The importance of serum creatine phosphokinase level in the early diagnosis, and as a prognostic factor, of Vibrio vulnificus infection.

BACKGROUND: Vibrio vulnificus infection causes rapidly progressive skin lesions and sepsis in compromised hosts with liver cirrhosis, and is often fatal. Early diagnosis and rapid treatment are important. OBJECTIVES: To clarify the characteristics of V. vulnificus infection that distinguish it from other cutaneous and soft-tissue bacterial infections and to confirm that serum creatine phosphokinase (CPK) levels are useful in early diagnosis, and are a prognostic factor for, V. vulnificus infection. METHODS: We analysed the clinical and laboratory findings (especially serum CPK levels) in eight patients with V. vulnificus infection who were treated at the Saga Medical School Hospital between January 1989 and December 1999. RESULTS: All eight patients had liver dysfunction and typical skin manifestations. Six had eaten raw seafood before onset. Seven patients had initial skin manifestations in their legs or feet and eventually died, despite prompt therapy in the intensive care unit. CPK levels of six of these seven patients were already elevated at their initial presentation. Only one patient, with skin manifestations solely on his left hand, showed and maintained a normal CPK level and survived. In 23 patients with cutaneous and soft-tissue infections (10 with necrotizing fasciitis, three with erysipelas, 10 with cellulitis), only three patients with necrotizing fasciitis and streptococcal toxic shock syndrome (STSS) showed CPK elevation. CONCLUSIONS: A high level of serum CPK in cutaneous or soft-tissue bacterial infection is considered useful for an early diagnosis of V. vulnificus infection and STSS. A history of eating raw seafood, underlying liver disease and multiple lesions suggest a diagnosis of V. vulnificus infection, rather than STSS.

Massive rectal bleeding due to ileal tuberculosis.

A patient with massive rectal bleeding due to ileal tuberculosis is reported. Technetium-99m labelled red blood cell scintigraphy indicated hemorrhage from the ileum, and laparotomy was then carried out. A 70-cm segment of ileum containing ulcers and erosions was resected, and epitheloid granuloma with Langhans-type giant cell was found in the resected specimen. Massive rectal bleeding is considered a rare presenting symptom of intestinal tuberculosis. Intestinal tuberculosis, including small intestinal tuberculosis, although uncommon, should be taken into consideration as a cause of rectal bleeding.

[Effect of sevoflurane on release of TNF-alpha and IL-1 beta from human monocytes].

Although isoflurane inhibits TNF-alpha and IL-1 beta release from human monocytes stimulated by LPS in dose dependent fashion, it is unclear whether sevoflurane has the same effects. Therefore, we investigated whether sevoflurane could inhibit TNF-alpha and IL-1 beta secretions from human monocytes stimulated by LPS in dose dependent fashion in vitro. Human monocytes stimulated by LPS were cultured for 3 h in the presence of sevoflurane 1% or 5%. Another group of human monocytes were cultured in the absence of sevoflurane. TNF-alpha and IL-1 beta increased after stimulation of LPS and these increases were not inhibited by sevoflurane in a dose dependent fashion. We conclude that sevoflurane does not inhibit TNF-alpha and IL-1 beta release from monocytes stimulated by LPS.

[The effect of isoflurane on the secretion of TNF-alpha and IL-1 beta from LPS-stimulated human peripheral blood monocytes].

The cytokines such as tumor necrosis factor and interleukin-1 secreted from macrophages/monocytes proved to play important roles in the pathogenesis of endotoxemia, severe pancreatitis and other surgical injuries. However, it is still unclear how inhalational anesthetic agents influence the secretion of these cytokines from macrophages/monocytes. We investigated the effects of isoflurane on TNF-alpha and IL-1 beta secretions from human peripheral blood monocytes stimulated by lipopolysaccharide. TNF-alpha and IL-1 beta secretions increased after LPS stimulation and this increase was inhibited by isoflurane in dose-dependent fashion. The inhibitory action of isoflurane disappeared between 1 and 3 hours after stopping isoflurane inhalation. We concluded that isoflurane could inhibit TNF-alpha and IL-1 beta secretions from peripheral blood monocytes stimulated by LPS in a dose-dependent fashion and that the inhibitory action of isoflurane was reversible.

[Milrinone suppresses TNF-alpha and IL-1 beta release in mouse peritoneal macrophages].

