Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACIDOSIS, DIABETIC”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed2001

[Severe accidental hypothermia in an elderly woman].

Profound hypothermia (core temperature of less than 28 degrees C) is a life threatening state and a medical emergency associated with a high mortality rate. The prognosis depends on underlying diseases, advanced or very early age, the duration prior to treatment, the degree of hemodynamic deterioration, and especially, the methods of treatment, including active external or internal rewarming. This is a case study of an 80-year-old female patient with severe accidental hypothermia (core temperature 27 degrees C). She was found in her home lying immobile on the cold floor after a fall. The patient was in a profound coma with cardiocirculatory collapse, and the medical staff treating her was inclined to pronounce her deceased. On her arrival at the hospital, she was resuscitated, put on a respirator and actively warmed. Very severe metabolic disorders were found, including a marked metabolic acidosis composed of diabetic ketoacidosis (she had suffered from insulin treated type 2 diabetes mellitus) and lactic acidosis with a very high anion gap (42) and a hyperosmotic state (blood glucose 1202 mg/dl). There were pathognomonic electrocardiographic abnormalities, J-wave of Osborn and prolonged repolarization. Slow atrial fibrillation with a ventricular response of 30 bpm followed by a nodal rhythm of 12 bpm and reversible cardiac arrest were recorded. The pulse and blood pressure were unobtainable. Despite the successful resuscitation and hemodynamic and cognitive improvement, rhabdomyolysis (CKP 6580 u/L), renal failure and hepatic damage developed. She was extubated and treated with intravenous fluids containing dopamine, bicarbonate, insulin and antibiotics. Her medical condition gradually improved, and she was discharged clear minded, functioning very well and independent. Renal and liver tests returned eventually to normal limits. Progressive bradycardia, hypotension and death due to ventricular fibrillation or asystole commonly occur during severe hypothermia. Respiratory and metabolic, sometimes lactic, acidosis, lethargy and coma, hypercoagulopathy, hyperosmolar state, acute pancreatitis and renal and hepatic failure are frequent complications of hypothermia. Underlying predisposing causes of hypothermia are diabetic ketoacidosis, cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency, malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction, sepsis and polypharmacy, and especially, the use of sedative and narcotic drugs. Our case demonstrates once again that CPR once begun should continue until the successful rewarming because "no one is dead until warm and dead".

Aged↗
PubMed2006

Sudden death in a patient newly diagnosed with diabetes having hyperosmolar non-ketotic acidosis with sickle cell trait.

Sickle cell trait (SCT) has a UK urban population rate estimated at 3.2%. The condition may remain unrecognised, but sudden death is a recognised feature. The sudden death of a 51-year-old man with SCT who presented with hyperosmolar non-ketotic acidosis (HONK) as his first presentation of diabetes is reported here. After admission to hospital, a rapid deterioration was seen in his condition, with loss of cardiac output, leading to death. He was found to have had acute-chest syndrome and hepatosplenic infarction on postmortem examination. The pathophysiology of sudden death in patients with SCT and the role of HONK in the patient's demise is discussed here.

Acidosis↗
PubMed1995

[A case of Sjögren's syndrome complicated with cryoglobulinemia, nephrogenic diabetes insipidus, and renal tubular acidosis].

A 68-year-old woman had been complained of xerostomia since she was 30 years old. Further symptoms of polyuria, polyposia and insomnia had been developed since she was 35 years old. The biopsy material from a minor salivary gland demonstrated the infiltration of lymphocytes into mesenchyme which was compatible with Sjögren's syndrome. She admitted to our hospital because of myalgia in bilateral gastrocnemius and petechiae in both lower extremities in addition to the complaints described above. Complete blood cell counts on admission revealed hemoglobin 9.7 g/dl, platelet count 12.5 x 10(4)/microliters, and white blood cell count 3,300/microliters. Marked polyuria, polyposia (more than 5,000 ml/day, respectively) and low urine gravity (1.005) were observed, although the serum creatinine level showed normal value. Serologic examination showed that the elevation of total serum protein concentration (9.5 g/dl) with marked elevation of serum IgG level (6,190 mg/dl). Her immunoglobulins contained cryoglobulin (cryocrit 20%), and immunoelectrophoresis demonstrated the existence of IgG-kappa monoclonal protein. A positive anti-nuclear antibody at 1:320 dilution, a positive rheumatoid factor and a positive antibody to SS-A (Ro) were also observed. The serial studies of blood gas analysis could not demonstrated the presence of metabolic acidosis. Together with the result of elevated plasma antidiuretic hormone level and results of vasopressin test, Fishberg's concentrating test and the tests of the overload of NH4Cl or bicarbonate, she was diagnosed Sjögren's syndrome with both diabetes insipidus and subclinical renal tubular acidosis. She was initially medicated with prednisolone (40 mg/day, orally), then she was given six courses of intravenous cyclophosphamide (750 mg/body/month).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed2005

Effect of keto-acidosis on seizure occurrence in diabetic patients.

