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At least 919 records · Page 51Linked to original sources
PubMed2005

Pancreatic beta and alpha cells are both decreased in patients with fulminant type 1 diabetes: a morphometrical assessment.

AIMS/HYPOTHESIS: We have previously reported that fulminant type 1 diabetes is characterised by an absence of diabetes-related antibodies and a remarkably abrupt onset. However, little is known about the mechanism of beta cell destruction in this diabetes subtype, and to obtain insights into the aetiology of the disease, we investigated residual endocrine cells and the expression of Fas and Fas ligand in fulminant type 1 diabetes. METHODS: Residual beta and alpha cells were morphologically assessed in pancreatic tissue obtained by biopsy from five patients with recent-onset fulminant type 1 diabetes and five patients with recent-onset typical autoimmune type 1 diabetes. In addition, the expression of Fas and Fas ligand was evaluated by immunohistochemistry. RESULTS: In fulminant type 1 diabetes, beta and alpha cell areas were decreased significantly, compared with autoimmune type 1 diabetes and control subjects. In contrast, the alpha cell area was not decreased significantly in autoimmune type 1 diabetes, compared with that in control subjects. No Fas expression in islets and Fas ligand expression in CD3(+) cells in the exocrine pancreas were found in the fulminant type 1 diabetic patients who underwent this evaluation. CONCLUSIONS/INTERPRETATION: Our study showed that beta and alpha cells are damaged in fulminant type 1 diabetes. In addition to the lack of Fas and Fas ligand expression, the results suggest that the mechanism of beta cell destruction in fulminant type 1 diabetes is different from that in autoimmune type 1 diabetes.

Acidosis↗
PubMed1993

Pearson bone marrow-pancreas syndrome with insulin-dependent diabetes, progressive renal tubulopathy, organic aciduria and elevated fetal haemoglobin caused by deletion and duplication of mitochondrial DNA.

We report a patient with a clinical picture consisting of small birth weight, connatal hypoplastic anaemia, vacuolised bone marrow precursors, failure to thrive, and, subsequently, by insulin-dependent diabetes, renal Fanconi syndrome, lactic acidosis, complex organic aciduria, and elevation of haemoglobin F and of adenosine deaminase activity. The clinical course was progressive and death occurred at age 19 months. A high proportion of mitochondrial (mt) DNA molecules with a deletion of nucleotides 9238 to 15575 were identified in several tissues; about half of the shortened mtDNA molecules were concatenated to form circular dimers. The clinical and laboratory findings support recent conclusions that Pearson syndrome is not confined to bone marrow and pancreas, as originally described, but is a multi-organ disorder associated with deletions in part of the mtDNA molecules. The tissue distribution and the relative proportions of the abnormal mtDNA molecules apparently determine the phenotype and clinical course.

Acidosis, Lactic↗
PubMed1987

[Interstitial nephropathies induced by meticillin: demonstration of distal tubule functional anomalies].

Renal tubular dysfunction was investigated in two patients with meticillin-induced interstitial nephritis. Some degree of renal failure persisted after the acute episode in both cases. The first patient was investigated 10 weeks after the onset of the nephropathy. Nephrogenic diabetes insipidus and distal tubular acidosis were demonstrated. The second patient was investigated 7 months after the onset of the nephropathy. A major impairment in urinary concentration ability was demonstrated. Neither patient had proximal tubular dysfunction. These data show that meticillin-induced interstitial nephritis may be responsible for distal tubular abnormalities, namely nephrogenic diabetes insipidus and distal tubular acidosis, which may persist long after the onset of the nephropathy.

Adult↗
PubMedDate not supplied

Severe lactic acidosis and renal involvement in a patient with relapsed Burkitt's lymphoma.

We describe an 8-year-old patient with relapsed Burkitt's lymphoma who developed complex metabolic problems, including renal diabetes insipidus and severe lactic acidosis. The lactic acidosis responded temporarily to chemo- and radiotherapy but not to bicarbonate or thiamine administration. These metabolic changes were most likely due to the lymphomatous infiltration of the kidneys. Severe lactic acidosis, without evidence of thiamine deficiency, seems to be a very rare event in children with cancer.

