Pseudoaldosteronism with increased serum cortisol associated with pneumonia, hypouricemia, hypocalcemia, and hypophosphatemia.

We describe here the interesting case of a 73-year-old hypertensive man with pseudoaldosteronism. He had been taking glycyrrhizin at a dose of 75 mg/day for 12 years because of mild liver damage, but had never experienced any previous symptoms associated with hypokalemia. He was referred to our hospital because of hypokalemic tetraparesis and rhabdomyolysis. At that time, we noted mineralocorticoid excess characterized by hypokalemia due to urinary K loss, exacerbation of hypertension due to increased tubular Na reabsorption, metabolic alkalosis, and suppression of both plasma renin activity and plasma aldosterone concentration. His urinary free cortisol excretion rate and the urinary ratio of free cortisol to free cortisone were markedly elevated. Thus we diagnosed pseudoaldosteronism that was related to the long-term use of glycyrrhizin. When he developed pseudoaldosteronism, he also contracted pneumonia, and exhibited elevated levels of serum cortisol and creatinine clearance (CCr) as well as hypouricemia, hypocalcemia, and hypophosphatemia. All normalized after the recovery from pneumonia and the administration of spironolactone. The extracellular volume expansion associated with increased tubular Na reabsorption by the aldosterone-sensitive distal nephron and the resulting increase in CCr caused an inhibition of proximal tubular reabsorption of uric acid, Ca, and inorganic phosphate, leading to their renal loss and therefore hypouricemia, hypocalcemia, and hypophosphatemia, respectively. In this patient, the increased circulating cortisol associated with the stress of inflammation caused by pneumonia triggered the development of pseudoaldosteronism.

Malignant lymphoma with tumor thrombus in the portal venous system.

We report a case of malignant lymphoma presenting with tumor thrombus of the portal venous system. Computed tomography showed a mass in the portal vein and mesenteric lymphadenopathy. Filling defects in the dilated portal vein also were identified by angiography. This type of the lymphoma is extremely rare, but it should be considered in the differential diagnosis of portal vein thrombus.

Helicobacter pylori infection delays the healing of acetic acid-induced gastric ulcer in Japanese monkeys.

To clarify the relationship between Helicobacter pylori and the healing of gastric ulcers, we investigated the healing of acetic acid-induced gastric ulcers in the antral mucosa of Japanese monkeys (n = 5) infected with H. pylori and in control monkeys without H. pylori infection (n = 6). Using H. pylori-infected Japanese monkeys as an experimental model, gastric ulcers were induced endoscopically with acetic acid. Healing of ulcers and factors that influenced healing were studied. Continuous colonization with H. pylori was confirmed in the infected group throughout the observation period; no H. pylori were isolated from the gastric mucosa of the control group. White scarring was not observed in any infected monkeys 4 weeks after ulcer formation, but was observed in one (20%) of five monkeys at 6 weeks and in all five monkeys eight weeks after ulcer formation. In the control group, white scarring was observed in one (16.7%) of six monkeys at 4 weeks and in six monkeys at 6 (P < 0.01 vs infected group) and 8 weeks. The ammonia concentration of the gastric secretions and the grade of inflammation were significantly increased in the H. pylori-infected group compared with the control group (P < 0.01 and P < 0.001, respectively). The volume of intracellular PAS-positive substance was decreased (P < 0.025-0.01) at the ulcer margin in the infected group compared with the ulcer margin in the control group. The proliferation of gastric epithelial cells was markedly accelerated at the ulcer margin in the infected group compared with the ulcer margin in control group (P < 0.025-0.01). Our results strongly suggest that H. pylori infection delays the healing of gastric ulcers.

Establishment of an animal model for chronic gastritis with Helicobacter pylori: potential model for long-term observations.

OBJECTIVES: To assess the suitability of an established experimental model for chronic gastritis associated with Helicobacter pylori for use in long-term observations. DESIGN: In a 3-year follow-up study of acute gastritis induced by H. pylori using an established experimental model with Japanese monkeys, we compared H. pylori-infected animals (n = 6) with a non-infected control group (n = 7). Colonization by H. pylori, gastritis scores, volume of intracellular periodic acid-Schiff-positive substances and the height of antral glands were investigated every 3 months for 3 years and compared with those of a control group. RESULTS: In the infected group, persistent colonization with H. pylori was demonstrated by culture and histological examinations. Gastritis scores were significantly higher than those of the control group, and the histological findings were quite similar to those of chronic active gastritis observed in humans. Simultaneously, significant decreases in the contents of periodic acid-Schiff-positive substances and in the height of antral glands were also demonstrated in infected animals. CONCLUSION: In Japanese monkeys, persistent colonization with H. pylori caused chronic gastritis quite similar to that observed in humans, thus providing a suitable animal model for evaluating the long-term prognosis of H. pylori infection.

[Experimental study in Japanese monkeys with Helicobacter pylori infection].

Japanese monkeys were studied for one month from 6 months (short-term) after inoculation of Helicobacter pylori, and two years (long-term). In the short-term study, macroscopic and histological gastritis were observed for 5 infected monkeys. The gastritis score, the ammonia concentration in the gastric secretion and the level of serum antibody (IgG) were higher for the infected group than for the control. In the long term study, H. pylori was always recovered for 2 years in the infected group, and the gastritis score was higher than the control. The intracellular periodic acid-Schiff (PAS) positive substances in the infected group decreased than that of the control. The tall of pyloric gland in the infected group was significantly decreased on 6 months from 1.5 years. These results suggest that the Japanese monkey can be used as experimental model of H. pylori infection and that H. pylori can induce chronic active gastritis similar to human.

Experimental gastritis induced by Helicobacter pylori in Japanese monkeys.

We used Japanese monkeys (Macaca fuscata) to establish an experimental model in order to clarify the pathogenicity of Helicobacter pylori in gastric and duodenal disorders. A suspension (5 ml; 10(9) CFU/ml) of H. pylori cells isolated from humans was sprayed around the antrum of the stomach of each of 12 of 17 animals with an endoscope. The remaining five animals were not inoculated; they served as a control group. On days 7, 14, and 28 after inoculation, the gastric mucosa samples were examined grossly and were biopsied for microscopic examination with an endoscope. H. pylori was recovered from 7 of the 12 inoculated animals (58%), and infiltration by neutrophils and monocytes was observed histologically. Macroscopic gastritis with erythema and erosions were noted for five of these animals. On day 28 after inoculation, five animals in the infected group were treated with ampicillin. In two infected but untreated animals, the bacteria persisted for more than 6 months. The result of the gastritis scoring of the antral mucosa and the ammonia concentration in the gastric secretion were significantly higher (P < 0.01 to 0.001) for the infected group than for the control group; however, these values decreased to levels comparable to those for the control group after treatment with ampicillin. Urease activity was positive in gastric biopsy specimens from five of the seven animals in the infected group after 7 days and from four of these animals after 14 days but was negative in all specimens from animals in the control group. The level of antibody (immunoglobulin G) in serum for the infected group was elevated but changed very little for the control group. These results suggest that this M. fuscata model can be used to study H. pylori infection and that H. pylori can induce gastritis.