Laparoscopic cholecystectomy using the subserosal layer dissection technique in dogs: 34 cases (2015-2021).

OBJECTIVES: To describe a standardised subserosal layer dissection technique and evaluate its outcomes in canine laparoscopic cholecystectomy. MATERIALS AND METHODS: Medical records of dogs undergoing laparoscopic cholecystectomy using the standardised subserosal layer dissection technique for the treatment of cholecystolithiasis, cholecystitis, and gall bladder mucocele at a single veterinary hospital from January 2015 to September 2021 were extracted. Operative time, subserosal layer dissection achievement rate, open conversion rate, and complication rate were evaluated. RESULTS: Thirty-four dogs were included. The most common preoperative diagnosis was cholecystolithiasis (n=29). Operative time was 190 minutes (range: 110 to 330 minutes). Subserosal layer dissection of more than 90% of the gall bladder bed was achieved in 27 (79%) dogs. Conversion to open surgery was required in three (8.8%) dogs. There were no cases of intraoperative bleeding, bile duct injury, or reoperation. CLINICAL SIGNIFICANCE: This study showed that laparoscopic cholecystectomy using the standardised subserosal layer dissection technique could be performed successfully in dogs. Future prospective clinical studies are needed to determine safety and effectiveness of this technique compared to standard techniques.

A prolonged course of Group A streptococcus-associated nephritis: a mild case of dense deposit disease (DDD)?

We herein report the case of a 12-year-old boy with dense deposit disease (DDD) evoked by streptococcal infection. He had been diagnosed to have asymptomatic hematuria syndrome at the age of 6 during school screening. At 12 years of age, he was found to have macrohematuria and overt proteinuria with hypocomplementemia 2 months after streptococcal pharyngitis. Renal biopsy showed endocapillary proliferative glomerulonephritis with double contours of the glomerular basement membrane. Hypocomplementemia and proteinuria were sustained for over 8 weeks. He was suspected to have dense deposit disease due to intramembranous deposits in the first and the second biopsies. 1 month after treatment with methylprednisolone pulse therapy, proteinuria decreased to a normal level. Microscopic hematuria disappeared 2 years later, but mild hypocomplementemia persisted for more than 7 years. Nephritis-associated plasmin receptor (NAPlr), a nephritic antigen for acute poststreptococcal glomerulonephritis, was found to be positive in the glomeruli for more than 8 weeks. DDD is suggested to be caused by dysgeneration of the alternative pathway due to C3NeF and impaired Factor H activity. A persistent deposition of NAPlr might be one of the factors which lead to complement dysgeneration. A close relationship was suggested to exist between the streptococcal infection and dense deposit disease in this case.

Short-term lithium treatment promotes neuronal survival and proliferation in rat striatum infused with quinolinic acid, an excitotoxic model of Huntington's disease.

We assessed the ability of lithium to reduce neurodegeneration and to stimulate cell proliferation in a rat model of Huntington's disease in which quinolinic acid (QA) was unilaterally infused into the striatum. LiCl (0.5-3.0 mEq/kg) was injected subcutaneously 24 h before and 1 h after QA infusion. At 7 days after QA injection, lithium significantly diminished the loss of neurons immunostained for Neuronal Nuclei (NeuN) in the injured striatum, but failed to prevent the reduction of NADPH-diaphorase-positive striatal interneurons. Lithium also reduced the number of neurons showing DNA damage or activated caspase-3. This neuroprotection was associated with an upregulation of Bcl-2 protein levels in the striatal tissue and an increase in the number and density of Bcl-2 immunostaining in striatal neurons. Bromodeoxyuridinie (BrdU) labeling in the lithium-treated injured striatum revealed the presence of large numbers of proliferating cells near the QA-injection site, with a reduction of BrdU-labeled cells in the subventricular zone (SVZ). All BrdU-labeled cells in the SVZ and the majority of BrdU-labeled cells near the QA-injection site were negative for either NeuN or glial fibrillary acidic protein (GFAP), suggesting that they are undifferentiated progenitor cells. However, a small number of BrdU-positive cells found in the QA-injected and lithium-treated striatum site were positive for either NeuN or GFAP. Our results suggest that lithium is neuroprotective in the QA-injection model of Huntington's disease not only due to its ability to inhibit apoptosis but also because it can stimulate neuronal and astroglial progenitor proliferation in the QA-injected striatum or their migration from the SVZ.

