Acquired C1-esterase inhibitor deficiency: Three case reports and commentary on the syndrome

Acquired C1-esterase inhibitor deficiency is a rare syndrome which usually presents with episodes of angioedema. Most patients have an underlying lymphoproliferative disorder. It is important to gastroenterologists, haematologists, immunologists and dermatologists, as these are the more likely specialties to which the patient will present. Recognition of the syndrome is important not only for diagnostic purposes but for investigating and treating any associated underlying lymphoproliferative disorders. In some instances the angioedema may precede the lymphoma by many years. Optimal patient management requires that both angioedema and the underlying lymphoma be recognized and treated.     

The effect of different calcium antagonists and a calcium agonist on the metabolism of propranolol by isolated rat hepatocytes

Summary— The influence of the dihydropyridine calcium entry blockers nicardipine, amlodipine, nifedipine, isradipine and of the dihydropyridine calcium entry promotor BAY K 8644 on the disappearance rate of propranolol by isolated rat hepatocytes was compared to the effect of diltiazem and verapamil, two non-dihydropyridine calcium channel blockers and known inhibitors of hepatic cytochrome P450 mixed function oxidases. All compounds dose-dependently inhibited the disappearance rate of propranolol. Nicardipine and isradipine were more potent in inhibiting the disappearance rate of propranolol than the other dihydropyridines and than diltiazem and verapamil. The inhibitory effect of nicardipine on the disappearance rate of propranolol was not stereoselective and was not influenced by age.     

Patterns of femoral head migration in osteoarthritis of the hip: a reappraisal with CT and pathologic correlation

Although medial, superior, and axial patterns of migration of the femoral head in osteoarthritis of the hip have been well described, it is not clear what anatomic and biomechanical factors determine the direction of migration. The authors studied 22 patients with bilateral (11 patients) or unilateral (11 patients) osteoarthritis by means of conventional radiography and computed tomography (CT) to define any relationships between migration in the coronal plane and that in the transverse plane and to determine whether femoral anteversion, acetabular anteversion, femoral neck-shaft angle, or acetabular inclination were related to particular migration patterns. Anterior migration was evident in 14 of the 19 hips with a superior migration pattern, whereas posterior migration was present in five of the seven hips with a medial migration pattern. In the remainder of cases, no migration in the transverse plane was present. Femoral anteversion as determined with CT, femoral neck-shaft angle, angle of acetabular inclination, and acetabular anteversion angle in this relatively small sample were all found to be within normal limits and appeared to have no influence on the occurrence of a specific pattern of femoral head migration.     

Low back pain: conservative treatment with artificial shock absorbers

A new method of conservative treatment for low back pain (LBP) was studied by follow-up investigation of 382 patients during the last five years. The attempt to reduce repetitive impulsive intervertebral impact in the troublesome S1-L5-4 area by significant improvement of the foot's attenuational capacity through artificial viscoelastic shock absorbing was prompted by the authors' work on decreased capability of LBP spines to attenuate axially propagated walking stresses. Viscoelastic shoe inserts were used in addition to light flexible shoes as artificial shock absorbing devices. Maximal amplitudes of bone oscillation during walking were reduced by about 40% by the viscoelastic inserts. Rapid and surprisingly significant improvement of pain syndrome and patient mobility occurred in about 80% of the patients. The accelerographic patterns recorded on a sacrum of patient with LBP were unusual for a healthy subject; they usually disappeared after treatment in LBP cases. Results suggested that poor walking impact attenuation was a true cause for prolonging intervertebral structures overstrain and consequent degeneration. It seemed logical that as spine damage could be explained primarily by prolonged impulsive overstrain, treatment must include viscoelastic inserts which increase foot shock absorbing capacity and help cushion the spine.     

Intrinsic factor-mediated absorption of cobalamin by guinea pig ileal cells

To investigate the fate of intrinsic factor and cobalamin during cobalamin absorption, we incubated enterocytes isolated from guinea pig ileum for periods of up to 30 min with ⁵⁷Co-labeled cyano-cobalamin bound either to human intrinsic factor or to rabbit intrinsic factor biosynthetically labeled with [³⁵S]methionine. When the labeled complex was incubated for 30 min with isolated ileal cells under conditions that block cellular metabolism, virtually all cellular radioactivity could be removed by washing the cell surface with EDTA or acid. In contrast, washing removed only half the radioactivity from cells incubated at 37°C in O₂. When residual cellular radioactivity was extracted and analyzed by gel filtration, 80-94% of both the ³⁵S and ⁵⁷Co radioactivity eluted in the same fractions as the original complex. The remaining 6-20% eluted as free [⁵⁷Co]cobalamin or [³⁵S]methionine. To examine events occurring after 30 min, we instilled into tied-off ileal loops of intact guinea pigs radiolabeled intrinsic factor-cobalamin complex and extracted nondissociable radioactivity 2-4.5 h later. The proportion of extracted ⁵⁷Co eluting as free cobalamin increased to 39-46%, that eluting as intrinsic factor-cobalamin complex declined to 22-45%, and 9-34% now eluted as a macromolecule that reacted with antitranscobalamin II antibody but not antiintrinsic factor antibody. Extracted ³⁵S radioactivity eluted in several peaks in addition to the intrinsic factor peak. These findings suggest that (a) after reversible attachment of intrinsic factor-cobalamin complex to its ileal surface receptor, an energy-dependent process prevents removal of the complex from the cell surface by EDTA or acid; (b) cobalamin dissociates from intrinsic factor and, as suggested by previous workers, binds to a molecule antigenically similar to transcobalamin II; and (c) intrinsic factor is slowly degraded and forms breakdown products that are detectable in ileal extracts.