CD3bright signals on γδ T cells identify IL-17A-producing Vγ6Vδ1+ T cells.

Interleukin-17A (IL-17A) is a pro-inflammatory cytokine that has an important role at mucosal sites in a wide range of immune responses including infection, allergy and auto-immunity. γδ T cells are recognized as IL-17 producers, but based on the level of CD3 expression, we now define the remarkable ability of a CD3(bright) γδ T-cell subset with an effector memory phenotype to rapidly produce IL-17A, but not interferon-γ. CD3(bright) γδ T cells uniformly express the canonical germline encoded Vγ6/Vδ1(+) T-cell receptor. They are widely distributed with a preferential representation in the lungs and skin are negatively impacted in the absence of retinoic acid receptor-related orphan receptor gammat expression or endogenous flora. This population responded rapidly to various stimuli in a mechanism involving IL-23 and NOD-like receptor family, pyrin domain containing 3 (NLRP3)-inflammasome-dependent IL-1ß. Finally, we demonstrated that IL-17-producing CD3(bright) γδ T cells responded promptly and strongly to pneumococcal infection and during skin inflammation. Here, we propose a new way to specifically analyze IL-17-producing Vγ6/Vδ1(+) T cells based on the level of CD3 signals. Using this gating strategy, our data reinforce the crucial role of this γδ T-cell subset in respiratory and skin disorders.

Metabolic alkalosis in a hemodialysis patient after ingestion of a large amount of an antacid medication.

A maintenance hemodialysis patient developed metabolic alkalosis in the absence of vomiting or nasogastric suction. The cause of the metabolic alkalosis was ingestion of an exogenous alkali in the form of Bromoseltzer. The metabolic alkalosis improved with hemodialysis using a low-bicarbonate bath.

Relapsing polychondritis.

BACKGROUND: Relapsing polychondritis (RPC) is a rare, chronic, and potentially fatal multisystemic inflammatory disorder targeting cartilaginous structures. This disorder is frequently associated with rheumatoid arthritis, systemic vasculitis, connective tissue diseases, and/or hematologic disorders. RPC afflicts patients with recurrent and often progressive episodes of inflammation with the potential for destruction of the affected structures. Tissues involved include the ears, joints, nose, larynx, trachea, eyes, heart valves, kidneys,and skin. Ocular manifestations commonly include episcleritis, scleritis, conjunctivitis, iridocyclitis, chorioretinitis, and proptosis. Lid edema, orbital inflammation, muscle palsies, and corneal melting may also occur. CASE REPORT: An 83-year-old man previously diagnosed with RPC presented to our clinic with acute unilateral chemosis, conjunctivitis, lid edema, proptosis, and extraocular muscle restriction. After orbital cellulitis was ruled out, further evaluation revealed posterior scleritis with choroidal detachment OS. A course of oral indomethacin and topical antibiotic-steroid combination drops was implemented in the treatment of the ocular manifestations. The quick positive response to the anti-inflammatory agents confirmed the diagnosis of ocular complications secondary to RPC. DISCUSSION: The presenting ocular signs and symptoms of RPC often resemble other commonly encountered ocular conditions. It is important for the eye care practitioner to be familiar with the ocular manifestations of RPC because the eyes are sometimes the initial site of involvement and may be a marker of severity. Early diagnosis and intervention may significantly improve the patient's outcome. This case report with literature review will hopefully bring to light features of this disease which will help the eye care practitioner in the diagnosis and management of this condition.

Hemodialysis-induced hypophosphatemia in a normophosphatemic patient dialyzed for ethylene glycol poisoning: treatment with phosphorus-enriched hemodialysis.

Hypophosphatemia developed in a normophosphatemic patient after 9 h of hemodialysis therapy (using a phosphate-free dialysate) administered for the treatment of ethylene glycol poisoning. The hypophosphatemia was promptly improved with additional hemodialysis treatment using a phosphorus-enriched dialysate.

Use of a phosphorus-enriched hemodialysate to prevent hypophosphatemia in a patient with renal failure-related pericarditis.

We describe a patient who suffered from renal failure-associated pericarditis and underwent daily 3.5-hour hemodialysis treatments for 17 days. The initially elevated serum phosphorus level gradually fell to below normal on days 11 and 12 as a result of the intensive dialytic therapy. Phosphorus was added to the "base concentrate" of a dual-concentrate, bicarbonate-based dialysate delivery system on days 13 to 17. Because of this phosphorus-enrichment, we were able to maintain the patient's serum phosphorus levels within normal limits in spite of continued daily dialysis treatments.

Treatment of acute methanol intoxication with hemodialysis using an ethanol-enriched, bicarbonate-based dialysate.

A patient poisoned with methanol was successfully hemodialyzed with an ethanol-enriched, bicarbonate-based dialysate. Along with a concomitant intravenous infusion of ethanol, the ethanol-enriched dialytic procedure was able to maintain an intradialytic plasma ethanol level of 80 to 102 mg/dL. The patient recovered without any sequelae of methanol intoxication.

Use of a phosphorus-enriched dialysate to hemodialyze patients with ethylene glycol intoxication.

A phosphorus-enriched dialysate was used to intensively hemodialyze two non-uremic and non-hyperphosphatemic patients poisoned with ethylene glycol. As a consequence of the use of such a dialysate, we were able to prevent a fall in plasma inorganic phosphorus levels in these patients in spite of the intensive dialytic therapy.