Chronic low back pain: new perspectives and treatment guidelines for primary care: Part II.

Low back pain is a leading cause of work-related disability and has important socioeconomic consequences. Although there is little evidence to determine the optimal treatment of chronic low back pain, treatment goals can be established. Primary care providers should focus simultaneously on pain management, improvement of activity and functional level, and fostering a greater understanding of chronic low back pain. This two-part article summarizes consensus guidelines developed by practitioners with expertise in pain management, family medicine, internal medicine, physical therapy, rheumatology, and managed care and provides direction for primary care providers on a multidisciplinary approach to the patient with chronic low back pain. This part examines pharmacologic methods.

Chronic low back pain: new perspectives and treatment guidelines for primary care: Part I.

Low back pain is a leading cause of work-related disability and has important socioeconomic consequences. Although there is little evidence to determine the optimal treatment of chronic low back pain, treatment goals can be established. Primary care providers should focus on pain management, improvement of activity and functional level, and fostering a greater understanding of chronic low back pain. This two-part article summarizes consensus guidelines developed by practitioners with expertise in pain management, family medicine, internal medicine, physical therapy, rheumatology, and managed care, and provides direction for primary care providers on a multidisciplinary approach to the patient with chronic low back pain.

Free protein S levels are elevated in familial C4b-binding protein deficiency.

In plasma, 40% of the protein S is free and functions as a cofactor for the anticoagulant effects of activated protein C. The remaining 60% of protein S is complexed to C4b-binding protein and is functionally inactive. A family with hereditary C4b binding protein deficiency has been identified with C4b-binding protein levels in an affected father and daughter of 37 micrograms/mL and 23 micrograms/mL, respectively; these values are significantly below the normal range for this protein of 180 micrograms/mL +/- 44 micrograms/mL (mean +/- 2 SD). The total protein S (free + bound) is normal in these individuals (23.2 micrograms/mL and 17.8 micrograms/mL, respectively; normal 19.1 micrograms/mL +/- 6.0 micrograms/mL). The free protein S levels are markedly increased at 22.5 micrograms/mL and 17.4 micrograms/mL, respectively (normal 5.9 micrograms/mL +/- 2.4 micrograms/mL). This experiment of nature shows that total protein S levels in plasma are not affected by the absence of C4b-binding protein and that chronic elevation of free protein S is not associated with increased hemorrhagic tendencies.

Hereditary complement (C6) deficiency associated with systemic lupus erythematosus, Sjögren's syndrome and hyperthyroidism.

Results of clinical, serologic and histologic studies documenting an association between hereditary C6 deficiency and a connective tissue disease are provided. The propositus had systemic lupus erythematosus with prominent discoid features, Sjögren's syndrome and hyperthyroidism. Serum C6 was undetectable by radial immunodiffusion and hemolytic assays. Serologic and typing studies performed on 9 family members suggested an autosomal codominant transmission. No correlation with a specific HLA phenotype was established.

C4 binding protein deficiency in a patient with atypical Behçet's disease.

Primary deficiency of the C4 binding protein (C4bp) was present in a patient with disease clinically resembling Behçet's disease. Her father and her sister were also deficient. This protein, as a cofactor for factor I, interferes with the assembly of, and accelerates the decay of, the classical C3 convertase. Thus, the deficiency favours C3 conversion by classical pathway activation. In addition to genital and oral ulceration, cutaneous vasculitis and synovitis, our patient had relapses complicated by angioedema, atypical for Behçet's disease. It is not clear whether her total disease, or only the complicating angioedema, was a consequence of the C4bp deficiency.

Nailfold capillaroscopy in type I diabetics with vasculopathy and limited joint mobility.

The nailfold capillary pattern of 48 Type I diabetic patients with longstanding disease and of 15 normal controls was studied using the technique of widefield nailfold capillaroscopy. Twenty-six diabetic patients had documented vascular disease (retinopathy) and 27 had flexion contractures of the hand. No distinctive morphologic capillary lesions were observed in any diabetic patient, nor were any differences in capillary loop number or density found between the diabetic and control groups. While vascular disease is a prominent feature of diabetes, it is not reflected in the appearance of the nailfold capillary pattern.

Pancreatic duct arteriovenous fistula and the metastatic fat necrosis syndrome.

This report summarizes the course of a patient with asymptomatic chronic pancreatitis associated with hemorrhage into the pancreatic duct and metastatic fat necrosis. Retrograde cannulation of the pancreatic duct and superior mesenteric arteriography established the presence of a pseudocyst with a pancreatic duct-arteriovenous (DAV) fistula as the cause of the syndrome. Ligation of feeder vessels with external drainage of the cyst as the initial surgical procedure stopped the bleeding but failed to prevent recurrence of the pancreatic duct-venous fistula. A pancreaticoduodenectomy with resection of the cyst and fistula was required to arrest destruction of distant tissues. Although serum and urine amylase concentrations were markedly elevated, serum lipase levels were normal throughout the patient's course. Elevation of serum lipase does not seem to be a necessary condition for the development of the metastatic fat necrosis syndrome.