MR of staphylococcal myelitis of the cervical spinal cord.

A homogeneously enhancing cervical cord lesion and multiple ring-enhancing brain lesions were detected with MR imaging in a 41-year-old woman with a staphylococcal septicemia. The brain and spinal cord lesions diminished in size after antibiotic therapy. Although no biopsy was performed, we believe, on the basis of the clinical outcome, that the spinal cord lesion represented a bacterial myelitis and that the lesion was prevented from developing into an abscess by early antibiotic therapy.

Abnormal crosstalk between pancreatic acini and macrophages during the clearance of apoptotic cells in chronic pancreatitis.

In chronic pancreatitis (CP), both the progressive loss of acinar parenchyma and aggressive fibro-inflammatory reactions ultimately lead to irreversible organ destruction. Dying cells are normally removed by macrophages and elimination is associated with anti-inflammatory cytokine switch. We investigated whether defective clearance of damaged acini by macrophages such as compromised phagocytosis or altered cytokine reaction occurs in CP and thus represents a causative link between acinar loss and fibro-inflammation. In a checkerboard-like co-culture system, we assessed normal and CP macrophages for their phagocytic and cytokine responses to dying pancreatic acinar cells of normal or CP origin by FACS, confocal microscopy, QRT-PCR, and ELISA. In CP, phagocytosis of apoptotic acini by macrophages was not impaired; however, the associated cytokine responses were gradually perturbed. Most interestingly, only normal acini suppressed TGFbeta1 expression and accumulation specifically in normal macrophage cultures, while CP acini lost this ability. Both types of apoptotic acini induced pro-inflammatory cytokine bursts of varying strength in both types of macrophages; however, the most significant difference (more than 50-fold higher expression of IL-1beta, IL-6, and IL-8) was evident between CP/CP and normal/normal combinations, indicating that acinar and macrophage alterations synergistically lead to the ultimate CP-specific bias. In combination with in situ data comparing circulating inflammatory cells to pancreatic resident ones, our results indicate that cytokine expression in inflammatory cells undergoes spatiotemporal modulation, most likely through a successive interplay of acinar, stromal, and circulating factors. Thus, clearance of injured pancreatic acini by macrophages is associated with a unique cytokine reaction which may constitute a basis for progression of SAPE (sentinel acute pancreatitis event) to the irreversible fibro-inflammation in CP.

Duodenum-preserving head resection in chronic pancreatitis changes the natural course of the disease: a single-center 26-year experience.

OBJECTIVE: To present preoperative and early postoperative data for 504 patients who underwent duodenum-preserving pancreatic head resection (DPPHR) for severe chronic pancreatitis (CP). BACKGROUND: The pancreatic head is considered to be the pacemaker of the disease in alcohol-induced CP. Indications for surgery in CP are intractable pain and local complications. DPPHR offers the advantage of treating the complications related to the inflammatory process in the head, relieving the pain syndrome, and preserving the bilioduodenal anatomy, and it may have the potential to change the natural course of chronic pancreatitis. METHODS: Between November 1972 and December 1998, 504 patients with chronic pancreatitis and an inflammatory mass in the pancreatic head were treated surgically after medical pain treatment for a median of 3.6 years. The procedure resulted in a hospital mortality rate of 0.8%. A continuous follow-up investigation lasting up to 26 years was conducted, during which the patients were reevaluated four times (1983, 1987, 1994, 1996). Between November 1982 and October 1996, 388 patients treated surgically were reinvestigated to evaluate the late outcome; the follow-up rate was 94% (25 patients were lost to follow-up). The reinvestigation evaluation included glucose tolerance test, exocrine pancreatic function test, pain status, physical status, professional and social rehabilitation, and quality of life. RESULTS: After an observation period of up to 14 years, 78.8% of the patients were completely pain-free and 12.5% had (yearly) pain. 91.3% were considered as pain-free; 8.7% had continuing abdominal pain; 12% had abdominal complaints. During the 14 years of follow-up, only 9% were admitted to the hospital for acute episodes of chronic pancreatitis. Endocrine function was improved in 11%; in 21%, diabetes developed de novo. The rate of hospital admission for acute episodes decreased from 69% before surgery to 9% after surgery. In the clinical management period of 9 years (median), the frequency of hospital admission dropped from 5.4 per patient before surgery to 2.7 after surgery. Fourteen years after surgery, 69% of the patients were professionally rehabilitated; in 72%, the quality of life index (Karnofsky criteria) was 90 to 100 and in 18%, it was <80. CONCLUSION: In patients with alcoholic chronic pancreatitis in whom an inflammatory mass has developed in the pancreatic head, DPPHR results in a change in the natural course of the disease in terms of pain status, frequency of acute episodes, need for further hospital admission, late death, and quality of life.