Cases reported "Diabetes Mellitus, Type 2"

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1/84. vitrectomy for cystoid macular oedema with attached posterior hyaloid membrane in patients with diabetes.

    AIM: To report the success of vitrectomy in eliminating cystoid macular oedema and improving vision in three eyes of two patients with diabetic cystoid macular oedema. In all of the eyes there was no ophthalmoscopic evidence of traction from a posterior hyaloid membrane or from proliferative tissue. methods: Pars plana vitrectomy was performed on three eyes of two patients with diabetic cystoid macular oedema who did not show traction upon examination with a slit lamp biomicroscope and a scanning laser ophthalmoscope. RESULTS: Cystoid changes disappeared 1, 3, and 5 days, postoperatively, and diffuse macular oedema resolved within 2 weeks. The visual acuity was improved and maintained. CONCLUSION: vitrectomy can be effective in some patients with diabetic cystoid macular oedema even in patients who lack evidence of traction by ophthalmoscopy.
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2/84. Triglyceride-induced diabetes associated with familial lipoprotein lipase deficiency.

    Raised plasma triglycerides (TGs) and nonesterified fatty acid (NEFA) concentrations are thought to play a role in the pathogenesis of insulin-resistant diabetes. We report on two sisters with extreme hypertriglyceridemia and overt diabetes, in whom surgical normalization of TGs cured the diabetes. In all of the family members (parents, two affected sisters, ages 18 and 15 years, and an 11-year-old unaffected sister), we measured oral glucose tolerance, insulin sensitivity (by the euglycemic-hyperinsulinemic clamp technique), substrate oxidation (indirect calorimetry), endogenous glucose production (by the [6,6-2H2]glucose technique), and postheparin plasma lipoprotein lipase (LPL) activity. In addition, GC-clamped polymerase chain reaction-amplified dna from the promoter region and the 10 coding LPL gene exons were screened for nucleotide substitution. Two silent mutations were found in the father's exon 4 (Glu118 Glu) and in the mother's exon 8 (Thr361 Thr), while a nonsense mutation (Ser447 Ter) was detected in the mother's exon 9. Mutations in exons 4 and 8 were inherited by the two affected girls. At 1-2 years after the appearance of hyperchylomicronemia, both sisters developed hyperglycemia with severe insulin resistance. Because medical therapy (including high-dose insulin) failed to reduce plasma TGs or control glycemia, lipid malabsorption was surgically induced by a modified biliopancreatic diversion. Within 3 weeks of surgery, plasma TGs and NEFA and cholesterol levels were drastically lowered. Concurrently, fasting plasma glucose levels fell from 17 to 5 mmol/l (with no therapy), while insulin-stimulated glucose uptake, oxidation, and storage were all markedly improved. Throughout the observation period, plasma TG levels were closely correlated with both plasma glucose and insulin concentrations, as measured during the oral glucose tolerance test. These cases provide evidence that insulin-resistant diabetes can be caused by extremely high levels of TGs.
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3/84. Mitochondrial dna point mutation at nucleotide pair 3316 in a Japanese family with heterogeneous phenotypes of diabetes.

    A mitochondrial dna (mtDNA) point mutation at nucleotide pair (np) 3316 has been reported in relation to diabetes. We recently encountered a non-obese family with this type of mutation. The proband in the affected family, a 49-year-old woman who had been previously diagnosed as having an insulin-requiring non-insulin-dependent diabetes mellitus (NIDDM), was referred to our hospital for treatment of diabetic gangrene in her left foot. Her insulin secretory capacity was markedly reduced, but the insulin sensitivity evaluated by the euglycemic hyperinsulinemic clamp technique was normal. In addition, her serum lactate level was markedly increased after a 5 min ambulation, although her serum pyruvate and ketones remained within the normal range. Twenty-year-old twin sons had been treated with insulin since the age of 7, when both were diagnosed with insulin-dependent diabetes mellitus (IDDM). The proband's mother, a 68-year-old, was nondiabetic at this time. MtDNA analysis revealed a point mutation at np 3316 in all family members, which was homoplasmic for the mutation on a photograph of agarose gel electrophoresis containing ethidium bromide under ultraviolet light. This mutation seemed to be maternally transmitted in the family, and the onset of diabetes was occurring earlier and the insulin secretory capacity was declining from generation to generation, so that these findings suggest that the point mutation at np 3316 is associated with various phenotypes of diabetes.
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4/84. 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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5/84. Providing timely and ongoing vision rehabilitation services for the diabetic patient with irreversible vision loss from diabetic retinopathy.