Superimposition of post-streptococcal acute glomerulonephritis on the course of IgA nephropathy: predominance of Th1 type immune response.

A 23-year-old man was admitted with macrohematuria and systemic edema appearing after an acute upper respiratory tract infection. He had been diagnosed 6 years earlier with IgA nephropathy (IgA-N). On admission, hypertension, nephrotic syndrome and hypocomplementemia were evident together with a high titer of anti-streptokinase (ASK). Renal biopsy showed severe glomerular mesangial proliferation, segmental endocapillary proliferation and crescent formation. Immunofluorescence microscopy (IF) showed strong deposition of C3 and reduced deposition of IgA. Electron microscopy showed a so-called "hump" on the epithelial side of the glomerular basement membrane. These features were consistent with post-streptococcal acute glomerulonephritis (PSAGN) superimposed on IgA-N. Following 2 weeks of observation, blood pressure, C3 level and ASK titer returned to normal ranges, although nephrotic syndrome was still evident, which necessitated oral prednisolone (30 mg/day) therapy. Another biopsy taken 2 months later demonstrated regression of endocapillary proliferation and IF showed decreased deposition of C3. Immunohistochemical staining of the specimen taken on admission revealed the presence of numerous T cells and macrophages in the interstitium. Macrophages were also seen in the glomerular tuft. Many interstitial infiltrating cells were positive for interferon-gamma, but their number diminished after treatment. Our findings suggest that PSAGN complicating pre-existing IgA-N activates cellular immunity and augments renal tissue injury.

Diffuse proliferative glomerulonephritis after bone marrow transplantation.

A 15-year-old boy developed nephrotic syndrome and acute renal failure 4 years after allogenic bone marrow transplantation (BMT) for lymphoid crisis of chronic myelocytic leukemia. On admission, he presented with clinical features of chronic GVHD including transient exacerbation of cholestatic liver injury. Renal biopsy showed diffuse proliferative glomerulonephritis with cellular crescents. The patient was treated with methylprednisolone pulse therapy (1 g/day, for 3 days) followed by oral prednisolone. Renal function gradually improved but nephrotic state was persistent. A second renal biopsy showed improvement of acute tubular necrosis and endocapillary proliferation and transformation of crescents into a fibrous form. After tapering of oral prednisolone, cyclophosphamide was started, which resulted in a gradual improvement of proteinuria. Several cases of nephrotic syndrome occurring after BMT have already been reported, but most cases had membranous nephropathy. In our case, renal biopsy revealed diffuse proliferative glomerulonephritis with findings of active cellular immunity, and aggressive treatment resulted in attenuation of these findings. Moreover, chronic GVHD-related liver injury was noted at the time of this episode. Our findings suggest that chronic GVHD may be complicated with diffuse proliferative glomerulonephritis through unknown cellular immune mechanism.

Sensor system using polarization analysis method to monitor oil-on-water in water purification plants and rivers.

Some 80% of accidental pollution in river water is caused by oil spills. Oil spills can cause serious damage such as suspension of water intake at water purification plants and major harm to ecosystems in the lower reaches of rivers. This is because oil-on-water tends to spread easily, quickly exacerbating the damage. To address this problem, an automated, continuous sensor system with high sensitivity can be used for early detection of spill accidents. We have developed a sensor system for detecting oil-on-water based on a polarization analysis method. Its advantages include: a) no direct contact with sample water; b) minimal maintenance; c) largely unaffected by foreign matter and waves on the water surface; and d) much higher sensitivity than simple visual observation. This paper describes the measurement principle and configuration of the sensor system, and discusses the results of sensitivity tests and tests on the influence of water turbidity, foreign matter and waves. We will also consider some of the limitations of the new system.

Initial experiences of tissue harmonic imaging in the diagnosis of fetal cardiac tumors.

The usefulness of tissue harmonic imaging in prenatal diagnosis is illustrated in two fetuses with a cardiac tumor. Tissue harmonic imaging provided more informative images than conventional B-mode imaging, enabling the detection of the site of attachment of the cardiac tumor and estimation of intracardiac blood flow. The advantages of tissue harmonic imaging over conventional B-mode imaging in prenatal diagnosis are discussed.

Predominance of Th1 immune response in diffuse proliferative lupus nephritis.

