Acute sphenoid sinusitis leading to contralateral cavernous sinus thrombosis: a case report.

INTRODUCTION: The objective of this article was to report a case of isolated, acute, right-sided sphenoid sinusitis that progressed to contralateral cavernous sinus thrombosis in an 18-year-old male patient. We describe the atypical presentation of this case and discuss the relevant anatomy, pathogenesis, presentation, diagnostic evaluation and treatment. CASE REPORT: A case report of sphenoid sinusitis leading to contralateral cavernous sinus thrombosis was reviewed and presented along with a comprehensive literature review of the relevant anatomy, pathophysiology, microbiology, diagnostic work-up and treatment options. CONCLUSION: Cavernous sinus thrombosis is a rare clinical entity in the antibiotic era. However, limited sphenoid sinusitis may progress to cavernous sinus thrombosis in spite of maximal medical treatment, as highlighted in this case report. The mainstay of treatment includes early diagnosis allowing aggressive intravenous antibiotics and appropriate surgical management.

Canal wall down tympanomastoidectomy: the 'on-disease' approach for retraction pockets and cholesteatoma.

It is well known that cholesteatoma is three-dimensional; hence, we feel that its surgical management requires a three-dimensional approach in order to achieve the best curative and functional results. Retraction pockets are undeniably caused by chronic and recurrent eustachian tube obstruction. However, we found that the presence of a large mastoid antrum was an important, additional aetiological factor in the formation of a retraction pocket and its progression to cholesteatoma formation, with bone destruction and subsequent complications. Canal wall down tympanomastoidectomy--the 'on-disease' approach--is an innovative, three-dimensional technique based on universally accepted surgical principles. We modified the technique to ensure complete exposure and thereby eradication of the disease, with a resultant small cavity. Working in a three-dimensional field, we began drilling at the posterior meatal wall, lowering it while simultaneously widening the cavity as the mastoid was drilled to reach the antrum and the aditus. The bridge was lowered and the incus removed to completely expose the entire disease. The facial ridge was debulked and the temporalis fascia graft placed so as to simplify the middle-ear cleft. We present a comprehensive report of this technique, based upon 600 patients studied retrospectively over a five-year period. After one-year follow up, 546 patients had a dry, healed cavity. Canal wall down tympanomastoidectomy performed by the on-disease approach ensures complete eradication of the disease, with excellent curative as well as functional results.

Prolactin-immunoglobulin G complexes from human serum act as costimulatory ligands causing proliferation of malignant B lymphocytes.

Several lines of evidence indicate that immunoglobulin-bound prolactin found in human serum is not a conventional complex between an anti-prolactin antibody and prolactin but a different type of association of prolactin with the Fab portion of IgG heavy chains. The complex of prolactin with IgG was purified from serum by anti-human prolactin affinity chromatography and was shown to contain close to 1 mole of N epsilon-(gamma-glutamyl)lysine crosslinks per mole of complex, a characteristic feature in structures crosslinked by transglutaminase. Interestingly, the complex caused a proliferation of cells from a subset of patients with chronic lymphocytic leukemia, while it was inactive in a cell proliferation prolactin bioassay. By contrast, human prolactin stimulated the proliferation of cells in the bioassay but had no effect on the complex-responsive cells from the patients. Competition studies with prolactin and free Fc fragment of IgG demonstrated a necessity for engaging both the prolactin and the immunoglobulin receptors for proliferation. More importantly, competition for the growth response by free prolactin and IgG suggests both possible reasons for the slow growth of this neoplasm as well as avenues for control of the disease.