A brain mass in a patient with Behcet's disease: a case report.

INTRODUCTION: This case report describes an uncommon presentation of Behcet's disease which manifested as neuro-Behcet's disease. Although it is not the first reported case in the medical literature, it is a possible differential in a patient presenting with a brain tumor. Since the diagnosis of neuro-Behcet's disease depends largely on the clinical picture and medical history, it should be considered prior to opting for invasive diagnostic methods. CASE PRESENTATION: Our patient is a 36-year-old white man from Kuwait. He presented with acute onset of headache, vomiting, and right-sided weakness. Magnetic resonance imaging of his brain showed a mass in the brain stem. He then revealed that he had a history of recurrent painful oral and genital ulcers for the past 10 years, which suggested a diagnosis of Behcet's disease. A brain biopsy was recommended by a neurosurgeon at the time, but the patient refused the procedure. After initiating steroid therapy, the mass began to regress and, eventually, was undetectable on subsequent imaging of his brain. CONCLUSIONS: This case of neuro-Behcet's disease reflects the need to consider this diagnosis in a patient of less than 40 years of age presenting with a suspected brain tumor. This may delay the need for invasive diagnostic methods, especially if such methods are not desired by the patient. In the management of suspected neuro-Behcet's disease, initiating steroid therapy and measuring the response is a reasonable option before seeking a definitive diagnosis via brain biopsy. If the response to steroids is minimal then a brain biopsy should be performed.

Influence of cold on stress ulceration and on gastric mucosal blood flow and energy metabolism.

"Ice-cold" gastric lavage is an important part of the treatment of bleeding from stress ulceration. The purpose of this study was to find out if cooling modifies ischemic injury of the gastric mucosa. Four series of experiments were performed in rabbits. In the first, we studied the influence of cooling on the rate of breakdown of gastric mucosal high energy phosphates during complete, ex vivo ischemia achieved by rapid excision of the stomach. We then studied the influence of cold versus warm gastric lavage on the severity of gastric mucosal injury and on the rate of breakdown of gastric mucosal adenosine phosphates during hemorrhagic shock. In a fourth series of experiments, we examined the influence of cold versus warm gastric lavage on gastric mucosal blood flow measured by injection of radioactive microspheres. Although the rate of breakdown of mucosal high energy phosphates was less rapid during a short period of complete, ex vivo ischemia when the stomach was cooled, this rate was more rapid during hemorrhagic shock under in vivo conditions when the stomach was lavaged with cold solution. The latter also increased the severity of shock-induced gastric mucosal injury. Cold gastric lavage reduced gastric mucosal blood flow before, during and after hemorrhagic shock.

Mechanism of stress ulcer. Influence of alpha-adrenergic blockade on stress ulceration and gastric mucosal energy metabolism.

In previous reports from this laboratory, it has been proposed that stress ulceration results from a severe gastric mucosal energy deficit due to shock-induced mucosal ischemia. In the experiments described in this report, the hypothesis was further tested by studying stress ulceration and gastric mucosal energy metabolism in rabbits subjected to hemorrhagic shock with or without the concomitant administration of an alpha-adrenergic blocking agent. Our data show that stress ulceration and gastric mucosal energy deficits are significantly less severe when shock is combined with alpha-adrenergic blockade.

Influence of hyperglycemia on survival after hemorrhagic shock.

Terms such as "insulin resistance" and "glucose intolerance" applied to shock-induced hyperglycemia suggest that this state may prejudice survival. However, our data indicate that posthemorrhage hyperglycemia improves short-term survival. Rabbits, either fed until the experiment or fasted for 24 hours, were shocked by rapid removal of 25% of their blood volume (BV) measured by 131IHSA. During the next 60 minutes, blood pressure (BP) was recorded, and the following variables were measured every 10 minutes: plasma volume (PV); arterial and venous plasma osmolality (PO), glucose, lactate, Na, K and hematocrit. Other fasted animals studied similarly received short intravenous pulses of hypertonic xylose after bleeding. The PO of fed animals, who all survived for 60 minutes rose to an extent accounted for by rises in glucose and lactate. A significant PV fluid gain was maintained for 60 minutes. The fasted animals, 42% of whom died before 60 minutes, had a flat glucose curve with a correspondingly small rise in PO. The PV fluid balance, after an initial small gain, became negative. Although a lower blood pressure in fasted rabbits was probably due to lack of PV refill, death resulted from hyperkalemia. Poor tolerance of fasted animals to shock is not attributable only to less glucose for energy metabolism, because when they received xylose, homeostatic features of fed animals were restored. The data suggest that, immediately after hemorrhage, glucose acts as a nonpermeant solute drawing fluid into the circulation. This study also shows that control of the nutritional status of animals used for shock models is important.

Mechanism of stress ulcer: influence of sodium taurocholate on gastric mucosal energy metabolism during hemorrhagic shock and on mitochondrial respiration and ATPase in gastric mucosa.

In previous reports from this laboratory, we have proposed that stress ulceration complicating hemorrhagic shock results from a gastric mucosal energy deficit due to shock-induced mucosal ischemia. We reasoned that if this hypothesis were correct, an agency known to augment the severity of stress ulceration would be expected to have an adverse effect on gastric mucosal energy metabolism. Others have shown that the severity of stress ulceration developing in animals subjected to hemorrhagic shock is increased by introducing bile salts into the stomach; conversely, the development of stress ulceration can be prevented by ligation of the pylorus or of the common bile duct. We have studied the influence of sodium tauurocholate on the respiration of gastric mucosal mitochondria and on gastric mucosal ATPase. We have also evaluated the influence of the intragastric introduction of taurocholate on the mucosal energy depletion produced by shock. The data presented in this report indicate that taurocholate uncouples oxidative phosphorylation of gastric mucosal mitochondria and inhibits gastric mucosal ATPase. The shock-induced gastric mucosal energy deficit was significantly more severe in the presence of added intragastric taurocholate.

Gastric mucosal energy metabolism and "stress ulceration".

Acute gastric erosions following hemorrhagic shock (stress ulceration) have been attributed to gastric hyperacidity, altered gastric secretion of mucus and an abnormal permeability of the gastric mucosa to H(+). This report aims at presenting evidence supporting an alternate hypothesis: the event linking shock-induced gastric mucosal ischemia to mucosal necrosis is a deficit in gastric mucosal energy metabolism. Our experimental procedure consisted of harvesting the stomachs of rats and rabbits by "stop-freeze" (liquid N(2)) at different intervals after the induction of hemorrhagic shock. Levels of adenosine-phosphates and of glycolytic intermediates in gastric mucosa were measured. We studied the changes in the levels of these substrates produced by shock as well as by factors capable, when combined with shock, of rendering the gastric mucosa more vulnerable to stress ulceration. The influence of shock and of these modifying factors were evaluated by comparison with data from appropriately designed control experiments. In parallel experiments we examined the frequency of stress ulceration (gross and microscopic) under these same standard conditions. There have emerged from these studies a number of observations all based upon data with the highest statistical significance. The data are consonant with the hypothesis stated above: an energy deficit severe enough to cause cellular necrosis is the event linking shock-induced gastric mucosal ischemia and stress ulceration.