OBJECTIVE: Lupus nephritis, which shows various histologic patterns, is a serious complication of systemic lupus erythematosus (SLE). We previously demonstrated the importance of Thl cell-mediated immune response in patients with diffuse proliferative lupus nephritis (DPLN). The aim of this study was to examine the relationship between the peripheral blood Th1/Th2 balance and the intrarenal immune response. METHODS: The Th1:Th2 ratio in peripheral blood was measured by intracellular staining for cytokines with flow cytometry. Immunohistochemical analysis of renal biopsy specimens was performed to clarify the characterization of local infiltrating cells in 3 groups of subjects: SLE patients with World Health Organization (WHO) class IV nephritis (DPLN) (group I; n = 13), SLE patients with WHO class V nephritis (group II; n = 9), and patients with minor glomerular lesions (group III; n = 7). In addition, the histologic activity index and chronicity index were evaluated and correlated with the Th1:Th2 ratio. RESULTS: Immunohistochemical studies showed higher numbers of CD68+ macrophages, CD3 + T cells, and interferon-gamma-positive cells in group I than in groups II or III. Renal tissues from patients in group I also showed up-regulation of expression of osteopontin and CD40, with a small number of infiltrating T cells expressing interleukin-4. Overall, the Thl:Th2 ratio in group I patients (SLE with DPLN) was high and correlated significantly with the histologic activity index, but not with the chronicity index. CONCLUSION: We have identified a predominance of Thl-type response in both peripheral and renal tissues of patients with DPLN, suggesting that the peripheral blood Thl:Th2 ratio directly reflects the local histopathologic findings. In patients with lupus nephritis, the peripheral blood Th1:Th2 ratio could be useful as a parameter that reflects the renal histologic activity or the strength of the local Thl response.

Overexpression of interleukin-6 aggravates viral myocarditis: impaired increase in tumor necrosis factor-alpha.

The process of inflammation and immune response is regulated by proinflammatory cytokines. Interleukin-6 (IL-6), one of the proinflammatory cytokines, plays a potentially critical role in viral-induced myocarditis. Our previous work demonstrates that exogenous IL-6 administration, given at the time of encephalomyocarditis virus (EMCV) inoculation in C3H/HeJ mice, has a protective effect on myocardium and improves survival rates. In the present study, we examined whether overexpression of IL-6 modified viral myocarditis. On day 3 and 10 after inoculation with EMCV, the ratio of heart weight to body weight and myocardial injury were significantly increased in IL-6 transgenic mice (IL-6TG). On day 3, a reduction of viral clearance was shown by the presence of elevated viral titers and viral replication in the heart of IL-6TG. The concentrations of serum tumor necrosis factor- alpha (TNF alpha) were dramatically increased in wild-type mice on day 1, in contrast, this change was not observed in IL-6TG. Treatment with recombinant human TNF (2 microg) significantly improved viral clearance in the IL-6TG hearts. Thus, overexpression of IL-6 promotes myocardial injury by interrupting both the cytokine network and viral clearance. These experiments suggest the possibility that IL-6 is one of the factors that accelerates tissue damage, including myocardial injury, in the viral myocarditis.

Cell-transforming activity and estrogenicity of bisphenol-A and 4 of its analogs in mammalian cells.

Estrogenicity is an important mechanism in hormonal carcinogenesis but not sufficient to explain the carcinogenic activity of all estrogens. Additional mechanisms, related to genetic alterations, in conjunction with estrogenicity mediated through the estrogen receptor, have been suggested. An environmental estrogen bisphenol-A (BP-A) and its analogs are widespread in our living environment. Because of the potential for human exposure, the possible relationship between carcinogenicity and estrogenicity of these bisphenols was studied using mammalian cells. We quantitatively compared the cell-transforming activity of BP-A and 4 of its analogs (BP-2, BP-3, BP-4 and BP-5) in Syrian hamster embryo (SHE) cells lacking estrogen-receptor expression. The transforming activity determined by the morphological transformation frequencies in SHE cells treated with the bisphenols ranked: BP-4 > BP-5 > BP-3 > BP-A > BP-2. We also compared the estrogenicity of the 5 bisphenols in MCF7 human breast cancer cells as determined by cell proliferation or progesterone receptor (PgR) expression assayed by RT-PCR. When MCF7 cells were treated with the bisphenols, the proliferative potency ranked: BP-A > BP-5 > BP-4 > BP-3 = BP-2. The level of mRNA for PgR in cells treated with the bisphenols was BP-A > BP-5 > BP-4 > BP-3 > BP-2. These indicate that the transforming activity does not correlate with the estrogenicity of the bisphenols, except for BP-2 that has the weakest activity at the both endpoints. In addition, our results suggest that bisphenols with few, if any, transforming and estrogenic activities could be altered by a modification of the chemical structure. Published 2001 Wiley-Liss, Inc.

