1/29. An unusual manifestation of diabetes mellitus.MEDICAL history: Type 2 diabetes mellitus for five years; unexplained 35-lb weight loss three years ago; Bell's palsy on right side many years ago. MEDICATIONS: glipizide, 10 mg/day. family history: Father died of leukemia at age 65; mother has kidney stones; no diabetes or neuromuscular disease. SOCIAL history: insurance salesman; heterosexual, promiscuous, uses condoms; smokes (25 pack years); does not drink. physical examination: Well-nourished, well developed, not in acute distress; had difficulty rising from a sitting position because of right lower extremity weakness. blood pressure, 154/74; pulse, 88; temperature, 36.6 degrees C; respiratory rate, 16. head, eyes, ears, nose, and throat: normal. neck: normal. heart: S4. Lungs: clear. abdomen: mildly obese. extremities: no cyanosis, clubbing, or edema; atrophy and weakness of right thigh and both calves; wide-based gait; able to walk on toes but not heels. Neurologic responses: cranial nerves intact; deep tendon reflexes, 1 symmetrically; plantar reflexes, flexor bilaterally. skin: macular rash in sun-exposed areas. LABORATORY FINDINGS: Hemoglobin, 13.2 gm/dL; mean corpuscular volume, 80 micron 3; white blood cell count, 7,200/mm3 (normal differential); platelet count, 137,000/mm3. serum: electrolytes, normal; blood urea nitrogen, 18 mg/dL; creatinine, 0.8 mg/dL; glucose, 308 mg/dL; total protein, albumin, liver enzymes, and creatine kinase, normal. urine: 1 glucose. Venereal disease test: nonreactive; hiv test: negative. DIFFERENTIAL diagnosis: dermatomyositis; heavy-metal poisoning; diabetic amyotrophy. HOSPITAL COURSE: The patient was given 50 mg/day of oral amitriptyline to alleviate the painful paresthesias and was switched to 20 U/day of subcutaneously injected neutral protamine Hagedorn (NPH) insulin to normalize the blood glucose level. Histologic studies of skin and muscle showed sun damage and neuropathic changes, respectively. There was no evidence of vasculitis. Screening for heavy-metal toxins produced negative results.- - - - - - - - - - ranking = 1keywords = atrophy (Clic here for more details about this article) |
2/29. 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.- - - - - - - - - - ranking = 0.63004844936089keywords = optic (Clic here for more details about this article) |
3/29. Mitochondrial dna mutation at np 3243 in a family with maternally inherited diabetes mellitus.Mitochondrial dna (mtDNA) gene defects may play a role in the development of maternally inherited diabetes mellitus and deafness (MIDD). A family from Southern italy who showed maternal transmission of type 2 diabetes mellitus with three individuals affected is described. A 10.4 kb deletion and mutations at nucleotide positions (np) 3243, 7445 and 11778 in the mtDNA of six relatives were sought. The mitochondrial np 3243 mutation of the tRNA Leu (UUR) gene was identified in a boy affected by optic atrophy and mental retardation, as well as in his diabetic mother. No other mutations or deletions were found. Our study points out the variable phenotypic expression of the np 3243 mtDNA mutation. This may suggest the presence of other mitochondrial or nuclear mutations required to modulate the phenotype. A clinical and metabolic follow-up of all family members was necessary to understand the role of the np 3243 mutation, especially in one child affected by optic atrophy and mental retardation. Further studies will be aimed at investigating the prevalence of mutations and deletions of mtDNA in type 2 diabetes mellitus.- - - - - - - - - - ranking = 3.2600968987218keywords = atrophy, optic (Clic here for more details about this article) |
4/29. Bell's palsy during interferon therapy for chronic hepatitis c infection in patients with haemorrhagic disorders.Two adult patients with life-long severe haemorrhagic disorders commenced on interferon-alpha2b therapy for chronic hepatitis c infection. Both developed Bell's palsy several weeks after commencing therapy, They were started on steroids and, in addition, the first patient discontinued interferon-alpha2b therapy while the second patient elected to continue with therapy. In both cases facial paralysis improved over the ensuing weeks. Bell's palsy is often idiopathic but has been reported. in association with herpesviruses. It is not a recognised complication of chronic hepatitis b or C infection, or interferon-alpha2b therapy. However, the interferons are associated with numerous adverse reactions including various neuropsychiatric manifestations and neurological syndromes. There are several reports of nerve palsies, including optic tract neuropathy, occurring during interferon therapy, and immune-based mechanisms are thought to play a role in the aetiopathogenesis. No reports of Bell's palsy in association with interferon therapy were identified in our literature search, although one possible case has been reported to the Committee of safety in medicine. Although Bell's palsy in our patients may have occurred by chance, a neuropathic effect of interferon-alpha2b on the facial nerve cannot be excluded and we urge physicians using interferons to be aware of this potential side-effect.- - - - - - - - - - ranking = 0.63004844936089keywords = optic (Clic here for more details about this article) |
5/29. Superior orbital fissure syndrome in a latent type 2 diabetic patient.Although isolated cranial nerve palsies are common in diabetic patients, multiple, simultaneous cranial neuropathies are rare. We describe the second case of a complete superior orbital fissure syndrome including the optic nerve in a middle-aged Papuan man with newly diagnosed diabetes mellitus. The differential diagnosis included septic cavernous sinus thrombosis and Tolosa Hunt syndrome, and management was initially directed at excluding these serious, treatable conditions.- - - - - - - - - - ranking = 0.63004844936089keywords = optic (Clic here for more details about this article) |