Tumor necrosis factor-alpha (TNF-alpha) exerts a wide spectrum of biological activities and contributes to the pathophysiology of septic shock. We studied whether milrinone suppresses TNF-alpha and IL-1 beta releases from mouse peritoneal macrophages. Mouse peritoneal macrophages were stimulated for 18 hr with lipopolysaccharide and different doses of milrinone. TNF-alpha release was suppressed in a dose-dependent fashion with milrinone, reaching half-maximal inhibition at 30 microM. Release of IL-1 beta was not suppressed with 25 microM of milrinone, but it was suppressed with 250 microM of milrinone. We conclude that TNF-alpha release is suppressed by therapeutically administered milrinone.

[Effects of DbcAMP on tumor necrosis factor and interleukin-1 production in human monocytes].

Recent reports have shown that dibutyryl cAMP (DbcAMP) blocks endotoxin-induced lung injury. To determine whether DbcAMP suppresses the production of tumor necrosis factor (TNF) and interleukin-1 (IL-1) in human monocytes, we measured the levels of TNF and IL-1 in response to E. Coli lipopolysaccharide (40 micrograms.ml-1) in vitro. We now show that DbcAMP suppressed dose-dependently the production of TNF in human monocytes, and DbcAMP totally suppressed it at the dose above 5 x 10(-4) M. However, DbcAMP did not suppress the production of IL-1 even at the dose of 5 x 10(-3) M in human monocytes. These data suggest that the productive mechanism of IL-1 may be different from that of TNF. Further, suppression of TNF by DbcAMP may contribute to the beneficial effects in animal models of septic shock or lung injury and this may have clinical implications.

[ACE Index in patients with respiratory failure].

To investigate whether ACE Index (ACE. Cardiac output-1) which excludes the influence of pulmonary perfusion volume is more useful than angiotensin converting enzyme (ACE) as an early marker of pulmonary endothelial injury and repair, we measured ACE, ACE index, and PaO2.FIO2-1 ratio several times during the stay in the ICU in two patients with respiratory failure. ACE index had a closer relationship to clinical course of respiratory condition and PaO2.FIO2-1 (r = 0.806, 0.889, respectively), in comparison with ACE. We conclude that ACE index could be more sensitive than ACE as an early marker of pulmonary endothelial injury and repair.

[Angiotensin converting enzyme index increases after open cardiac surgery].

To investigate whether pulmonary endothelial cells are damaged after open cardiac, open chest, or head-neck surgery, we measured angiotensin converting enzyme (ACE) and calculated ACE index (ACE.cardiac output-1) to exclude the influence of pulmonary perfusion volume in 38 patients. There were no significant differences among three groups in serum ACE (9.93 +/- 2.46 IU.l-1 after open cardiac surgery, 8.50 +/- 2.75 IU.l-1 after open chest surgery, 10.71 +/- 2.23 IU.l-1 after head-neck surgery). ACE index after open cardiac surgery was significantly higher than those after open chest and head-neck surgery (2.43 +/- 0.85, 1.67 +/- 0.69, 1.64 +/- 0.50 respectively). These results suggest that ACE index detects pulmonary endothelial cell damage caused by reperfusion after cardiopulmonary bypass. We conclude that ACE index is more useful than ACE as an early clinical marker of pulmonary endothelial cell damage.

[Effect of endotoxin on plasma angiotensin-converting enzyme in dogs].

We calculated angiotensin converting enzyme (ACE) index (ACE/CO) to exclude the influence of pulmonary perfusion and investigated the relationship among ACE, ACE index, hemodynamic changes in 6 endotoxin dogs. Systemic arterial pressure and cardiac output (CO) decreased significantly after 3 mg.kg-1 of endotoxin administration, but neither pulmonary arterial pressure nor pulmonary arterial wedge pressure changed. Lung wet/dry ratio was higher. Although endotoxin administration caused the pulmonary capillary endothelial damage in this experiment, plasma ACE showed a nonsignificant increase. The main reason may be related to the reduction of surface area of pulmonary capillary endothelial cells caused by the decrease in cardiac output. The increased ACE index lasted for 15 to 90 min and began to return to baseline at 120 min after endotoxin administration. We conclude that ACE index is more useful than plasma ACE as an early marker of the pulmonary capillary endothelial damage induced by endotoxin.