Spontaneous retroperitoneal hematoma: our experience

We report 15 cases of spontaneous retroperitoneal haematoma. The etiology and the diagnostic and therapeutic procedures were evaluated. The haematoma source was the adrenal gland in 4 patients and the causes were pheochromocytoma (1), adenoma (1), myelolipoma (1) and idiopathic (1). In 10 patients the source was the kidney and the causes were angiomyolipoma rupture (6), renal cell carcinoma (3) and ureteral calculi (1). In the remaining case, the haematoma was produced by fibrinolytic and anticoagulant therapy in a patient with acute myocardial infarction. The imaging diagnostic techniques employed were abdominal ultrasonography and CT scan, which allowed the diagnosis of haematoma and showed his size and extension in all the cases. With these two techniques, and with the retrograde pyelography in one patient, we obtained the etiologic diagnosis in 12 of the 15 cases. Surgical treatment was performed in 12 patients (adrenalectomy in 2, simple nephrectomy in 3, radical nephrectomy in 5 and partial nephrectomy in 2).     

Influence of acid-base alterations on myocardial sensitivity to catecholamines

Summary The influence of respiratory and metabolic acid-base alterations on the myocardial sensitivity to catecholamines was studied in the isolated rat atria. The ability of noradrenaline for increasing the atrial rate was enhanced during alkalosis and conversely, it was decreased by acidosis. These changes in sensitivity shifted the concentration-effect curve for noradrenaline to the right by about 0.5 log unit when the pH was lowered from 7.60 to 7.00. No changes in the maximum attainable response were detected. Essentially the same shifts of the concentration-effect curves were obtained with changes in pH brought about by altering the pCO₂ or at constant pCO₂. The decrease in the pH produced a similar shift to the right of the concentration-effect curve for isoprenaline, after the extraneuronal uptake inhibition by hydrocortisone and also in atria tissue with low content of endogenous noradrenaline (reserpine-pretreated and newborn rats). The ability of isoprenaline for increasing cyclic AMP levels in atrial tissue was also enhanced by alkalosis and decreased by acidosis. However, the shift to the right of the concentration-effect curve for cyclic AMP induced by the decrease in the pH was greater than the shift detected in the chronotropic-effect curve. In addition a decrease in the maximum increment of cyclic AMP was detected under acidosis, in spite of equal maximal chronotropic response.Our results support the hypothesis that the alterations in the sensitivity to catecholamines induced by the changes in pH are not due to a release of endogenous noradrenaline nor to alterations of the mechanisms which remove catecholamines from the biophase. The fact that cyclic AMP response to catecholamines was also reduced by acidosis strongly suggests that the mechanism(s) involved is located in the earlier steps of the events leading to the chronotropic effect of the -agonists.     

Presynaptic muscarinic receptor subtypes involved in the inhibition of acetylcholine and noradrenaline release in bovine cerebral arteries

