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Biomedical subjects

G Gamba

Publications and source records attributed to G Gamba.

At least 163 records · Page 9Linked to original sources
PubMedDate not supplied

Role of angiotensin II in the antinatriuresis that follows acute volume depletion.

The aim of this study was to examine the contribution of the renin angiotensin system to the antinatriuresis that follows acute volume depletion. Four groups of six dogs each were studied. The first group was exposed to saline expansion (8% body weight) (SE). The second group was exposed to acute volume depletion (2% body weight) followed in one hour by saline expansion (AVD). The third and fourth groups were similar but in dogs treated with high doses of captopril (SE + C and AVD + C). Dogs were anesthetized with phenobarbital. Control measurements were made for 30 minutes before and 60 minutes during saline expansion. Glomerular filtration rate (inulin), renal blood flow (para-aminohippuric acid) and mean arterial pressure were similar in the four groups during the experiment. The increase in fractional sodium excretion from the control period to the end of saline expansion was in the SE group from 0.6 +/- 0.2 to 6.4 +/- 1% and in the SE + C group from 1.1 +/- 0.3 to 8.5 +/- 1.3%. In contrast, in the AVD group it only rose from 0.8 +/- 0.2 to 3.5 +/- 0.7% and in the AVD + C group from 1.3 +/- 0.4 to 4.1 +/- 0.6%. Therefore, the increment in sodium excretion during saline expansion was significantly lower in dogs exposed to acute volume depletion, independent of the treatment with captopril. The blunted natriuresis cannot be explained by differences in GFR, RBF or MAP. These results suggest that renin angiotensin system is not the responsible agent of the sodium retention that follows acute volume depletion.

Acute Disease↗
PubMedDate not supplied

Bicarbonate therapy in severe diabetic ketoacidosis. A double blind, randomized, placebo controlled trial.

Intravenous sodium bicarbonate has been used for a long time in the treatment of diabetic ketoacidosis. However, there are no clinical studies showing its effectiveness in improving arterial pH in this condition. We therefore designed this study to investigate if bicarbonate therapy improves the rate of increase of arterial pH and to find out its effects on the recovery rate of the other metabolic abnormalities. Twenty patients with severe diabetic ketoacidosis (pH less than 7.15) entered a double-blind, randomized, placebo controlled trial: nine were included in the bicarbonate group and eleven in the placebo group. All patients were studied during the first 24 hours of treatment. Their management was similar, except for the use of sodium bicarbonate in one group and 0.9% saline solution in the placebo group. Heart rate, respiratory rate, arterial pressure, mental status, blood gases, blood glucose, sodium, potassium, and urea were assessed at the beginning of treatment, and then at 2, 6, 12 and 24 hours. No clinical or metabolic differences were found between groups. Two hours after therapy was begun, the arterial pH rose in the bicarbonate group from 7.05 +/- 0.08 to 7.24 +/- 0.04, while it only rose from 7.04 +/- 0.08 to 7.11 +/- 0.09 in the placebo group (p less than 0.02). Simultaneously, arterial bicarbonate increased from 2.87 +/- 1.2 to 6.1 +/- 1.5 mEq/L in the bicarbonate group and from 2.55 +/- 0.81 to 3.6 +/- 2 mEq/L in the placebo group (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Purpura fulminans as clinical manifestation of atypical SLE with antiphospholipid antibodies: a case report.

Purpura Fulminans and DIC were the main clinical manifestations of the antiphospholipid syndrome observed in a 62-year-old man. The patient was well until 44 years of age when he began to suffer from recurrent thrombophlebitis, without other symptoms suggestive of immune disease. At the time of hospital admission the pt. appeared acutely ill, showing high fever, severe anemia, massive urinary blood loss, multiple purpuric patches evolving to hemorrhagic bullae and gangrene rapidly spreading over about 30% of the total body area. No signs of neurological involvement or of visceral thrombotic occlusions were present. Clotting tests were consistent with a diagnosis of DIC, further confirmed by skin biopsy showing the presence of thrombi in dermal arterioles. The autoantibody research was positive as follows: Waaler-Rose 1:40, Anti-DNA 1:80; ANF 1:640, aCA IgG 100 GPL. LA was diagnosed according to standard criteria: prolonged KCT and RVVT not corrected by a mixture of normal plasma and abnormal TTI. Plasma exchange in association with heparin and prednisone was effective in arresting the progression of the skin lesion; nevertheless the patient died ten days after hospital admission for sepsi and acute renal failure.

Autoantibodies↗
PubMedDate not supplied

Clotting abnormalities in children during maintenance chemotherapy for acute lymphoblastic leukemia.

BACKGROUND: Many of the drugs used in the treatment of acute lymphoblastic leukemia in children may induce modifications in different organs and functions. Following the observation of a recurrent, mild delay in the prothrombin time in ALL children during maintenance chemotherapy, we explored the main parameters of the clotting function. METHODS: 17 children with acute lymphoblastic leukemia were studied during maintenance chemotherapy for clotting function screening evaluation; 15 healthy children, matched for age and sex, were used as controls. RESULTS: A uniform pattern of slight prolongation of the prothrombin time with significantly reduced levels of factors VII, IX, and a trend toward reduced activity of factor X was observed in the absence of any demonstrable anticoagulant factor. CONCLUSIONS: Antileukemic maintenance chemotherapy is associated with a subclinical modification of the clotting parameters that is not responsible for hemorrhagic diathesis. Long-term administration of anti-metabolites (6-mercaptopurine and methotrexate) could be responsible for this reversible impairment.