Transforming growth factor-beta/Smads signaling induces transcription of the cell type-restricted ankyrin repeat protein CARP gene through CAGA motif in vascular smooth muscle cells.

Transforming growth factor (TGF)-beta plays a major role in the development of vascular diseases. Despite the pleiotropic effects of TGF-ss on vascular smooth muscle cells (VSMCs), only a few genes have been characterized as direct targets of TGF-beta in VSMCs. Cardiac ankyrin repeat protein (CARP) has been thought to be expressed exclusively in the heart. In the present study, we showed that CARP is expressed in the vasculature after balloon injury and in cultured VSMCs in response to TGF-beta. Analysis of a half-life of the cytoplasmic CARP mRNA levels and the transient transfection of the CARP promoter/luciferase gene indicates that the regulation of CARP expression is increased by TGF-beta at the transcriptional level. Transfection of expression vectors encoding Smads significantly activated the CARP promoter/luciferase activity. Deletion analysis and site-specific mutagenesis of the CARP promoter indicate that TGF-beta response element is localized to CAGA motif at -108 bp relative to the transcription start site. Electrophoretic mobility shift assays showed that the binding activity to the CAGA motif was increased in nuclear extracts of cultured VSMCs by TGF-beta. Cells transfected with adenovirus vector expressing CARP showed a significant decrease in DNA synthesis. Overexpression of CARP enhanced the TGF-beta-mediated inhibition of the DNA synthesis. These data indicate that CARP is a downstream target of TGF-beta/Smad signaling in VSMCs and suggest a role of CARP in mediation of the inhibitory effects of TGF-beta on the proliferation of VSMCs.

Hypercalcemia induced by metastatic bone cancer in a patient with chronic renal failure.

We present a diagnostically challenging case of hypercalcemia in a 50-year-old Japanese woman with chronic renal failure due to chronic interstitial nephritis. She had a history of a radical mastectomy for breast cancer at the age of 30. Despite her chronic renal failure, serum levels of calcium and alkaline phosphatase were abnormally high, and levels of intact parathyroid hormone and of parathyroid hormone-related protein were undetectable on repeated assays. Bone scintigram revealed multiple hot lesions in the ribs, which were suggestive of bone metastases of breast cancer. After treatment with tamoxifen citrate was initiated, her serum calcium levels returned to the normal range and hot lesions were no longer evident on bone scintigraphy in 14 months. Thus, our patient's hypercalcemia was considered to be related to bone metastases of breast cancer. Physicians should be aware of existence of malignancy in the patient with chronic renal failure and hypercalcemia.

Genome analysis with restriction endonucleases recognizing 4- or 5-base pair sequences of adenovirus type.

PURPOSE: To detect the genetic changes in adenovirus type 4 (Ad4) by DNA restriction endonuclease analysis during 1993-1995, when no epidemic outbreak of conjunctivitis occurred. METHODS: We evaluated 16 Ad4 strains from patients with acute viral conjunctivitis at four eye clinics in Sapporo, northern Japan. Seven strains were obtained during the period from December 1993 through March 1994 (first period). Nine strains were obtained during the period from March through May 1995 (second period). These strains were analyzed using DNA restriction endonucleases, TaqI and HinfI. RESULTS: The seven strains obtained during the first period showed identical DNA digestion patterns. The nine strains obtained during the second period showed two DNA digestion patterns using TaqI: five strains showed the same digestion pattern as that seen in the strains obtained during the first period, and four showed a different pattern. The genetic changes in Ad4 during 1993-1995 were less frequent than those reported previously during 1985-1989. CONCLUSION: It is suggested that the decrease in the incidence of infection in 1993-1995 was related to the decrease in the incidence of mutation in the Ad4 DNA.