    BACKGROUND: diabetic retinopathy (DR) remains the leading contributor to severe vision loss in the united states among persons 20 to 70 years of age. Despite advances in disease management and treatment, patients with vision loss from DR continue to constitute a significant portion of patients served in vision rehabilitation service (VRS) settings. These patients present special challenges to VRS providers because of early onset, fluctuations in and the complex nature of vision loss, unique visual demands of disease management, and associated multi-system losses. case reports: After introductory epidemiologic review, a case presentation format is used to illustrate solutions a multidisciplinary VRS can offer the special visual challenges of the person with diabetes with vision loss from DR. Four patients are presented--ages 30 to 70 years--with varying degrees and types of vision loss, with different lifestyle demands and disease management needs. The cases address vocational issues, vision fluctuation, coordinating adaptive solutions to complex visual losses, and meeting diabetic needs to measure medication, insulin, and blood glucose levels, to maintain skin care, diet, exercise, transportation, family roles, and support systems. CONCLUSIONS: The unique and complex needs of people with diabetes who experience vision loss can be well addressed through timely and ongoing VRS consultations, in conjunction with medical/ocular disease management.
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6/84. prevalence of macular pattern dystrophy in maternally inherited diabetes and deafness. GEDIAM Group.

    OBJECTIVE: To evaluate the prevalence of macular pattern dystrophy (MPD) in maternally inherited diabetes and deafness (MIDD), a new subtype of diabetes mellitus that cosegregates with a mutation of mitochondrial dna (i.e., the substitution of guanine for adenine at position 3243 of leucine transfer rna) and to report the clinical characteristics of MPD. DESIGN: Prospective cohort study. PARTICIPANTS: Forty-six patients from 29 families with an adenine-to-guanine mutation of mitochondrial dna were recruited from a French collaborative multicenter study. Thirty-five patients had MIDD, 8 were asymptomatic children of MIDD patients, and 3 had melas syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes). The 33 MIDD patients with diabetes were matched for diabetes duration and gender with 33 patients with "common" type-2 diabetes to compare the prevalence of diabetic retinopathy (DR) in both series. methods: All patients had a full ophthalmologic examination and fundus photographs. MAIN OUTCOME MEASURES: The presence and severity of MPD and DR were assessed in each patient. RESULTS: Thirty MIDD patients (85.7%) of 35 exhibited bilateral MPD characterized by linear pigmentation surrounding the macula and optic disc. In 24 of these 30 patients, visual acuity was 20/25 or more in both eyes. The prevalence of DR was 6% in MIDD patients with diabetes versus 15% for patients with common type-2 diabetes (a difference that was not significant, P = 0.23). The fundus of each of the eight asymptomatic children was normal. MPD was present in one of the three cases of MELAS. CONCLUSION: The prevalence of MPD in MIDD is high. Its detection may be helpful for the diagnosis of this new subtype of diabetes, for which specific treatments may be proposed.
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7/84. 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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8/84. myoglobin clearance and removal during continuous venovenous hemofiltration.

