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Biomedical subjects

D Garzoni

Publications and source records attributed to D Garzoni.

5 recordsLinked to original sources

Inaccurate self-monitoring of blood glucose readings in patients on chronic ambulatory peritoneal dialysis with icodextrin.

Patients on chronic ambulant peritoneal dialysis (CAPD) are increasingly likely to be treated with a new solution of corn starch-derived glucose polymers called icodextrin. This solution involves a very low carbohydrate absorption leading to a better glycemic control in diabetic patients. However these glucose polymers pass to the blood and are metabolized to oligosaccharids which interfere with blood glucose in distinct capillary glucose analyzers leading to overestimation of glycemia. We assessed the accuracy of glucose measurements with the three most commonly used glucose analyzers compared to venous plasma glucose measurement at our institution in 8 patients (4 patients with type 2 diabetes) on CAPD using icodextrin. Glycemia was measured simultaneously in plasma of venous blood using a reference laboratory method and in capillary blood using Accu-Chek sensor (Rotkreuz, Switzerland) (glucose dehydrogenase method), Glucotrend 2 (Rotkreuz, Switzerland) (glucose-dye-oxyreductase method) and Ascensia elite (Zurich, Switzerland) (glucose oxidase method) glucose analyzers. Only glucose readings with Ascensia elite correspond correctly with venous plasma glucose results (+0.3 mmol/l; n. s.), whereas glycemia was significantly overestimated by Accu-Chek sensor (+4.3 mmol/l; p<0.0001) and Glucotrend 2 glucose analyzers (+3.7 mmol/l; p<0.0001). Thus we conclude that distinct glucose analyzers overestimate real blood glucose concentration and are not suitable for monitoring glycemia in patients on CAPD with icodextrin. On the basis of our results, these patients should use glucose analyzers using glucose oxidase methods. All glucose analyzers should be cross-checked with a laboratory reference method before the application in patients on CAPD with icodextrin is recommended.

Blood Glucose↗

[Lupus nephritis].

Lupus nephritis is a serious complication of systemic lupus erythematodes. It is important to establish the correct diagnosis in order to initiate the optimal treatment for a specific patient. Early therapy will prevent organ damage which otherwise can dramatically increase morbidity and mortality. This article provides information about pathogenesis, manifestations, laboratory investigations, histopathology and treatment of lupus nephritis. Besides the indication for treatment the various immunosuppressive protocols are discussed. Moreover, a specific treatment option is proposed and the follow up is described.

Clinical Trials as Topic↗

[C-reactive protein and early diagnosis of kidney transplant rejection].

C-reactive protein (CRP), which is known to rise rapidly in the serum after tissue injuries or inflammation, was measured daily after renal transplantation during hospitalization up to day 28 in 45 consecutive patients. In 16 patients who developed neither an infection nor rejection the CRP level normalized within 3 to 5 days. In 7 out of 14 patients with graft rejection the CRP level rose 1 to 3 days before the clinical signs of rejection. 11 patients with overt infection all had a CRP rise. 6 other patients had a CRP rise: in 5 the clinical situation explained this rise but in the sixth no explanation was found. We conclude from our results that periodic measurement of CRP (for example twice a week), even under aggressive immunosuppression, can help in the early diagnosis of graft rejection after renal transplantation. In the event of infection CRP loses its usefulness with respect to graft rejection and the daily measurements have no further point.

C-Reactive Protein↗

[Clinical aspects of staphylococcal endocarditis].

Patients with staphylococcus endocarditis hospitalized at the Cantonal Hospital Lucerne from 1971 to 1988 are reviewed. A total of 50 patients fulfilled the diagnostic criteria (in 60% of the cases the diagnosis was definite, in 26% probable, and in 14% possible). These 50 patients with staphylococcus infection account for 29% of all patients with infective endocarditis seen during this time interval. Staphylococcus endocarditis affected the mitral valve in 48%, the aortic valve in 36% and--unexpectedly often--the tricuspid valve in 30%. In 54% previously normal valves were infected. Diminished host defence (predominantly intravenous drug addiction and diabetes) was a predisposing feature in 52% of the patients. The average duration of symptoms before diagnosis was 11 days, and in patients with right heart endocarditis it was 21 days. In 20% the condition was not diagnosed before autopsy. The clinical picture was relatively nonspecific: 50% of patients had no diagnostic heart murmur and 10% had no fever. The dominant--often misleading--symptoms were due to embolic complications. Two thirds of the cases with right heart endocarditis had pulmonary emboli. In 38% of the patients endocarditis resulted in heart failure. Overall mortality was 51% and correlated with age and the presence of heart failure, uncontrolled infection or cerebral embolism. In contrast to the high mortality in patients with mitral valve infection (61%), only one of the 11 patients with isolated right heart endocarditis died.

Endocarditis, Bacterial↗

Necrotising enterocolitis and neuraminidase-producing bacteria.

In 9 out of 26 newborns with necrotising enterocolitis (NEC) exposure of the Thomsen-cryptantigen (T-antigen), probably due to the action of circulating bacterial neuraminidase, was demonstrated on red blood cells. The serological titres seemed to correlate with the clinical course of the disease. Neuraminidase-producing clostridia were isolated in two of the patients. Reaction between the exposed T-antigen and anti-T-agglutinins, normally present in human blood, may lead to difficulties during blood transfusion. This potential transfusion hazard is best avoided by routine T-antigen-tests and by transfusion of packed or washed red blood cells to T-antigen-positive patients.

Antibody Specificity↗