Induction of VEGF gene transcription by IL-1 beta is mediated through stress-activated MAP kinases and Sp1 sites in cardiac myocytes.

Interleukin-1 beta (IL-1 beta) is a multipotent cytokine participating in a variety of cardiovascular diseases. In this study, we examined the effects of IL-1 beta on the expression of vascular endothelial cell growth factor (VEGF) and pursued the molecular mechanisms underlying this effect. Treatment of cultured neonatal rat cardiac myocytes with IL-1 beta increased the levels of VEGF mRNA in a time- and a concentration-dependent manner. These effects were completely abolished by SB203580 and SB202190 (p38 MAPK inhibitors) but not by PD98059 (MEK1 inhibitor), calphostin C (protein kinase C inhibitor), or genistein (tyrosine kinase inhibitor). While IL-1 beta phosphorylated c-Jun N-terminus protein kinase (JNK) rapidly and transiently, the effect of IL-1 beta on p38 mitogen-activated protein kinase (MAPK) was gradual and persistent. Transient transfection assays showed that IL-1 beta increases the transcription from the VEGF promoter. A series of 5;-deletion and site-specific mutation analyses indicated that IL-1 beta as well as overexpression of p38 MAPK and JNK activate VEGF promoter activity through two G+C-rich sequences located at -73 and -62. Electrophoretic mobility shift and supershift assays showed Sp1 and Sp3 proteins specifically bind to the G+C-rich sequences. The half-life of VEGF mRNA was significantly increased in cells treated with IL-1 beta. Together, these results indicate that IL-1 beta induces VEGF gene expression at both transcriptional and post-transcriptional levels, and IL-1 beta evokes p38 MAPK and JNK signalings, which in turn stimulate the transcription of the VEGF gene through Sp1-binding sites. These findings suggest the role of IL-1 beta as a cytokine inducing VEGF in cardiac myocytes, and imply that activation of stress-activated MAP kinases regulate Sp1 sites-dependent transcription.

[Hypertensive putaminal hemorrhage with extensive subarachnoid hemorrhage presenting extravasation of contrast material during angiography: case report].

The authors describe a case of hypertensive putaminal hemorrhage with extensive subarachnoid hemorrhage. On admission, the patient aged 71 presented right-sided motor weakness. CT scan on admission revealed left putaminal hemorrhage with extension into the ipsilateral thalamus and lateral ventricle as well as into the subarachnoid space of the suprasellar, ambient, interhemispheric and contralateral sylvian cisterns. To exclude vascular lesions, left carotid angiography was performed just after admission. The lateral view was unremarkable, but the anterior-posterior view demonstrated extravasation of contrast material from the left lateral lenticulostriate artery. The angiographic sylvian point was shifted to the lateral side. No abnormal vessels were revealed. CT scan after angiography showed exacerbation of both intracerebral and subarachnoid hemorrhages, but the consciousness level was unchanged. CT-guided stereotactic aspiration of the hematoma was performed 4 days after the onset, but failed to remove much hemtoma. The patient died of aspiration pneumonia 9 days after onset. The authors emphasize that extensive subarachnoid hemorrhage in cases with hypertensive putaminal hemorrhage may be an important finding which indicates high risk of rebleeding.

Therapeutic effects of ulinastatin on experimental crescentic glomerulonephritis in rats.

Ulinastatin is a potent protease inhibitor purified from the human urine that has been used clinically to treat acute pancreatitis and circulatory shock. In the current study, we evaluated the therapeutic effects of Ulinastatin in a rat model of crescentic glomerulonephritis (CrGN) and investigated its putative mechanisms. Wistar-Kyoto rats were injected with nephrotoxic serum and received daily intraperitoneal injection of Ulinastatin. Ulinastatin treatment significantly reduced proteinuria and glomerular crescentic formation. Moreover, glomerular infiltration of neutrophils and ED1+ cells (monocytes/macrophages) was significantly suppressed by Ulinastatin. In contrast, the glomerular deposition of heterologous (rabbit) and autologous (rat) antibodies was not changed. Neither serum complement activation nor the anti-rabbit immune response was affected by Ulinastatin administration. Our results suggest that Ulinastatin has preventive effects on rat experimental CrGN, mediated at least in part by inhibiting intraglomerular infiltration of inflammatory cells.

High prevalence of herpes simplex virus type 2 in acute retinal necrosis syndrome associated with herpes simplex virus in Japan.

