluramine 20 mg per day (at 4:00 p.m.). Because many obese patients skip breakfast and eat more in the afternoon and evening, medication was dosed in order to cover these high-risk eating periods. overall, these patients lost a mean of 22.4% of their initial weight (range 18.6% to 32.8%) over an average of 8.4 months (range 3.5 to 16 months). These cases suggest that short-term weight loss can be achieved with a low dose of fenfluramine when both medications are given in the afternoon to better target the eating patterns of obese subjects.
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2/112. Syndromal obesity due to paternal duplication 6(q24.3-q27).

    The likelihood of a paternally expressing imprinted gene in chromosome region 6(q23-24) has been highlighted by cases of transient neonatal diabetes mellitus (TNDM) in which paternal uniparental disomy (UPD) for chromosome 6 or paternal duplication 6(q23-qter) was detected. We present the case of a 38-year-old man with moderate to severe intellectual delay, short stature, small hands and feet, eye abnormality, small mouth, and obesity (without hyperphagia) beginning in mid-childhood. The perinatal and neonatal histories were normal. The patient had a duplication within 6q. fluorescence in situ hybrisation studies were performed with single and dual hybridisations using a chromosome 6 library probe, short and long arm subregional probes, 6q23-24, 6q25.3-6qter locus-specific probes, and a 6q telomere probe. The hybridisation results defined an inverted duplication of 6q24.3 to 6q27. dna studies with microsatellite markers from 6p and 6q showed regular biparental inheritance of chromosome 6 and confirmed that the duplication was paternal in origin. Our patient appears to be the first one known to have paternal duplication of chromosome area 6(q24-q27) who did not have TNDM as an infant. He has remained nondiabetic, although obesity, without hyperphagia, has been a constant problem since its onset in mid-childhood.
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3/112. Patient case studies.

    Three contrasting cases of obese patients with type 2 diabetes mellitus are presented, which illustrate the management difficulties faced by clinicians. The first raises the issue of when to commence an oral hypoglycaemic agent in a newly diagnosed but asymptomatic obese patient; the second case addresses the problem of when to commence insulin in the face of continuing weight gain and poor glycaemic control; the final case is an example of the vicious metabolic spiral which so many patients enter, with increasing body weight, poor diabetic control and associated co-morbidities. The discussion that follows each case presentation recognises the considerable cardiovascular risk faced by such patients and provides guidance about possible management pathways including adjunctive anti-obesity pharmacotherapy.
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4/112. Bone amyloidoma in a diabetic patient with morbid obesity.

    Bone localisations of amyloidosis are rare, usually diffuse and associated with myeloma. We report the case of a patient with massive obesity complicated by diabetes, hypertension, sleep apnea and liver steatosis, who complained of rapidly worsening bilateral polyradiculalgia of the lower limbs. After sufficient weight loss made nuclear magnetic resonance imaging feasible, a spinal tumour was visualised on the 5th lumbar vertebra, extending to soft tissues. Total excision was performed, and pathological studies revealed an amyloid bone tumour with no evidence of myeloma.
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5/112. Bilateral giant adrenal myelolipoma and polycystic ovarian disease.

    We report a case of a nonfunctioning, synchronous, bilateral, very large adrenal myelolipoma in an obese woman. She had diabetes mellitus and oligomenorrhea due to polycystic ovarian disease, and for that, she was taking progesterone medication for over 12 years. The principal clinical findings, the etiology and pathogenesis, the diagnostic-tools including US-guided fine-needle biopsy to preoperative differential diagnosis, are discussed. copyright copyright 1999 S. Karger AG, Basel
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6/112. Improvement in severe insulin resistance with frequent injections of lispro insulin.

    Extreme insulin resistance is common in obese african americans with type 2 diabetes. This case report describes an obese African-American woman who was treated with subcutaneous injections of lispro insulin every 2 hours with resultant decrease of mean daily blood glucose from 264.7 mg/dL to 111 mg/dL and in insulin requirement from 479 U/24 hours to 60 U/24 hours. This case demonstrates that extreme insulin resistance is reversible in the short term.
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7/112. Restructuring the therapeutic environment to promote care and safety for the obese patient.

    Fifty-four percent of American adults are overweight. obesity is a chronic disease associated with a number of conditions, such as diabetes, heart disease, hypertension, certain types of cancers, and breathing problems. The direct and indirect costs related to obesity exceed $70 billion annually. Because of the many cost and quality issues related to obesity, national attention is turning toward the special needs of this population. Strategies to restructure therapeutic intervention with attention to risk management, economic implications, and patient satisfaction are important considerations when managing the obese patient.
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8/112. Mutation analysis of the human adipocyte-specific apM-1 gene.

