IgG4-related disease of the hepatobiliary tract : 2 case reports and review of the literature.

IgG4-related disease is a rare inflammatory disorder that may mimic many infectious, malignant, and autoimmune conditions. The biliary tract is frequently involved, but hepatic lesions are rarely seen. Diagnosis is often delayed due to the absence of specific clinical and radiological signs, and the lack of an accurate diagnostic marker. Differential diagnosis includes cholangiocarcinoma, primary sclerosing cholangitis and intrinsic or metastatic liver disease. Corticosteroids are the cornerstone of therapy but treatment has not been standardized and relapse is common. Based on two cases of IgG4-related hepatobiliary disease, we review the current literature on this pathological entity.

Efficacy of SF 68 in the treatment of acute diarrhea. A placebo-controlled trial.

BACKGROUND: The therapeutic value of Bioflorin, a preparation containing Enterococcus SF 68 strain, was evaluated in adult patients with acute diarrhea. METHODS: In a double-blind randomized trial we compared the effect of SF 68 strain in a dose of 150 x 10(6) colony-forming units three times a day for 5 days compared with placebo on the duration of diarrhea in 211 adults. RESULTS: Patients receiving SF 68 had a reduced duration of diarrhea compared with placebo, with a highly statistically significant difference between treatments. The proportion of patients with continuing diarrhea during the 2nd day of treatment was 61% in patients receiving SF 68 and 96% in those receiving placebo (P < 0.01). During the 3rd day diarrhea was still present in 8% of patients given SF 68, compared with 66% of those given placebo (P < 0.01). The mean (+/-SD) duration of diarrhea was 1.69 days (0.6) in patients given SF 68 compared with 2.81 days (0.9) in those given placebo. When pathogens were found in the first stool culture, they could not be detected at post-treatment examination. No adverse reactions were observed. CONCLUSIONS: Oral bacteriotherapy with SF 68 strain shortens the duration and the severity of diarrhea in adults and represents a safe and effective approach to re-establishing a balanced microbial flora in this condition.

Splenic abscess: a diagnostic challenge.

Splenic abscess is uncommon and remains a diagnostic challenge. We present two cases. Both patients had predisposing factors that may have led to the splenic abscess. At admission, both patients presented clinical and roentgenographic signs, suggestive but nonspecific for splenic suppuration. Of particular interest was the isolation of Salmonella typhimurium in our first patient. The literature on splenic abscess is reviewed.

Analysis of the receptor specificity of tolerance induction in stress versus opioid-related prolactin secretion in rats.

The effects of restraint stress and opiates on prolactin secretion in male rats have been measured. Both induced a short-lived increase in prolactinaemia. Experimental evidence indicates that both opioids and restraint stress bring about their actions by the activation of opioid receptors. When restraint stress was followed by administration of the specific kappa-agonist bremazocine, a second prolactin peak was observed. In contrast, morphine (predominantly a mu-agonist) lost its prolactin-stimulating capacity when given after a period of restraint stress. This indicates cross-tolerance between restraint stress and morphine. Tolerance was overcome when the dose of morphine was doubled, and an increase in prolactin secretion could again be obtained. The cross-tolerance phenomenon argues that a common opioid receptor is involved in morphine- and restraint stress-stimulated prolactin release. In another set of experiments, in which morphine administration replaced restraint stress as a means of inducing tolerance, a second rise in prolactinaemia was seen only with bremazocine and not with a further administration of morphine. This suggests a morphine (mu) receptor-specific development of tolerance. Two consecutive administrations of bremazocine also produced tolerance, in this case for the kappa-receptor. This illustrates the rapid and receptor-specific development of tolerance for the prolactin-releasing capacity of opioid compounds.

The growth hormone secretory response to fentanyl in rat: an involvement of mu type receptors.

Fentanyl, a selective mu opioid receptor agonist, administered intravenously, influences growth hormone secretion in conscious male rats. A dose-response study demonstrated that the maximum growth hormone release was obtained with 10 micrograms/kg while higher doses were less or not effective. MR-2266 (6 mg/kg i.v.), a mu and kappa opioid receptor antagonist, and bremazocine (0.1 mg/kg i.v.) a mu opioid receptor antagonist with kappa agonistic properties, both potently inhibited the growth hormone response to fentanyl (10 micrograms/kg i.v.). In contrast, the effect of fentanyl on growth hormone release was not blocked in rats treated with either ICI-154129 (30 mg/kg i.v. or 150 micrograms/kg intracerebroventricularly a selective delta opioid receptor antagonist, or U-50488 (10 mg/kg i.v.), a specific kappa opioid receptor agonist. These results suggest that opioid receptors of the mu type are involved in the fentanyl-induced growth hormone release.

Electron microscopic detection of Whipple's bacillus in sarcoidlike periodic acid-Schiff-negative granulomas.

We describe a patient with Whipple's disease without apparent intestinal involvement at initial presentation. Electron microscopy demonstrated the typical bacilli in PAS-negative lymph node and muscle biopsy specimens.

The effect of beta-endorphin on basal and TRH-stimulated TSH release in conscious male rats.

