Osseous metaplasia in a recurrent symptomatic rectal lesion: a rare occurrence.

BACKGROUND: Osseous metaplasia of the gastrointestinal tract is exceedingly rare. Associated with colorectal cancer, juvenile polyps , and inflammatory polyps, the exact etiology is still unknown. We present a case report on a young male with recurrent rectal polyps and rectal bleeding. Histopathology revealed an inflammatory polyp with focal osseous metaplasia. CASE PRESENTATION: A 30-year-old male without significant past medical history but with a significant smoking history of 10 pack-years. He initially presented to the colorectal clinic approximately 8 months prior with complaints of rectal pain and bleeding. The patient subsequently underwent colonoscopy which demonstrated a friable 2-cm mass at the dentate line. He was taken to the operating room for a transanal mass excision which, at the time, pathologic examination demonstrated a hyperplastic polyp with no evidence of dysplasia or malignancy. The patient returned to the clinic 8 months later with similar complaints of rectal bleeding. He denied any constitutional symptoms, weight loss, abdominal pain, diarrhea, or constipation. Upon rectal examination, he was noted to have a soft palpable mass blood on digital rectal exam. The patient was taken for repeat colonoscopy and was found to have a recurrent mass at the dentate line. Given the recurrent mass, the patient was taken for a re-excision in the operating room. Histopathology returned showing a 1.8 × 1.5 × 1.5 cm inflammatory polyp with focal osseous metaplasia. CONCLUSION: Osseous metaplasia of the gastrointestinal tract is a rare occurrence that can be associated with benign polyps or malignancy. Certain markers have been shown to be linked to this process and polypectomy remains the gold standard of treatment; however, further research is warranted.

Wound healing is accelerated by agonists of adenosine A2 (G alpha s-linked) receptors.

The complete healing of wounds is the final step in a highly regulated response to injury. Although many of the molecular mediators and cellular events of healing are known, their manipulation for the enhancement and acceleration of wound closure has not proven practical as yet. We and others have established that adenosine is a potent regulator of the inflammatory response, which is a component of wound healing. We now report that ligation of the G alpha s-linked adenosine receptors on the cells of an artificial wound dramatically alters the kinetics of wound closure. Excisional wound closure in normal, healthy mice was significantly accelerated by topical application of the specific A2A receptor agonist CGS-21680 (50% closure by day 2 in A2 receptor antagonists. In rats rendered diabetic (streptozotocin-induced diabetes mellitus) wound healing was impaired as compared to nondiabetic rats; CGS-21680 significantly increased the rate of wound healing in both nondiabetic and diabetic rats. Indeed, the rate of wound healing in the CGS-21680-treated diabetic rats was greater than or equal to that observed in untreated normal rats. These results appear to constitute the first evidence that a small molecule, such as an adenosine receptor agonist, accelerates wound healing in both normal animals and in animals with impaired wound healing.

Medial-to-lateral laparoscopic colon resection: a view beyond the learning curve.

BACKGROUND: Since the authors' report on the lateral approach to laparoscopic colon resection (LCR), medial-to-lateral (M-L) segmental resection has continued to evolve. This report analyzes their learning curve experience with a standardized three-trocar M-L technique, which demonstrates the influence of operative volume on proficiency and outcome. METHODS: From January 1999 to December 2004, 100 consecutive patients underwent a standardized three-trocar M-L segmental LCR. Patient demographics, indications for surgery, operative proficiency (time), and outcome (i.e., blood loss, conversion to open surgery, length of hospital stay, morbidity, and mortality) were recorded. A learning curve analysis was performed using a t-test and analysis of variance (ANOVA). RESULTS: The 100 M-L LCRs included sigmoid (55%), right (34%), left (6%), and transverse (5%) approaches. Overall learning curve proficiency was influenced by increasing operative experience (p = 0.02). However, significant and consistent improvement in the learning curve occurred only after 38 LCRs (p < 0.008). Notably, all conversions to open surgery (3%) occurred during the early learning curve. Similarly, early LCR patients experienced greater morbidity (mean, 21% vs 12%) and mortality (mean, 5% vs 2%) than their later counterparts. CONCLUSION: To obtain optimum proficiency in performing LCR, a minimum of 38 M-L procedures is required. Operative and patient outcomes improve beyond the early learning curve.