    myoglobin has a relatively high molecular weight of 17,000 Da and is poorly cleared by dialysis (diffusion). However, elimination of myoglobin might be enhanced by an epuration modality based on convection for solute clearances. We present a single case of myoglobin-induced renal failure (peak creatine kinase level: 313,500 IU/l) treated by continuous venovenous hemofiltration (CVVH). Our purpose was to evaluate the efficiency of such a modality using an ultrafiltration rate of 2 to 3 l/h for myoglobin removal and clearance. The hemofilter was a 0.9 m(2) polyacrylonitrile (AN69) membrane Multiflow-100 (Hospal-Gambro, St-Leonard, canada) and the blood flow rate was maintained at 150 ml/min by an AK-10 pump (Hospal-Gambro, St-Leonard, canada). The ultrafiltration bag was placed 60 cm below the hemofilter and was free of pump control or suction device. serum myoglobin concentration was 92,000 microg/l at CVVH initiation and dropped to 28,600 microg/l after 18 h of the continuous modality. The mean sieving coefficient for myoglobin was 0.6 during the first 9 h of therapy and this decreased to 0.4 during the following 7 h. Mean clearance of myoglobin was 22 ml/min, decreasing to 14 ml/min during corresponding periods, while the mean ultrafiltration rates were relatively stable at 2,153 /- 148 ml/h and 2,074 /- 85 ml/h, respectively. In contrast to myoglobin, the sieving coefficeint for urea, creatinine, and phosphorus remained stable at 1.0 during the first 16 h of CVVH. More than 700 mg of myoglobin were removed by CVVH during the entire treatment. In conclusion, considerable amounts of myoglobin can be removed by an extracorporeal modality allowing important convective fluxes and middle molecule clearances, such as CVVH at a rate of 2 to 3 l/h using an AN69 hemofilter. If myoglobin clearance had been maintained at 22 ml/min, 32 l of serum would have been cleared per day. However, the sieving coefficient of myoglobin decreased over time, probably as a consequence of protein coating and/or blood clotting of the hemofilter. Whereas myoglobin can be removed by CVVH, it remains unknown at this point if such a modality, applied early, can alter or shorten the course of myoglobinuric acute renal failure.
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9/84. Treatment of severe proliferative retinopathy and diabetic maculopathy.

    Strict blood glucose control, early detection and surveillance of diabetic retinopathy by means of validated screening programmes, and judicious use of laser photocoagulation can greatly reduce the risk of visual loss in diabetes. Some patients however, have aggressive neovascular disease resistant to laser treatment, or present at a late stage with advanced fibroproliferative disease, and may progress rapidly to blindness. In the elderly with Type 2 disease, diabetic maculopathy is more common and requires a different therapeutic approach. The present article describes two diabetic patients and discusses the management of patients with severe proliferative retinopathy or diabetic maculopathy.
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10/84. Hepatocellular injury in a patient receiving rosiglitazone. A case report.

    BACKGROUND: Rosiglitazone maleate (Avandia, SmithKline Beecham, philadelphia, pennsylvania) is a new oral hypoglycemic agent approved for the treatment of type 2 diabetes. It acts primarily by increasing insulin sensitivity. In controlled trials, there has been no evidence of rosiglitazone-induced hepatocellular injury. OBJECTIVE: To report a case of hepatocellular injury in a patient receiving rosiglitazone. DESIGN: Case report. SETTING: Community teaching hospital. PATIENT: 61-year-old man receiving rosiglitazone, 4 mg/d for 2 weeks. INTERVENTION: Discontinuation of rosiglitazone therapy. MEASUREMENTS: Clinical evaluation and assessment of liver function test results were done daily during hospitalization and periodically after discharge. The outpatient record was also reviewed. RESULTS: After receiving rosiglitazone for 2 weeks, the patient presented with anorexia, vomiting, and abdominal pain. liver function tests revealed severe hepatocellular injury. Discontinuation of rosiglitazone therapy led to rapid improvement of liver function and resolution of symptoms. CONCLUSION: Rosiglitazone may be associated with hepatocellular injury. We believe that patients receiving rosiglitazone should have liver enzyme levels monitored earlier and more frequently than initially recommended.
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