The inhibitory effect of beta-endorphin (EP) or other opioids on TSH secretion is, in contrast to their stimulating properties on PRL release, still a matter of debate. In the present study a dose of 1 microgram beta-EP injected intracerebroventricularly (IVT) in unstressed conscious male rats, though highly effective on PRL release, did not affect basal TSH levels, nor the TRH-induced TSH secretion. The previously reported inhibition of TSH release by opioids may therefore be an effect only seen when pharmacological doses are used.

The effect of bombesin on basal, alpha-methyl-p-tyrosine, haloperidol, morphine, bremazocine and stress-induced prolactin secretion.

Intravenously administered bombesin lowered basal PRL levels in conscious male rats and prevented the morphine, bremazocine and stress-induced PRL secretion. The same dose of bombesin had no effect on PRL levels in alpha-methyl-p-tyrosine pretreated rats and did not affect haloperidol-stimulated PRL release. These results show that bombesin given intravenously acts as an inhibitor of PRL secretion and suggests that it does not act on the lactotrope itself but rather by an increase of the inhibitory dopaminergic tone.

In vivo and in vitro effect of naloxone on prolactin response to TRH in rat.

In adult male Wistar rats submitted to a standardized noise stress, intravenous TRH induced a prolactin (PRL) secretory response. Prior IV naloxone administration not only lowered plasma PRL levels in those stressed rats but abolished also the stimulatory action of TRH. This effect was further studied by superfusion experiments on enriched PRL cell suspensions (70% lactotrophs) from female adult Wistar rats. Naloxone kept unaffected the basal PRL secretion but lowered significantly that induced by TRH. These experiments suggest a dual effect of naloxone on rat PRL secretion, one exerted on central opioid receptors lowering stress-related increased basal PRL levels, the other inhibiting the TRH-dependent PRL secretion exerted at the lactotroph level itself.

Linear Percoll gradient centrifugation of rat anterior pituitary cells. A simple method for prolactin cell enrichment.

Prolactin (PRL) cells were purified from nulliparous normal female adult Wistar rat pituitary cell suspensions by linear Percoll density gradient centrifugation, a procedure yielding single cells. Lactotrophs were found in two different layers, the first containing 70% PRL cells in the density range 1.055 to 1.065 g/ml, the second with 28% PRL cells in the range 1.070 to 1.080 g/ml. Both cell fractions contained more than 90% viable cells with an intact ultrastructure. The physiological integrity of the 70% enriched PRL cells was assessed by their basal PRL secretion, their secretory response to TRH and dopamine, and their cAMP production in a basal situation and after incubation with dopamine.

Opioid modulation of thyrotropin releasing hormone induced prolactin secretion.

It is known that opioids stimulate prolactin (PRL) secretion by an action on hypothalamic neurons, but in vitro studies have suggested a direct action on the lactotrophs. The present study was performed on male rats known to have little or no PRL response to TRH. A beta-endorphin (beta EP) injection in the third ventricle stimulated PRL secretion and induced furthermore a PRL secretory reaction to TRH injected intravenously 20 min later. Pretreatment with naloxone 10 min before beta EP injection abolished not only the PRL response to beta EP but also the conjugated effect of beta EP and TRH. Pretreatment with naloxone methyl bromide (Br-naloxone), a quaternary naloxone derivative, which does not cross the blood-brain barrier, had no effect on the PRL response to beta EP but prevented the conjugated effect of beta EP and TRH on PRL secretion. Pretreatment of the animals with -methyl-parathyrosine resulting in a dopamine depletion or with haloperidol, a dopamine antagonist, could not induce lactotroph responsiveness to TRH. These results suggest that beta EP in male rat sensitizes the PRL cell to TRH by a direct effect and not through an inhibition of the dopaminergic tone.

Thyroid hormone reserve in asymptomatic autoimmune thyroiditis.

Basal (B) and peak (P) serum levels of thyroxine (T4), free thyroxine (FT4), triiodothyronine (T3), free triiodothyronine (FT3), and TSH were measured before and after oral TRH (40 mg) administration in 79 subjects affected with asymptomatic autoimmune thyroiditis (AAT) and in 69 normal subjects. The area under the curve (AUC) and peak values of T4, FT4, T3 and FT3 were considered as parameters of thyroid hormone reserve. Intrathyroidal iodine (ITI) was measured by the X-ray fluorescence method. The AAT subjects were divided into three groups on the basis of their basal and peak TSH values. In group I, these parameters were similar to those in the normal controls; in group II, basal TSH remained normal but peak TSH was significantly increased, and in group III both values were significantly increased. Group I differed from the controls by a decrease in P FT4 and AUC FT4, whereas in groups II and III B FT4 was also significantly lowered. T3 levels were similar in all groups except in group III, in whom they dropped. ITI was already lower in group I than in the controls. Its decline went further in groups II and III. An inverse correlation with significant r values was evidenced between log B and P TSH on one hand and log B FT4, P FT4 and AUC FT4 on the other. When group III was excluded, log P TSH was positively correlated with log B T3, P T3, AUC T3, and AUC F T3.(ABSTRACT TRUNCATED AT 250 WORDS)