Communicating the diagnosis of multiple sclerosis - a qualitative study.

Studies on communicating the diagnosis of multiple sclerosis (MS) are few, and all reveal communication and information deficits. We explored the personal experience of diagnosis communication of people with MS and health professionals, using a qualitative methodology. Data were obtained from two sets of focus group meetings (FGM) with people with MS (total 23; 16 females; age range: 23-70) and one FGMs with health professionals (four neurologists, three psychologists, two nurses). The methods of framework analysis were applied to meeting transcripts to identify key topics and categories. The experience of communicating/receiving an MS diagnosis was highly varied; all patients reported the moment as powerfully evocative and unforgettable. Very poor levels of support and information were sometimes given. Although diagnosis communication had improved in more recent experience, all felt it should be further improved with appropriate setting (privacy, no interruptions, sufficient time), information tailored to the individual, and continuity of care. Such improvements imply a more meaningful patientneurologist relationship, and also structural and organisational changes.

Specialty-related differences in the epidemiology, clinical profile, management and outcome of patients hospitalized for heart failure; the OSCUR study. Oucome dello Scompenso Cardiaco in relazione all'Utilizzo delle Risore.

AIMS: This study was designed to identify potential specialty-related differences in the epidemiology, clinical profile, management and outcome of patients hospitalized for congestive heart failure in departments of cardiology or internal medicine. METHODS AND RESULTS: From 1 July to 31 December 1998, we prospectively recorded epidemiological and clinical data from patients with congestive heart failure consecutively admitted to 11 departments of cardiology and 12 departments of internal medicine in Liguria, a northern area of Italy. The overall study population included 749 patients; 22% were treated by cardiologists and 78% by internists (P<0.0001). Patients managed by cardiologists were more likely to undergo echocardiography (92% vs 37%), Holter monitoring (25% vs 3%) and exercise stress testing (20% vs 0.5%) than those managed by internists (P=0.001). At discharge, patients treated by cardiologists were more likely to be prescribed beta-blockers (41% to 4%) and ACE inhibitors (100% to 74%) than those treated by internists (P<0.0001), and the latter medication at higher dosages by cardiologists than internists. In addition, patients followed by cardiologists were younger (70+/-9 to 79+/-1 years;P<0.0001), more likely to be male (61% to 50%;P=0.011) and to have coronary artery disease (57% to 45%;P<0.006) than those followed by internists. Conversely, patients followed by internists were more likely to have diabetes, chronic obstructive pulmonary disease, atrial fibrillation and renal failure (P<0.03). In the overall study population, 53 patients (7%) died during hospitalization. Patients treated by cardiologists had a mortality not significantly different from that of patients treated by internists (10% and 6%, respectively;P=0.067), although congestive heart failure was more severe on admission in patients treated by cardiologists. CONCLUSION: Cardiologists follow published guidelines for congestive heart failure more strictly than internists, but treat a smaller number of patients who are younger, have more severe congestive heart failure and fewer co-morbidities than those managed by internists.

Successful treatment of mitomycin C-associated hemolytic uremic syndrome by plasmapheresis.

Therapeutic attempts have generally failed to reverse the rapid progression of renal failure after mitomycin C (MMC)-induced hemolytic uremic syndrome (HUS). A patient who developed HUS after MMC and who showed pathologic changes in the kidney consistent with thrombotic microangiopathy is reported. Treatment with plasmapheresis was followed by a favorable outcome and significant recovery of renal function. Accordingly, this therapeutic modality should be considered for patients with MMC-induced HUS.

[Chronic renal insufficiency associated with tuberous sclerosis]. / Insufficienza renale cronica associata a sclerosi tuberosa.

Despite the high incidence of renal involvement by hamartomatous proliferative lesion, the occurrence of chronic renal failure in patients with tuberous sclerosis in unusual. This rare association in a 37 year old woman is described. The literature is reviewed and the pathological, clinical, diagnostic and therapeutic aspects of this entity are discussed.

Renal ammoniagenesis in an early stage of metabolic acidosis in man.

Total renal ammonia production and ammonia precursor utilization were evaluated in patients under normal acid-base balance and in patients with 24-h NH4Cl acidosis by measuring (a) ammonia excreted with urine and that added to renal venous blood, and (b) amino acid exchange across the kidney. In 24-h acidosis not only urinary ammonia excretion is increased, but also total ammonia production is augmented (P less than 0.005) in comparison with controls. By evaluating the individual role of acid-base parameters, urine pH and urine flow in influencing renal ammonia production, it was shown that the degree of acidosis and urine flow are likely major factors stimulating ammoniagenesis. Both urine pH and urine flow are determinant in the preferential shift of ammonia into urine. In 1-d acidosis, renal extraction of glutamine was not increased and the total ammonia produced/glutamine N extracted ratio was higher than in controls (P less than 0.005) and was inversely correlated with the log of arterial bicarbonate concentration (P less than 0.001). In the same condition, renal glycine and ornithine uptake took place; the more severe the acidosis, the greater was the renal extraction of these amino acids (P less than 0.001). These data indicate that at the early stages of metabolic acidosis, in spite of a brisk increase in ammonia production, the mechanisms responsible for the increased glutamine use, which are operative in chronic acidosis, are not activated and other ammonia precursors, besides glutamine, are probably used for ammonia production.

[Activity of renal enzymes producing ammonia from glutamine in the absence of phosphate in the rat: 1. Effect of chronic metabolic acidosis]. / Attività degli enzimi che producono ammoniaca dalla glutamina in assenza di fosfato nel rene di ratto: 1. effetto della acidosi metabolica cronica.

Phosphate- independent glutaminase (PIG) and gamma-glutamyl transpeptidase (gamma GT) activities were evaluated in renal cortex homogenates of rats under normal acid-base balance or chronic metabolic acidosis (CMA). An incubation medium containing glutamine 2 mM, no phosphate, pH 7,40, was used. PIG activity was measured as glutamate production and total gamma GT activity as ammonia production. In normal rats gamma GT activity was significantly higher (0,84 +/- 0,05 mumol/min/g wet wt.) than PIG activity (0,48 +/- 0,06 mumol/min/g wet wt.) (p less than 0,01). In CMA there was a significant increase in PIG activity and an even higher increase in gamma GT activity (p less than 0,01 compared to controls in both cases). The glutamate production/ammonia production ratio was 0,57 +/- 0,05 in normal rats, and 0,37 +/- 0,03 in CMA ( p less than 0,025). These data suggest that the increase in PIG activity and, to a further extent, the increase in gamma GT activity may play an important role in augmenting renal ammonia production in CMA.

Effects of metabolic alkalosis, metabolic acidosis and uraemia on whole-body intracellular pH in man.

1. Whole-body intracellular pH (pHi) was measured by the 14C-labelled DMO method in twenty-four control subjects, eighteen normal subjects with induced acute metabolic alkalosis, ten normal subjects with induced acute metabolic acidosis, twelve normal subjects with chronic acidosis and in fifteen patients with chronic renal insufficiency and acidosis. 2. The change in pHi per unit change in extracellular pH is significantly larger in acute metabolic alkalosis than in acute metabolic acidosis. In chronic metabolic acidosis, pHi decreased in proportion to the total amount of ammonium chloride administered; pHi was normal in patients with uraemic acidosis. 3. These observations confirm the role that tissue buffers play in the protection of the cellular environment in some forms of acidosis. When the acid load overwhelms tissue buffer capacity, pHi becomes a function of extracellular pH. 4. Cells seem more protected from acute acidosis than from acute alkalosis.