1/107. Effects of diabetes mellitus on patients with acute intermittent porphyria.OBJECTIVES: To study the effects of diabetes mellitus in patients with acute intermittent porphyria (AIP). Haeme deficiency in the liver of AIP patients stimulates an increase in ALA-synthase which triggers an escalating metabolic chain reaction, leading to an increase in the porphyrin content. This reaction can be reduced by treating AIP patients with haeme arginate or with glucose. DESIGN: A population-based study of all patients > 18 years of age having dna-verified AIP (n = 328) living in the two most northerly counties of sweden (Norrbotten and Vasterbotten, with 550,000 inhabitants) of whom 16 had type 2 diabetes. prevalence of diabetes was studied retrospectively in 26 AIP patients with hepatocellular carcinoma (HCC). RESULTS: None of the patients showed symptoms of AIP after the onset of their diabetes. Three patients had had recurrent, severe attacks for many years but when their diabetes became manifest, their urinary ALA and PBG levels decreased and the AIP symptoms resolved, to the relief of the patients. Amongst the 26 AIP patients with HCC, only one with signs of diabetes was identified (impaired glucose tolerance test). CONCLUSIONS: This study raises the possibility that diabetes mellitus may be beneficial for patients with severe AIP.- - - - - - - - - - ranking = 1keywords = liver (Clic here for more details about this article) |
2/107. pregnancy outcome in aboriginal women with NIDDM in the Sioux Lookout Zone.PURPOSE: To review the pregnancy outcomes of Aboriginal women with non-insulin-dependent diabetes mellitus (NIDDM) in the Sioux Lookout Zone of Northwestern ontario, canada. METHOD: Retrospective chart review of deliveries of all women with a confirmed diagnosis of NIDDM was carried out between 1989 and 1992. RESULTS: During this period, 26 infants were born to 19 women with the diagnosis of NIDDM. Mean birth weight was 4,075 grams, with an average gestational age at delivery of 38 weeks. Three newborns required cesarean delivery, one required forceps, and one a vacuum extraction. There were four cases of shoulder dystocia. There were one stillbirth, one maternal death, and two cases of congenital heart disease. Ten newborns had neonatal jaundice and only two had neonatal hypoglycemia. These results suggest there is significant risk associated with NIDDM in pregnancy.- - - - - - - - - - ranking = 3keywords = liver (Clic here for more details about this article) |
3/107. Non-insulin-dependent diabetes mellitus with type I multiple symmetrical lipomatosis: a case report.Type I multiple symmetrical lipomatosis (MSL; Madelung's disease) is characterized by lipomas in the nape of the neck and the supraclavicular and deltoid regions, resulting in a bull-necked appearance (Madelung's collar). It is most common in alcoholic men between 35 and 50 years of age. Type I MSL has been reportedly associated with hyperinsulinemia, but its association with diabetes mellitus is rarely discussed. We describe a case of non-insulin-dependent diabetes mellitus (NIDDM) associated with type I MSL. A 47-year-old alcoholic man presented with a seven-year history of hyperglycemia and progressive neck swelling with dysphagia for one year. physical examination showed diffuse and symmetrical swelling of the bilateral posterior aspects of the neck. biochemistry profiles revealed elevated concentrations of fasting serum glucose (276 /- 16 mg/dl), triglycerides (358 /- 79 mg/dl) and total cholesterol (323 /- 28 mg/dl). Endocrinologic studies showed normal thyroid function. neck sonography revealed diffuse thickening and swelling of the fatty structures of both sides of the neck. Normal sonography showed no fatty deposition in the liver. Maxillary and neck computerized tomography revealed diffuse fat accumulation in the submental and posterior neck regions, with no extension to the superior mediastinum. Fine needle aspiration cytology of the neck masses showed only fat cells. The patient received an oral hypoglycemic agent (glibenclamide 5 mg bid) for blood glucose control and lovastatin (20 mg before bed-time) for hyperlipidemia, and ceased drinking alcohol. The neck swelling resolved markedly after 15 months of medical treatment. This suggests that, in addition to the cessation of alcohol consumption, the reduction of blood glucose and lipid concentrations by medication may also assist in resolving the accumulated fat of type I MSL in patients with NIDDM.- - - - - - - - - - ranking = 2.7707030546365keywords = liver, fatty (Clic here for more details about this article) |