It has been observed anecdotally that diabetics are usually non-ketotic at the time of their seizure presentation. In order to establish some validity on this observation, we reviewed the medical records of patients with diagnoses of diabetes and seizure. Study subjects were diabetics presenting with seizures. Control subjects were random sampling of all diabetics. In 51 diabetics presenting with seizures, 38 were nonketotic and 13 were ketotic. In the control group of 119 diabetics, 63 were non-ketotic and 56 were ketotic. There were no significant differences in the serum levels of glucose, sodium, potassium, chloride, and calcium between the seizure and control groups. Multiple regression analysis showed that non-ketotic patients were at risk for developing seizures with an odds ratio of 4.03 (p=0.001). Male sex and type 1 diabetes were also risk factors while age was not a risk factor. Keto-acidosis may play a role in preventing epileptic seizures from occurring in diabetic patients.

Case-Control Studies↗
PubMedDate not supplied

The balance between glucocorticoids and insulin regulates muscle proteolysis via the ubiquitin-proteasome pathway.

In uremia, accelerated muscle protein degradation results from activation of the ATP-ubiquitin proteasome proteolytic pathway. Like uremia, other conditions (e.g., acidosis and diabetes) activate this pathway in rat muscles and are associated with excess glucocorticoids (GC) and impaired insulin action. To define the stimuli responsible for muscle wasting in IDDM, the roles of glucocorticoids, insulinopenia and acidosis in streptozotocin (STZ) - induced diabetes were studied. Proteolysis in isolated epitrochlearis muscles from acutely (3d) diabetic rats was 52% higher than pair-fed, sham-injected rats; this increase was eliminated by an inhibitor of the proteasome or by blocking ATP synthesis. In muscles of STZ-diabetic rats, the levels of ubiquitin-conjugated proteins and mRNAs encoding ubiquitin, the ubiquitin-carrier protein, E2(14k) and the C3, C5 and C9 proteasome subunits were increased. Transcription of ubiquitin and C3 proteasome subunit genes in muscle was also increased by IDDM. Oral NaHCO(3) eliminated acidemia but did not prevent accelerated muscle proteolysis. Corticosterone excretion was higher in IDDM rats and adrenalectomy (ADX) prevented these catabolic responses; physiologic doses of glucorcoticoids restored the excessive protein catabolism in ADX-STZ rats. Giving IDDM rats replacement insulin also normalized protein degradation in muscles. In conclusion, reduced insulin together with physiologic levels of glucocorticoids activate the ubiquitin-proteasome pathway by a mechanism that includes enhancing ubiquitin conjugation and proteolysis by the proteasome. The balance between these stimuli could regulate muscle proteolysis in uremia.

Acidosis↗
PubMed2006

Pemetrexed-induced acute renal failure, nephrogenic diabetes insipidus, and renal tubular acidosis in a patient with non-small cell lung cancer.

We report a patient with metastatic non-small cell lung cancer who developed renal toxicities manifest as acute renal failure associated with nephrogenic diabetes insipidus and distal renal tubular acidosis following sequential therapy with pemetrexed. The nephrotoxicity occurred concomitantly with severe myelosuppression. We postulate renal tubular toxicity may account for distinct patterns of injury including acute renal failure and tubular cell dysfunction of the distal nephron.

Acidosis, Renal Tubular↗
PubMed2000

[Multiorgan dysfunction syndrome complicating hyperosmolar hyperglycemic syndrome as the primary feature of juvenile diabetes].

Diabetic ketotic acidosis and hyperosmolar hyperglycemic syndrome are regarded as the most serious diabetes complications. Acute renal failure frequently develops simultaneously with the symptoms of multiorgan disfunction and might be a factor indicating the severity of the primary disease. Authors present a case of a 11-year-old boy with acute renal failure due to defective perfusion and disseminated intravascular coagulation as the complications of hyperosmolar hyperglycemic syndrome. This syndrome was the first feature of juvenile diabetes. Intensive treatment of fluid and electrolyte disorders, mechanic ventilation, renal replacement therapy, and close collaboration of trained nephrologist with intensive care unit specialists allowed to cure critical health states and improve the course of diabetes.

Child↗
PubMed2006

Unexplained acidosis of malnutrition: a study by ion-exchange chromatography/mass spectrometry.