Summary Experiments were performed in bovine cerebral arteries preincubated with [³H]-choline or [³H]-noradrenaline to analyze the presynaptic muscarinic receptors involved in inhibition of acetylcholine and noradrenaline release induced by electrical stimulation (4 Hz, 200 mA, 0.3 ms, 1 min). For this purpose, the actions of several muscarinic receptor antagonists on the ³H overflow and on the carbacol-induced inhibition of this overflow were assessed. The evoked [³H]-acetylcholine release and [³H]-noradrenaline release were markedly reduced by the presence of tetrodotoxin, Ca²⁺-free medium, and the inhibitor of both choline transport and choline acetyltransferase, AF64A. Chemical sympathetic denervation with 6-hydroxydopamine (6-OHDA) decreased the uptake of[³H]-noradrenaline, and AF64A reduced mainly the uptake of [³H]-choline, but also of [³H]-noradrenaline. Carbachol reduced the evoked [³H]-noradrenaline and [³H]-acetylcholine release; the IC₅₀ values were 0.37 and 0.43 mol/l, respectively.Atropine and 4-DAMP, but not AF DX 116, methoctramine or pirenzepine, increased the evoked [³H]-acetylcholine release. However, these muscarinic antagonists failed to modify the evoked [³H]-noradrenaline release. Carbachol inhibited the release of both acetylcholine and noradrenaline. The inhibition was blocked by the antagonists. The rank orders of potency (based on plC₅₀ values) were, in the case of [³H]-acetylcholine release, atropine > 4-DAMP >AF-DX 116 >- pirenzepine >- methoctramine, and, in the case of [³H]-noradrenaline release, atropine > 4-DAMP > AF-DX 116 >- methoctramine >-pirenzepine. These results suggest (1) that the prosynaptic receptors that modulate endogenous acetylcholine release are likely of the M₃ subtype, whilst those involved on the effect of the exogenous agonist Carbachol are of M₂ subtype, and (2) that those which inhibit noradrenaline release are probably a mixture of M₂ and M₃ subtypes as well. The autoinhibition of the acetylcholine release was funtionally active under our experimental conditions, while noradrenaline release does not appear to be modulated by muscarinic receptors in physiological conditions.Send offprint requests to G. Balfagón at the above address     

Managing sore throat: a literature review. I. Making the diagnosis.

OBJECTIVE: To assess the justification for the routine use of investigations in the diagnosis of bacterial causes of sore throat. DATA SOURCES: The literature from 1945 to 1990 was systematically screened to identify studies that addressed diagnosis of bacterial infection and the efficacy of antibiotics in sore throat, using the key-words "pharyngitis" and "tonsillitis". RESULTS: Difficulties were identified with clinical methods and investigations that identify streptococcal infections. The practice of throat-swab culture--the "gold standard"--appears to have developed as a strategy to protect patients from acute rheumatic fever. However, this method may be limited in its usefulness for protection against acute rheumatic fever because: (i) in many cases in which the streptococcus is isolated from symptomatic patients there is no serological evidence of infection; (ii) there are very high asymptomatic carrier rates of the streptococcus; (iii) even after adequate treatment with penicillin there are high bacteriological failure rates; and (iv) those organisms that can be isolated from the mucosal surface are a poor representation of organisms lying deep in the tissues. Evaluation of other diagnostic techniques such as Gram's stain and rapid antigen testing, as well as decision analysis, has also been hampered by the difficulties encountered with use of this inadequate gold standard. CONCLUSION: There is little indication from the literature that any routine system of identifying bacterial causes of sore throat is helpful to the clinician.     

Evaluation of a training program to improve clinical competencies of pharmacists serving skilled nursing facilities

Forty-eight pharmacists from the New York area were selected for specialized training in consultant clinical services to skilled nursing home facilities. A skills curriculum was developed, and the pharmacists participated in 15 training sessions which included lectures by nationally recognized experts, audiovisual presentations, and on-site clinical workshops. Evaluations were based upon clinical preprogram v. clinical postprogram testing, comparisons with clinical pharmacy experts, and attitudinal pre- and postprogram testing. It was found that the training course did improve the skills of the trainees but they still performed at a level below recognized clinical pharmacy experts. Future programs should stress fewer topics, but in more detail, and should focus upon monitoring techniques, laboratory results, and more on-site experiences.     

Beneficial effect of verapamil added to chronic ACE inhibitor treatment on renal function in hypertensive elderly patients