Acidosis, Lactic↗
PubMed2004

Glibenclamide-induced acute haemolytic anaemia revealing a G6PD-deficiency.

A 58-year-old woman was admitted at diagnosis of type 2 diabetes without keto-acidosis. Blood glucose was normalized initially with insulin. Whilst taking glibenclamide, she developed acute haemolysis. She was homozygous for glucose-6-phosphate dehydrogenase (G6PD) deficiency and had no other factors predisposing haemolysis. We reviewed the literature and discuss the relationship between glibenclamide and haemolytic crisis and between G6PD-deficiency and diabetes.

Anemia, Hemolytic↗
PubMed1997

Pathogenesis of cerebral edema after treatment of diabetic ketoacidosis.

We studied the roles of acidosis, plasma osmolality, and organic osmolytes in the pathogenesis of cerebral edema in an animal model of diabetes mellitus. Normonatremic rats with streptozotocin-induced non-ketotic (NKD) and ketotic (DKA) diabetes were sacrificed before or after treatment with hypotonic saline and insulin. Brains were analyzed for water, electrolyte, and organic osmolyte content. Brain water decreased by 2% in untreated DKA and NKD despite a 12% increase in plasma osmolality due to hyperglycemia. After treatment of both NKD and DKA, brain water increased equivalently by 8%. The cerebral edema that occurred after treatment was associated with decreased brain sodium content and no change in total major brain organic osmolytes in both NKD and DKA. However, brain content of the individual osmolytes glutamine and taurine increased after treatment of DKA. In a separate study, brain water and solute content of rats with DKA were compared after treatment with either hypotonic or isotonic fluid. Animals treated with isotonic fluid had significantly less cerebral edema and higher brain sodium content than those treated with hypotonic fluid. In our studies, brain swelling after treatment of DKA and NKD was primarily due to a rapid reduction of plasma glucose and osmolality, and was not caused by sodium movement into the brain. Acidosis did not appear to play a major role in the pathogenesis of cerebral edema after treatment of DKA.

Animals↗
PubMed2004

Experiences of a poison center with metformin-associated lactic acidosis.

Metformin is widely used in the treatment of type 2 diabetes, though it is recognized to be associated with the risk of lactic acidosis. A case of pronounced lactic acidosis with cardiac arrest (pH 6.60, lactate 17.5 mmol/l, base excess - 30, standard bicarbonate 2.5 mmol/l, core body temperature 27.8 degrees C) is presented in a 61-year-old woman under metformin therapy. The key laboratory abnormalities observed during the intensive care treatment including repeated hemodialysis are described. The patient showed a complete recovery with residually reduced mental capabilities. Furthermore, an explorative data analysis of our poison center database from 1995 until 2003 concerning metformin was performed. In 109 inquiries for metformin a lactic acidosis (mean pH 6.87 +/- 0.11, mean lactate 20.9 +/- 8.1 mmol/l) was present in 14 cases (9 female, 5 male, average age 57.7 years) with 8 patients under regular metformin therapy and 6 patients who ingested large amounts of metformin to attempt suicide. 4 patients did not survive the severe metabolic disturbance. The present report demonstrates that metformin-associated lactic acidosis is a rare but critical complication of metformin therapy of type 2 diabetes as well as in acute suicidal ingestion of metformin. Early diagnosis and rapid correction of the metabolic acidosis using hemodialysis provides the possibility of a positive outcome even in severe cases. If metformin-associated lactic acidosis is suspected we recommend early involvement of a poison center.

Acidosis, Lactic↗
PubMed1992

Correlates of brain edema in uncontrolled IDDM.