PURPOSE: To determine the type of herpes simplex virus in acute retinal necrosis syndrome associated with herpes simplex virus. METHODS: Herpes simplex virus type 1, herpes simplex virus type 2, varicella-zoster virus, Epstein-Barr virus, and cytomegalovirus were examined by polymerase chain reaction in intraocular specimens from 16 patients with acute retinal necrosis syndrome. Anti-herpes simplex virus type 1 and anti-herpes simplex virus type 2 type-specific antibodies in serum from the patients were detected by enzyme immunoassay. RESULTS: Of 16 patients with acute retinal necrosis syndrome, seven were polymerase chain reaction positive for herpes simplex virus type 2 and nine were positive for varicella-zoster virus. Anti-herpes simplex virus type 2 antibody was positive and anti-herpes simplex virus type 1 antibody was negative in the sera of the seven patients with herpes simplex virus type 2 DNA-positive acute retinal necrosis syndrome. In contrast, anti-herpes simplex virus type 2 antibody was absent in all nine varicella-zoster virus DNA-positive acute retinal necrosis syndrome patients. CONCLUSION: Herpes simplex virus type 2 has been demonstrated to be the major causative agent in acute retinal necrosis syndrome associated with herpes simplex virus by molecular biological and serological methods. Negative preexisting anti-herpes simplex virus type 1 antibody may play an important role in acute retinal necrosis syndrome associated with herpes simplex virus type 2.

Effects of cilostazol on heart rate and its variation in patients with atrial fibrillation associated with bradycardia.

BACKGROUND: Heart-rate (HR) variability is an important predictor of mortality in patients with heart disease. We examined the effects of cilostazol, a quinolinone derivative, on HR and HR variability in patients with chronic atrial fibrillation associated with bradycardia episodes. PATIENTS AND METHODS: Thirteen patients with chronic atrial fibrillation associated with bradycardia episodes (minimal HR <40/min and/or pauses, ie, episodes with an RR interval > 2.5 sec) received cilostazol (100 or 200 mg/day) orally for at least 2 months and 24-hour Holter electrocardiography was performed before and after the start of cilostazol administration. RESULTS: Minimal HR was significantly increased, by an average of 14 beats/min (bpm), at 3.3 +/- 0.8 weeks (mean +/- SD) after the start of cilostazol treatment. The number of pauses was significantly decreased. As a consequence, mean HR was increased by an average of 18 bpm. Maximal HR was also increased by an average of 19 bpm. The circadian variation of the HR, determined by cosine fitting, was not changed by cilostazol treatment. The time-domain HR variabilities, ie, the SD of the mean RR interval and the SD of the 5-minute mean RR intervals, were also unchanged. New York Heart Association functional class was significantly improved and the plasma atrial natriuretic polypeptide level was significantly decreased after the initiation of cilostazol treatment. CONCLUSION: Cilostazol improves the slow HR episodes associated with chronic atrial fibrillation and maintains the HR circadian variation and time-domain variability, indicating that cilostazol has therapeutic utility for the treatment of the slow HR associated with chronic atrial fibrillation.

Chronic intestinal pseudo-obstruction due to dialysis-related amyloid deposition in the propria muscularis in a hemodialysis patient.

Dialysis-related amyloidosis (DRA) is one of the most serious complications interfering with rehabilitation in dialysis patients. Here, we report a case of beta2-microglobulin (beta2M)-related amyloidosis, in which the patient developed a severe intestinal pseudo-obstruction. The patient was a 42-year-old male who had been undergoing hemodialysis for 13 years, and who had no history of osteoarticular involvement of DRA. The first symptoms of the disease were severe abdominal fullness and nausea after meals. The whole intestinal wall biopsy revealed massive amyloid deposition in the propria muscularis. The patient became malnourished and died of acute subendocardial infarction 3 years after the onset. An autopsical examination revealed a massive deposition of amyloid, which was positively stained with anti-beta2M antibody but not AA amyloid, predominantly in the gastrointestinal muscular layer, including the tongue, esophagus, stomach, small intestines, colon, and rectum. These results suggest that the gastrointestinal involvement of beta2M-related amyloidosis might occur during the course of hemodialysis treatment, and that this possibility should be considered if patients suffer from intestinal pseudo-obstruction without osteoarticular symptoms.