This study analysed the effect of low doses ofverapamil added to chronic treatment withangiotensin-converting enzyme (ACE) inhibitors onblood pressure and serum creatinine levels in eightelderly hypertensive patients who had a steadyincrease of serum creatinine while on ACE inhibitors.The study was performed in eight elderly hypertensivesubjects, five men and three women (mean age 70 ±2 years; systolic blood pressure 173 ± 4 mmHg; diastolic blood pressure 99 ± 1 mm Hg) andserum creatinine of 1.60 ± 0.27 mg/dl beforetreatment. During an average of 25 weeks, ACEinhibitors significantly reduced both systolic anddiastolic blood pressures, but serum creatinine levelswere increased over basal levels (0,68 ± 0,20 mg/dl, p < 0.05). During an average of 10 weeks,the addition of verapamil did not decrease bloodpressure further, but serum creatinine levels werereduced to baseline. Our study suggests that theaddition of verapamil to ACE inhibitors can reverseACE-induced increase in creatinine levels in elderlyhypertensive patients in whom this side effect isobserved. This revised version was published online in August 2006 with corrections to the Cover Date.     

CD34+ cells from acute myeloid leukemia, myelodysplastic syndromes, and normal bone marrow display different apoptosis and drug resistance-associated phenotypes.

Myelodysplastic syndromes and acute myeloid leukemia (AML) are heterogeneous disorders in which conflicting results in apoptosis and multidrug resistance (MDR) have been reported. We have evaluated by multiparameter flow cytometry the expression of apoptosis- (APO2.7, bcl-2, and bax) and MDR-related proteins [P-glycoprotein (P-gp), multidrug resistance protein (MRP), and lung resistance protein (LRP)] specifically on bone marrow (BM) CD34+ cells, and their major CD32-/dim and CD32+ subsets, in de novo AML (n=90), high-risk myelodysplastic syndrome (n=9), and low-risk myelodysplastic syndrome (n=21) patients at diagnosis, and compared with normal BM CD34+ cells (n=6). CD34+ myeloid cells from AML and high-risk myelodysplastic syndrome patients displayed higher expression of bcl-2 (P <0.0001) and lower reactivity for APO2.7 (P=0.002) compared with low-risk myelodysplastic syndrome and normal controls. Similar results applied to the two predefined CD34+ myeloid cell subsets. No significant differences were found in the expression of P-gp, MRP, and LRP between low-risk myelodysplastic syndrome patients and normal BM, but decreased expression of MRP (P <0.03) in AML and high-risk myelodysplastic syndromes and P-gp (P=0.008) in high-risk myelodysplastic syndromes were detected. Hierarchical clustering analysis showed that low-risk myelodysplastic syndrome patients were clustered next to normal BM samples, whereas high-risk myelodysplastic syndromes were clustered together and mixed with the de novo AML patients. In summary, increased resistance to chemotherapy of CD34+ cells from both AML and high-risk myelodysplastic syndromes would be explained more appropriately in terms of an increased antiapoptotic phenotype rather than a MDR phenotype. In low-risk myelodysplastic syndromes abnormally high apoptotic rates would be restricted to the CD34- cell compartments.     

Continuous care in the cancer patient: palliative care in the 21<Superscript>st</Superscript> century

Continuous care for the cancer patient is an open concept that is not only applicable only to the terminal stage. Such a simplification could generate inequities of therapy and discrimination. Historically, oncology services have been structured as networks dispensing chemotherapy and radiotherapy rather than services dedicated to the integrated care of the cancer patient. This situation has changed in a continuous and progressive manner over the past few years, as reflected in the latest Spanish Libro Blanco de Oncología. We are still far from reaching the optimum level of integrated care, possibly because we have not, as yet, achieved services that are structured and appropriate for the care-needs of the patient and, perhaps, to the lack of the necessary personnel. We must always make sure that cancer patients receive the best possible treatment, irrespective of whet-her the disease is in relapse. Oncologists must not “give up”, indicating that, in addition to using the most effective anticancer treatments available, they should deploy their best knowledge and experience to control the symptoms of cancer while providing psycho-social help to the patient and family. This is best conducted with a communication that is adjusted to the changing needs of the patient over the longterm clinical process, and should be provided by a multidisciplinary team, according to the needs of the patient and the family. Within a program of integrated care, it is possible to coordinate the existing care structures without creating parallel health networks so as to cover the needs of the greatest number of cancer patients in advanced stage of the disease.