Adolescent↗
PubMedDate not supplied

[Membranous glomerulonephritis. Experience at the Instituto Nacional de la Nutrición Salvador Zubirán].

The purpose of this retrospective study was to study the incidence of idiopathic and secondary forms of membranous nephropathy in our institution, its clinical course and progression to chronic renal failure, and the risk factors associated with it. Two hundred fourteen (16%) of the 1,287 renal biopsies obtained between 1962 and 1988 were primary glomerular diseases and 28 of this 214 (13%) were idiopathic membranous nephropathy. On the other hand 59 of 1,287 biopsies were membranous nephropathy of whom 28 were idiopathic, 27 secondary to systemic lupus erythematosus, 2 due to drugs, one associated with rheumatoid arthritis, and one more with breast cancer. The clinical picture was: nephrotic syndrome in 84%, hypertension in 15%, non-nephrotic proteinuria in 14%, chronic renal failure in 8.4%, and renal vein thrombosis in 6.3%. In the idiopathic group 75% of the patients were male while in the lupus group 85% were female. For the analysis of progression to chronic renal failure we excluded 5 patients with renal failure when the biopsy was taken, 2 because the nephropathy was due to drugs, one associated with breast cancer, and nine were within the first year of follow-up. Thus, for this analysis the group consisted of 22 patients with idiopathic form and 20 with systemic lupus erythematosus. The idiopathic and lupus groups were similar except for a lower serum albumin in the former. The progression to renal failure was seen in 9 patients: six in the idiopathic group and the other 3 in the lupus group; this difference was not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMedDate not supplied

Amikacin nephrotoxicity in patients with chronic liver disease.

Chronic liver disease is a risk factor for aminoglycoside nephrotoxicity. We conducted this study to identify the incidence and risk factors associated with it. A total of 45 patients with liver disease and 329 controls were included, with a toxicity incidence of 17.7%, similar to that in controls. Chronic liver disease patients received lower amikacin doses than calculated on the basis of creatinine clearance (498 +/- 1187 vs 611 = 313 mg/day). Serum albumin, both at the beginning of the treatment and at the end was lower in patients who developed toxicity, and bilirubin levels were higher in these patients at the end of the treatment. Apparently, a dose reduction may lessen the risk for amikacin nephrotoxicity in patients with chronic liver disease. We conclude that hypoalbuminemia and hyperbilirubinemia are risk factors in this complication.

Amikacin↗
PubMedDate not supplied

Hypoalbuminemia as a risk factor for amikacin nephrotoxicity.

Hypoalbuminemia has been recently informed by us as a risk factor in aminoglycoside nephrotoxicity. Since amikacin has a low serum binding capacity to albumin, the present study was designed to determine if the higher risk of amikacin nephrotoxicity in patients with hypoalbuminemia was due to low serum albumin per se or to malnutrition. One-hundred and thirteen ward patients who received endovenous amikacin for greater than 36 hours were studied prospectively. All were evaluated for the following factors: age, sex, diagnosis, serum creatinine, serum albumin, and nutritional status. They were followed with serum creatinine twice a week until cessation of therapy. Amikacin pharmacokinetics was studied in 11 subjects: 6 patients had a serum albumin less than 3.0 g/dL and 5 greater than 3.0 g/dL, but there were no differences in age, sex, weight, diagnosis, arterial pressure and nutritional status. The overall incidence of toxicity was 11%. In patients with serum albumin less than 3.0 g/dL it was 17.3% and in those greater than 3.0 g/dL it was 2.2%, p less than 0.05. There was no difference in the nutritional status between toxicity and non-toxicity groups. In the pharmacokinetic study, the peak levels obtained one hour after amikacin administration were higher in patients with serum albumin less than 3.0 g/dL than in those with normal serum albumin (12.7 +/- 1.6 vs 9.0 +/- 1.2, p less than 0.002). In conclusion hypoalbuminemia is a risk factor in aminoglycoside nephrotoxicity regardless of the nutritional status.

Adult↗
PubMedDate not supplied

[The safe transportation of children in automobiles].

The Author emphasizes the significant number of children who sustain fatal accidents during their transport on motor vehicles and relates the Act recently promulgated by the Italian Parliament on the mandatory use of particular restraining devices as well as safety harness for children.

Accidents, Traffic↗
PubMedDate not supplied

[The in-vivo effect of dihydroergocristine on human platelet function].

An acute test was run on healthy volunteers to assess the effect of i.v. dihydroergocristine methansulphonate on platelet function. The number of platelets was virtually unaffected, whereas adhesion to glass was significantly reduced. A direct and specific effect was noted on the 1st, adrenaline aggregation wave, while the 2nd wave (expression of ADP) induced aggregation did not appear to have been significantly altered. It is felt that further examination of the alpha-adrenergic block induced by the drug should be under-taken in view of the recent literature data which explain the inability of commonly employed anti-aggreganting drugs, such as acetylsalicylic acid, to prevent and treat atherothrombosis, in spite of the encouraging experimental results.

Adenosine Diphosphate↗