Evolution of the lateral canthoplasty: techniques and indications.

Lateral canthoplasty is a useful method to restore eyelid function and to protect the ocular surfaces. The success of the procedure depends on the proper analysis of periorbital anatomy as it relates to the specific indication for lateral canthoplasty. We report the experience with 1565 lateral canthoplasties with emphasis on the evaluation of newer techniques that better address anatomic and functional requirements. Between 1981 and 1994, 1565 lateral canthoplasties were performed in 684 patients. Of these, 1369 "reconstructive" lateral canthoplasties were performed in 586 patients and 196 "cosmetic" lateral canthoplasties were performed in 98 patients. All operations were performed by a single surgeon (Jelks), and follow-up ranged from 1 to 14 years. The evolution of the operative technique for lateral canthoplasty has been toward an operation that corresponds with the anatomy of the individual. Indications for the procedure include lateral canthal dystopia, horizontal lid laxity, ectropion, entropion, lid margin eversion, lid retraction with or without soft-tissue deficiency, and aesthetic improvement. The types of procedures performed will be reviewed in detail. The evaluation of the newer forms of lateral canthoplasty as unique reconstructive tools and as adjuncts to aesthetic surgery will be discussed.

The anti-inflammatory mechanism of sulfasalazine is related to adenosine release at inflamed sites.

The anti-inflammatory mechanism of sulfasalazine is not well understood. It has recently been shown that sulfasalazine inhibits 5-aminoimidazole-4-carboxamidoribonucleotide (AICAR) transformylase, an enzyme involved in de novo purine biosynthesis. We recently demonstrated that methotrexate promotes intracellular AICAR accumulation, thereby increasing adenosine release and diminishing inflammation, so we tested the hypothesis that sulfasalazine similarly promotes intracellular AICAR accumulation. We studied adenosine release and the state of inflammation in in vitro and in vivo models of the inflammatory process. The adhesion of stimulated neutrophils (FMLP) to endothelial cells preincubated with sulfasalazine was inhibited in a dose-dependent manner. Elimination of extracellular adenosine by addition of adenosine deaminase or inhibition of adenosine by the adenosine A2 receptor antagonist 3,7-dimethyl-1-propargylxanthine (DMPX) completely reversed the anti-inflammatory effect of sulfasalazine (at concentrations <1 microM in this in vitro model. To determine whether this phenomenon was relevant to inhibition of inflammation in vivo, we studied the effect of sulfasalazine (100 mg/kg/day by gastric gavage for 3 days) on leukocyte accumulation in the murine air pouch model of inflammation. Treatment with sulfasalazine markedly decreased the number of leukocytes that accumulated in the inflamed (carrageenan, 2 mg/ml) air pouch. Injection of either adenosine deaminase or DMPX, but not the A1 receptor antagonist 8-cyclopentyl-dipropylxanthine, significantly reversed the anti-inflammatory effects of sulfasalazine treatment. Sulfasalazine increased the exudate adenosine concentration from 127 +/- 64 nM to 869 +/- 47 nM. Moreover, sulfasalazine treatment promoted a marked increase in splenocyte AICAR concentration from 35 +/- 6 to 96 +/- 3 pmols/10(6) splenocytes, which is consistent with the in vitro observation that sulfasalazine inhibits AICAR transformylase. These results indicate that sulfasalazine, like methotrexate, enhances adenosine release at an inflamed site and that adenosine diminishes inflammation via occupancy of A2 receptors on inflammatory cells. Our studies provide evidence that sulfasalazine and methotrexate may be described as a newly recognized family of anti-inflammatory agents that share the property of using adenosine as an antagonist of inflammation.