Keto-acidosis is usually associated with uncontrolled diabetes and typically poses few diagnostic problems when presenting as hyperglycaemia, metabolic acidosis and a high anion gap. An emaciated patient suffering from Duchenne Muscular Dystrophy and volume depletion presented with acidosis of unknown origin. Preliminary investigations appeared to rule out lactic acidosis, diabetic keto-acidosis and acidosis due to base loss. We have previously reported a technique utilizing liquid chromatography coupled to mass spectrometry (LC-MS) which can be used to characterize the underlying aetiology of acidosis and applied it to ultrafiltrate derived from a blood sample taken from this patient. The anion profile obtained on the chromatogram showed elevated levels of acetoacetate and hydroxybutyrate but no evidence of lactic acidosis, nor was the profile typical of that seen in 'unexplained' acidosis. We concluded that the patient was suffering from keto-acidosis associated with starvation and dehydration, the biochemical features being obscured by both the patient's chronic malnutrition and minimal muscle mass. A combination of enteral feeding and rehydration led to prompt resolution of the patient's metabolic acidosis.

Acetoacetates↗
PubMed1984

Ultrastructure of heart muscle in short-term diabetic rats: influence of insulin treatment.

The ultrastructure of myocardium was examined in short-term diabetic rats. Morphometric analysis showed the volume of myocytic mitochondria, sarcoplasmic reticulum and lipid droplets to be significantly increased compared with those of control animals. Further measurements of mitochondria and sarcoplasmic reticulum indicated that the augmentation of these compartments was accountable by the enlargement of pre-existing mitochondria, which were swollen, and of pre-existing tubules of sarcoplasmic reticulum, the lumen of which was dilated. After insulin treatment the morphological changes were returned to normal which indicates that they were not due to the toxic effect of streptozotocin but were caused by the diabetic state per se. This suggestion is further supported by the finding that experimentally induced metabolic acidosis without diabetes did not cause any morphologically detectable changes in the heart muscle. It is concluded that short-term diabetes in the rat causes mitochondrial swelling, dilatation of sarcoplasmic reticulum and accumulation of lipid in cardiac myocytes, and that these changes are preventable with insulin treatment. We suggest that insulin may have an important role in the maintenance of metabolism in heart muscle.

Acidosis↗
PubMed1997

Pancreatic insufficiency due to antituberculous therapy.

OBJECTIVE: To describe a case of chronic pancreatic insufficiency related to antituberculous therapy. CASE SUMMARY: A 57-year-old man developed rash, fever, and hepatitis (aspartate aminotransferase 369 IU/L, alanine aminotransferase 506 IU/L), 6 weeks after starting isoniazid, rifampin, ethambutol, and pyrazinamide. He also developed severe metabolic acidosis secondary to diabetic ketoacidosis and lactic acidosis (serum bicarbonate 7 mEq/L, glucose 1778 mg/dL, and lactate 4.0 mEq/L). Acute pancreatitis was diagnosed on the basis of a mildly elevated amylase concentration (392 U/L) and radiologic evidence of pancreatic inflammation. He developed pancreatic insufficiency with steatorrhea and an abnormal secretin test. He continues to require pancreatic enzyme replacement and insulin therapy. Rechallenge was not performed. DISCUSSION: Hypersensitivity syndromes have been reported for various drug therapies, including antituberculous agents. Hypersensitivity syndrome reactions are characterized by fever, rash, and internal organ involvement. Rifampin has been reported to cause acute pancreatitis in up to 2.7% of patients. Drug-induced chronic pancreatitis, however, is reported to be extremely rare. This is the first reported case of chronic pancreatic insufficiency occurring in the setting of a hypersensitivity syndrome reaction to antituberculous drugs. CONCLUSIONS: Chronic pancreatic insufficiency should be considered as a possible long-term sequelae of a hypersensitivity syndrome reaction to antituberculous therapy.

Antitubercular Agents↗
PubMed1975

[Infusion theraphy in disorders of the acid-base equilibrium].

The acid-base balance is primarily regulated by renal and respiratory mechanisms affecting concentration of carbonic acid and bicarbonate in the extracellular fluid. The most important indication for intravenous therapy is diabetic keto-acidosis, lactate acidosis and the acidosis following poisoning. Calculation of the required amounts of buffer as well as corresponding formulars for therapy are of limited value and have always to be considered in relation to the actual clinical status.

Acid-Base Imbalance↗
PubMed2003

[Metformin-associated lactic acidosis remains a serious complication of metformin therapy].

We report 4 cases of lactic acidosis in diabetic patients usually treated with metformin. For the first 3 patients, the clinical history was similar because lactic acidosis was precipitated by gastro-intestinal disorders whereas all of them were simultaneously treated with several nephrotoxic drugs. These 3 patients presented with acute renal failure on arrival at hospital. Their issue was fatal whereas any obvious cause of overproduction of lactate was found. The fourth case, which was due to a voluntary intoxication, was the only one presenting with a favourable evolution. The metformin plasma and red blood cell levels were performed for 2 of 4 patients and confirmed the overdose. These observations remind that metformin-associated lactic acidosis remains a serious complication, and that medical doctors must respect strictly contra-indications and guidelines for withdrawing metformin.

Acidosis, Lactic↗