Chronic pancreatitis resulting from primary hydatid disease of the pancreas: a case report and review of the literature.
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Biomedical subjects
Publications and source records attributed to F Rosenberg.
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We present a case of a 54-year-old woman with rapidly progressive renal failure of uncertain origin, who developed pleuropericarditis and livedo reticularis 6 weeks after initiation of hemodialysis (HD). The presentation with acute renal failure, the development of serositis, and the dramatic clinical response to empiric steroid therapy initially suggested the diagnosis of a systemic inflammatory disorder or vasculitis. Renal biopsy, performed 3 days after presentation, suggested crystal deposition disease, and subsequent investigations, using both dialysate oxalate concentrations and liver biopsy, led to the diagnosis of primary hyperoxaluria (PH). We discuss this atypical adult presentation of PH and propose a role for the use of steroids in the management of the acute inflammatory symptoms of oxalosis. We also briefly discuss the current medical management of patients with PH, including transplantation.
The objective of this study was to correlate between macrophage inflammatory protein-1beta (MIP1beta) and viral loads in untreated, HIV-infected individuals. For that purpose, HIV-positive patients were tested for number of copies of HIV-RNA in plasma and for intracellular MIP1beta in freshly explanted CD8 and CD4 lymphocytes and monocytes. Results demonstrate that the levels of MIP1beta in the various cell populations were significantly higher in the HIV group than in age-matched healthy individuals. Moreover, patients with low CD4 cell counts (<500/microl) and relatively high viral loads exhibited much higher levels of intracellular MIP1beta than patients with lower viral loads and CD4 counts >500/microl. We conclude therefore that although MIP1beta is induced in the various cell populations as a result of HIV infection in vivo, a high intracellular level of MIP1beta appears to be linked to a deterioration in the immune status of the patients.
A 46-year-old man presented with shock and adult respiratory distress syndrome. Investigations revealed an adrenal mass that was diagnosed, by fine-needle aspiration biopsy, as pheochromocytoma. Because biopsy is contraindicated in patients with pheochromocytoma, this confusing presentation underscores the value of excluding this diagnosis by biochemical means before performing fine-needle aspiration of adrenal tumours.
Many atypical manifestations that can be inaugural in giant cell arteritis are well known. Three cases with facial edema as the first manifestation are described. Similar cases reported to date are reviewed.
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Plasma ionized calcium [Ca++] concentrations are decreased in patients having lactic acidosis. To further investigate this observation, we prospectively studied nine critically ill patients who had lactic acidosis and measured arterial pH, PCO2, [Ca++], lactate, and albumin concentrations. We found a strong association between decreased [Ca++] and increased plasma lactate concentrations (r2 = 0.78, p less than or equal to 0.001). This unexpected association--[Ca++] usually increases with increasing acidosis--might be clinically important and the mechanism deserves further investigation.
The postantibiotic effect of oxacillin on Staphylococcus aureus ATCC 6538P was determined under different test conditions by reference (viability counting) and semiautomated (electronic counting) methods. Differences in durations of the postantibiotic effect obtained with the two counting methods were not statistically significant. The semiautomated method provided a more rapid and convenient alternative to viability counting.
Electrophysiological and electron microscopic techniques were used to investigate the actions of potassium depolarization, black widow venom (BWSV), Ca2+-ionophore A 23187 and hyperosmotic solution on mouse hemidiaphragms poisoned in vitro with botulinum A toxin (BoTx) and tetanus toxin (TeTx). These neurotoxins reduced the frequency of miniature endplate potentials (m.e.p.ps) from 5/s of the control to 2/min and 21/min, respectively. High potassium (25 mmol/l) increased the m.e.p.p.-frequency at BoTx- and TeTx-poisoned endplates to 30/min and 50/s, respectively. The ultrastructure of endplates showed no obvious changes. BWSV (0.04 glands/ml) was just as effective in promoting transmitter release from BoTx-treated endplates as in control preparations. Electron micrographs revealed depletion of vesicles as well as swollen and disrupted mitochondria. When preparations were pretreated with TeTx, BWSV only moderately increased transmitter release and no alterations of the ultrastructure could be observed. At TeTx- or BoTx-poisoned endplates Ca2+-ionophore A 23187 usually produced an extreme reduction of m.e.p.p.-frequency (0.005/s), sometimes preceded by a short burst-like release. The ultrastructure of these endplates was not obviously affected. Application of hyperosmotic solution to BoTx- or TeTx-poisoned preparations further reduced the already low m.e.p.p.-frequency. These results further demonstrate that TeTx and BoTx act at different sites in the transmitter releasing process.
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Intracellular recordings of the spontaneous activity from mammalian spinal cord neurons in culture demonstrated different sensitivities of excitatory and inhibitory synaptic transmission for the action of tetanus toxin (Tetx) and botulinum toxin type A (Botx). The effects of Tetx and Botx on spontaneous and nerve-evoked transmitter release were compared under identical experimental conditions in experiments on in vitro poisoned mouse diaphragms. At 37 degrees C completely paralyzed endplates are characterized by a very low frequency of spontaneous miniature endplate potentials (m.e.p.p.s) and by a 100% failure to evoke endplate potentials (e.p.p.s) in response to single nerve stimuli. Striking differences in the action of both toxins have been observed when the very low transmitter release probabilities of paralyzed nerve-muscle preparations were increased by tetanic nerve stimulation and/or application of potent K+-channel blockers and/or by reduction of temperature to 25 degrees C. While Botx did not change the short latency between nerve impulse and postsynaptic response, Tetx produced a temporal dispersion of the quantal release suggesting that the toxins act at different sites in the chain of events that result in transmitter release. To find further evidence to support the different actions of the toxins the spontaneous transmitter release was studied in more detail. Tetx blocked preferentially the release of so-called large mode m.e.p.p.s without affecting the frequency of the small mode ones. In contrast, Botx strongly inhibited both the small and large mode m.e.p.p.s.(ABSTRACT TRUNCATED AT 250 WORDS)
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1 The ubiquitous actions of the cyclo-oxygenase inhibitors are described. 2 These include the inhibitory effect on prostaglandin synthesis and the direct effect of aspirin on lymphocytes and their ability to produce lymphokines. 3 Aspirin reduces some types of platelet aggregation possibly involving inhibition of the precursors of thromboxane A2 and prostacyclin. 4 The therapeutic implications in relation to transient ischaemic attacks, coronary artery disease and reno-allograft rejection are discussed. 5 The beneficial and adverse effects on the gastro-intestinal tract are described. 6 The effects of aspirin-like drugs on the genito-urinary tract are described with particular reference to their adverse effects on labour and their therapeutic effect on dysmenorrhoea.
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In order to study the response of patients with multiple myeloma of the bones (MM) to various anti-cancer drugs (Melphalan M, Cyclophosphamide Cy, Nitrosourea NU, Vincristine V, Adriamycine A and Prednisone P), 70 MM received the following treatment : 1) Induction therapy : a) M and P or b) M and Cy and P ; 2) Levelling with partial or complete response : V Cy P (in case a) or V M Cy P (in case b) ; 3) Relapse : A and NU. The following results were obtained : 1) Only 42.6% of patients respond to induction therapy ; 2) Fewer than 10% of patients showing a response reach a second levelling with Vincristine ; 3) 50% of those not showing a response reach a levelling between --20 and --50 and have prolonged survival ; 4) Only 20% of non responders are improved by Cy P or A and NU. The median actuarial survival is 42 months. Among the responders two poor prognosis factors must be underlined : hypercalcemia and the speed of response.