6/29. diabetes mellitus secondary to glycogen storage disease type iii.BACKGROUND: diabetes mellitus is a rare complication of glycogen storage disease type III (GSD III). CASE REPORT: We describe a 47-year-old man with GSD III who developed diabetes mellitus. He was diagnosed as having GSD III at the age of 18 years, and his glucose tolerance was normal at that time. liver dysfunction and muscle atrophy gradually progressed, and the patient developed diabetes mellitus at the age of 45. When the post-prandial hyperglycaemia worsened, we instituted treatment with an alpha-glucosidase inhibitor, voglibose, and this improved glycaemic control without any adverse effects. CONCLUSIONS: We recommend serial evaluation for complications of GSD III, and propose that an alpha-glucosidase inhibitor may be a favourable drug in treating diabetes mellitus secondary to GSD III.- - - - - - - - - - ranking = 1keywords = atrophy (Clic here for more details about this article) |
7/29. Human recombinant dna insulin-induced lipoatrophy in a patient with type 2 diabetes mellitus.OBJECTIVE: To present the first case of lipoatrophy occurring in a patient with type 2 diabetes mellitus who was treated with human recombinant dna (rDNA)-derived insulin as her only exposure to exogenous insulin. methods: We describe the clinical findings in a 47-year-old woman with lipoatrophy after injection of human rDNA insulin for type 2 diabetes, and we review the related literature. RESULTS: Although a few case reports have documented lipoatrophy in patients with type 1 diabetes treated with human insulin, to our knowledge no previous reports have described patients with type 2 diabetes in whom lipoatrophy developed after injection of human rDNA insulin. This was our patient's first exposure to exogenous insulin. No definite factor was found to be contributory to the development of lipoatrophy in this case, even though several factors may be related. CONCLUSIONS: This is the first published case report of lipoatrophy occurring in a patient with type 2 diabetes mellitus who received human rDNA insulin as her only exposure to exogenous insulin.- - - - - - - - - - ranking = 10keywords = atrophy (Clic here for more details about this article) |
8/29. Long-term follow-up of idiopathic central serous chorioretinopathy without laser.PURPOSE: The purpose of this study was to observe the varied types of manifestations in the fundus of patients with idiopathic central serous chorioretinopathy (ICSC) without laser treatment and also to assess the ultimate visual outcome in such cases in a long-term follow-up ranging from 7 to 23 years. methods: This study is confined to 5 selected cases of ICSC which fairly represent the different types of late stage manifestations of the disease in the fundus. Case records from our hospital, as well as available records of previous treatment elsewhere were reviewed. A complete ophthalmological examination, routine laboratory investigations and fluorescein fundus angiography (FFA) were repeated in each case on the day of final evaluation. RESULTS: Pigmentary disturbances in the macular area resembling to some extent age-related macular degeneration (AMD), extensive retinal pigment epithelial (RPE) atrophy and macular haemorrhage have been observed in the fundus of the reviewed cases. CONCLUSIONS: ICSC runs an unpredictable course and there are no definitive clinical clues to predict its ultimate outcome. recurrence of the condition is a possibility for a considerable period of time.- - - - - - - - - - ranking = 1keywords = atrophy (Clic here for more details about this article) |
9/29. Visual loss after coronary artery bypass surgery.Anterior ischemic optic neuropathy is caused by microvascular occlusion of the prelaminar or laminar portion of the optic nerve head. The main types are arteritic, non-arteritic, and autoimmune. Few cases were reported following coronary artery bypass surgery. A 63-year-old man, who is both diabetic and hypertensive, underwent coronary artery bypass graft complicated postoperatively by sudden visual loss in his right eye. The diagnosis was non-arteritic anterior ischemic optic neuropathy. Possible predisposing factors were crowded disc and internal carotid artery stenosis.- - - - - - - - - - ranking = 1.8901453480827keywords = optic (Clic here for more details about this article) |
10/29. Syndrome of lipodystrophy, hyperlipidemia, insulin resistance, and diabetes in treated patients with human immunodeficiency virus infection.OBJECTIVE: To describe the syndrome of lipodystrophy, hyperlipidemia, insulin resistance, and diabetes in patients with human immunodeficiency virus (hiv) infection treated with protease inhibitor drugs. methods: This is a case series of patients referred from an infectious disease clinic to a diabetes-endocrinology clinic in an academic medical center because of severe metabolic problems that occurred during the course of otherwise-successful treatment of hiv infection. The clinical course, abnormalities on physical examination, laboratory data, and complications are described and analyzed. The pathogenesis of the syndrome is discussed and compared with that of type 2 diabetes, lipoatrophic diabetes, and mouse models of lipodystrophy. RESULTS: In six male patients receiving antiretroviral therapy for hiv infection, a syndrome of lipoatrophy of the face, legs, and buttocks, hyperlipidemia (predominantly hypertriglyceridemia), and type 2 diabetes mellitus was noted. Two patients had pronounced abdominal obesity, in contrast to their thin extremities. Five of the six patients were receiving protease inhibitor drugs, which have been thought to contribute to metabolic abnormalities. In two patients, ischemic heart disease had developed. CONCLUSION: protease inhibitors frequently cause insulin resistance and lipoatrophy in subcutaneous adipose tissue. These abnormalities are associated with visceral adiposity, hyperlipidemia, diabetes, and cardiovascular consequences and represent an important and unsolved problem in the treatment of hiv-infected patients.- - - - - - - - - - ranking = 2keywords = atrophy (Clic here for more details about this article) |
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