    BACKGROUND: The aim of this study was to analyse the human adipocyte-specific apM-1 gene for sequence variations. methods: sequence analysis was performed in 344 randomly chosen blood samples using a capillary sequencer. RESULTS: Whereas no mutations were detected in intronic regions and in 2.7 kb of the promoter, two sequence variations were found within the coding sequence of apM-1. For both mutations, a polymerase chain reaction-(PCR) based restriction fragment length polymorphism (RFLP) analysis was developed, which provided a rapid screening method. A conservative T --> G transition at nucleotide 45 within exon-2 [Gly15Gly] was detected with an allelic frequency of 0.9 for the wild-type allele and 0.1 for the mutated allele. In addition, a missense point mutation at nucleotide 331 within exon-3 [Tyr111His] was detected with an allelic frequency of 0.97 for the wild-type allele and 0.03 for the mutated allele. This mutation replaces a tyrosine by an histidine within the carboxyterminal globular domain of apM-1. Concerning the Gly15Gly polymorphism, the TT genotype was found in 275 subjects (79.9%), the TG genotype in 67 subjects (19.5%) and the GG genotype in 2 subjects (0.6%): one with maturity onset diabetes of young age (MODY-diabetes) and one with Lipoatrophic Diabetes Syndrome (LPDS). Concerning the Tyr111His polymorphism, the TT genotype was found in 328 subjects (95.4%), the TC genotype in 15 subjects (4.3%) and the CC genotype in 1 subject (0.3%). CONCLUSION: The existence of two yet unknown mutations within the apM-1 gene was demonstrated and RFLP analysis was established for rapid screening. Well defined cohorts of patients are necessary to determine the putative role of apM-1 gene mutations in the pathogenesis of metabolic disorders.
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9/112. gout in Maoris.

    Historical evidence suggests that the Maori people of new zealand were virtually untroubled by gout or obesity at a time when these disorders, along with other elements of the gouty diathesis, were rife in the best fed and hardest drinking sections of the Northern European population. By the mid 20th century, however, the apparent decline of the gout in europe and north america and the breakup of the gouty diathesis in those lands had been more than compensated by their large-scale reappearance in the Maori and in other indigenous inhabitants of the Pacific Basin who, at first sight, appeared to have become one large gouty family. Half the Polynesian population of new zealand, Rarotonga, Puka Puka, and the Tokelau islands proved to be hyperuricemic by accepted European and North American standards, the associated gout rate reaching 10.2% in Maori males aged 20 and over. The trends towards hyperuricemia and gout, on the one hand, and towards obesity, diabetes mellitus, hypertension, and associated degenerative vascular disorders, on the other hand, which manifest themselves separately in some Polynesian Pacific Islanders, run together in the Maori and Samoan people, presenting a combined problem of considerable importance to the public health. The appearance of these traits under conditions of plenty in the descendants of hardy and wide-ranging Polynesian voyagers, suggests the emergence of a formerly favorable ancestral polygenic variation through selection for survival under harder conditions. This may now have lost its primitive survival value with a paradoxic shift towards increased prevalence of obesity and the gouty diathesis in more affluent environmental conditions. This may now constitute a genetic load, with recent environmentally determined increase in morbidity and mortality rates from degenerative vascular disorders. There is no satisfactory evidence that overproduction of uric acid differs in mechanism from its European counterparts, although more work remains to be done to determine whether there is any difficulty in renal handling of an increased uric acid load. A high Maori morbidity rate from gout and morbidity and mortality rates from associated components of the gouty diathesis in the face of readily available skilled medical advice and care, indicate the need for greater future attention to help education and health care delivery, at least while conditions of plenty continue. Continuation of previous epidemiologic surveillance may then be required in order to provide a continuing index of the effectiveness of these measures, as well as an opportunity for further research into the interrelationships of these associated disorders.
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10/112. Acute lymphoblastic leukemia in one of two siblings with alstrom syndrome.

    alstrom syndrome is a rare autosomal recessive disease; less than 60 cases have been reported. No Chinese patient with this disease has been reported previously in the literature. Here, we describe an 11-year-old Chinese boy with this condition. His elder sister also had alstrom syndrome, and his father had non-insulin-dependent diabetes mellitus. Both siblings had degenerative retinopathy, obesity, mental retardation, perceptive hearing loss, short stature, non-insulin-dependent diabetes mellitus, nephropathy, hyperlipidemia, acanthosis nigricans, and hepatic dysfunction. The boy also developed acute lymphoblastic leukemia, which was confirmed by cytochemistry and immunophenotyping findings. He received chemotherapy and radiotherapy for the malignancy. The present case suggests that acute lymphoblastic leukemia may be coincident with or may be a previously undescribed systemic manifestation of alstrom syndrome.
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