4/107. 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 = liver (Clic here for more details about this article) |
5/107. 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.- - - - - - - - - - ranking = 0.88535152731826keywords = fatty (Clic here for more details about this article) |
6/107. hepatitis a-induced diabetes mellitus, acute renal failure, and liver failure.A 38-year-old otherwise healthy man presented with hepatic failure (aspartate aminotransferase of 7212 U/L, alanine aminotransferase of 6629 U/L, total and direct bilirubin of 10.7 mg/dL) and acute renal failure (creatinine of 11.6 mg/dL and blood urea nitrogen of 42 mg/dL), which required hemodialysis when the creatinine increased to 21 mg/dL, with a blood urea nitrogen of 115 mg/dL, and the patient became oliguric. On admission, this patient also had a lipase of 1833 U/L, amylase of 211 U/L, glucose of 210 mg/dL, and reactive IgM antibody for acute hepatitis a. The hepatitis and acute renal failure resolved in 3 months, but this patient continues to have type II diabetes mellitus 7 years after the hepatitis a infection. This case illustrates that hepatitis a infection may be severe with liver failure, acute renal failure, and permanent diabetes mellitus as sequale of this infection.- - - - - - - - - - ranking = 5keywords = liver (Clic here for more details about this article) |
7/107. 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.- - - - - - - - - - ranking = 1keywords = liver (Clic here for more details about this article) |
8/107. Hepatic failure in a patient taking rosiglitazone.BACKGROUND: Rosiglitazone maleate is the second approved oral hypoglycemic agent of the thiazolidinedione class. The first, troglitazone, has been associated with liver failure, occasionally resulting in liver transplantation or death. There have been no reports to date of rosiglitazone-associated elevations in the alanine aminotransferase level or hepatotoxicity. OBJECTIVE: To report the clinical characteristics of liver failure developing in a patient receiving rosiglitazone. DESIGN: Case report. SETTING: University hospital. PATIENT: 69-year-old man taking rosiglitazone, 4 mg/d. INTERVENTION: Discontinuation of rosiglitazone therapy and treatment with lactulose, vitamin k, fresh frozen plasma, ventilatory assistance, and intensive care unit support. MEASUREMENTS: Blood test monitoring, including toxicology screening, liver function tests, coagulation studies, serum chemistries, and complete blood counts. RESULTS: After 21 days of rosiglitazone therapy, hepatic failure developed. Other causes of hepatic failure, such as viruses and toxins, were excluded, although it is possible that congestive heart failure was also a causative factor. The patient recovered fully with supportive care. CONCLUSION: Rosiglitazone may be associated with hepatic failure.- - - - - - - - - - ranking = 4keywords = liver (Clic here for more details about this article) |
9/107. 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.- - - - - - - - - - ranking = 3keywords = liver (Clic here for more details about this article) |
10/107. gliclazide-induced acute hepatitis.There are few reports in the literature related to sulfonylurea-induced hepatotoxicity. We describe the case of acute hepatitis induced by gliclazide, a second generation sulfonylurea. A 60-year-old woman with diabetes mellitus (type 2) developed an acute icteric hepatitis-like illness 6 weeks after the initiation of gliclazide therapy. Other causes of acute hepatocellular necrosis were excluded. Liver histology showed marked portal inflammation with lymphocytes, monocytes and eosinophils, associated with lobular inflammation (indicative of a histological pattern consistent with drug-induced hepatitis). The drug was immediately withdrawn and the patient was given glibenclamide. The patient recovered clinically and, in less than 4 weeks, her serum bilirubin and aminotransferases returned to normal levels. We believe that this is the first description of acute hepatitis caused by an idiosyncratic adverse reaction to gliclazide or to one of its metabolites. In conclusion, this case strongly suggests that gliclazide can induce acute icteric liver necro-inflammation which may be misdiagnosed clinically as acute viral hepatitis. In patients who show abnormal liver function tests, the immediate discontinuation of gliclazide is recommended.- - - - - - - - - - ranking = 2keywords = liver (Clic here for more details about this article) |
| | Next -> |