Blood glucose, plasma sodium, bicarbonate (HCO3-), vasopressin, and hematocrit were monitored before and during treatment in patients with uncontrolled insulin-dependent diabetes mellitus (IDDM). These parameters were correlated with simultaneous serial cranial computed tomography readings of brain edema. Six of seven patients had positive computed tomography readings for brain edema on admission. Initial brain edema correlated directly with blood glucose (r = 0.79, P = 0.033) and inversely with HCO3- (r = -0.76, P = 0.047). At 6 h, brain edema still correlated with acidosis (HCO3-; r = -0.79, P = 0.033) but no longer with blood glucose. At that time, however, brain edema correlated with the rate of change in blood glucose (r = 0.915, P = 0.005). Results of interactive stepwise regression analysis suggest that the change in the calculated effective plasma osmolality plays a predominant role in the progression of brain edema during therapy (r = 0.995, P less than 0.001). Thus, although hyperglycemia and acidosis probably predispose to diabetic brain edema, osmotic factors may be major predictors of its evolution. No relationships were detected between brain edema and initiation of insulin therapy, plasma vasopressin, or changes in hematocrit. The factors responsible for initial brain edema and its progression, statistically identified in this study, require reassessment of common theories that attribute brain edema exclusively to therapy.

Adolescent↗
PubMed1986

[Food poisoning in patients with diabetes mellitus].

The clinical picture of food toxoinfections in patients with diabetes mellitus is characterized by a more severe and protracted course. On the other hand, food toxoinfections promote diabetes mellitus decompensation and the development of diabetic ketoacidosis. Since diabetes mellitus and food toxoinfections have a number of symptoms in common the authors suggest the diagnostic working schedule. Grave and medium-grave food toxoinfections in patients with diabetes mellitus mandate refusing the intake of oral antidiabetic drugs and long-acting insulins. It is recommended that insulin may be administered in divided doses.

Acidosis↗
PubMed1987

[Hemostasis and microcirculation in patients with diabetic ketosis].

Indices of acid-base equilibrium (ABE), the level of ketone bodies, coagulation and platelet procoagulant hemostasis, and erythrocyte aggregation were studied in 102 patients with diabetes mellitus, of them in 58 patients with diabetic ketoacidosis and in 10 practically healthy persons. The most frequent cause of the development of diabetic ketoacidosis was poorly controlled treatment of diabetes and infections. The most frequent type of ABE disorder in patients with diabetic ketoacidosis was metabolic acidosis with secondary compensatory respiratory alkalosis. Ketoacidosis was characterized by hemostatic disorders after hypercoagulation type, an increase in platelet and erythrocyte aggregation activity with secondary activated fibrinolysis.

Acid-Base Equilibrium↗
PubMed2002

[Development of severe lactic acidosis during radio frequency ablation conducted for the treatment of hepatocellular carcinomata in a patient with liver cirrhosis].

A 60-year-old male with liver cirrhosis (Child-Pugh class B) underwent laparotomic radio frequency ablation for the treatment of a solitary hepatocellular carcinoma (-4.5 cm in diameter). Severe lactic acidosis (base excess < -12 mEq.l-1, lactate > 150 mg.dl-1) developed during the intraoperative period, when neither his hemodynamics nor arterial oxygenation was significantly impaired. The blood loss was small (-200 g), and the serum hemoglobin level was maintained -10 g.dl-1 during the procedure. There was no evidence for impairment of either peripheral perfusion or renal function. In addition, there was no evidence for development of either splanchnic ischemia or diabetic ketoacidosis. Thus, the acidosis appeared to be caused by significant impairment of liver function possibly resulting from the ablation (total ablation time = -60 min). The core temperature increased rapidly (-1.5 degrees C/60 hr) immediately after the ablation was started, suggesting that a large amount of heat was produced in the ablated area and/or that the vicinity of the ablated area was richly supplied by blood flow. As a result, intact liver cells in the vicinity of the tumor probably suffered from thermal injuries. In conclusion, depending on preoperative liver function, ablated area, and/or blood flow in the vicinity of ablated area, the ablation may become significantly invasive.

Acidosis, Lactic↗