Growth hormone resistance in uremia

Growth retardation is a major complication in children with uremia. Protein restriction, calorie deficit, metabolic acidosis, renal osteodystrophy, and endocrinologic disturbances contribute to the growth failure. The effect of these factors on growth retardation can be attenuated in part by therapy with vitamin D metabolites, adequate nutrition, alkalization, and dialysis. Linear growth in children with uremia is markedly retarded despite normal or increased levels of circulating serum growth hormone. An increased growth hormone level in children with uremia is due to normal growth hormone secretion from the pituitary gland and impaired growth hormone clearance in the kidney. However, the elevated growth hormone level does not lead to a commensurate rise in serum insulin-like growth factor I (IGF-I); the serum IGF-I level is decreased or normal in relation to the degree of renal failure. This discrepancy suggests growth hormone resistance in the liver in uremia. Recent molecular techniques open a new era in studying the gene expression for growth hormone or IGF-I. There is no doubt today that growth hormone treatment has the beneficial effect of growth promotion in children with uremia, which also suggests endogenous growth hormone resistance in target organs or target cells in uremia.     

Venous clots: evaluation with MR imaging

In vitro and in vivo studies were performed to determine the proton relaxation and imaging characteristics of static blood and acute and organized clot in canine jugular veins. In vivo, it was found that two inversion recovery sequences using a short inversion time (100 msec) demonstrated better differentiation of signal intensity of intravascular clot from surrounding soft tissues than did standard T1- and T2-weighted sequences. In vitro, quantitative measurements showed marked reduction of both T1 and T2 relaxation time of acute clot compared with stagnant blood. In addition, the T1 relaxation time, and to a lesser extent the T2 relaxation time, shortened as the clot aged, indicating a potential role for magnetic resonance imaging in determining the age of venous thrombi.     

Wallerian degeneration in a patient with Schilder disease: MR imaging demonstration

Wallerian degeneration in the corticospinal tract was demonstrated by magnetic resonance (MR) imaging in a patient with Schilder disease. The histochemical stages of myelin breakdown that allow its demonstration by MR imaging are reviewed.     

Significance of diastolic pulmonary artery pressure peaks

We describe a patient undergoing elective surgery for treatment of an abdominal aortic aneurysm in whom an abrupt change in the contour of the pulmonary artery pressure (PAP) trace indicated the development of an intermediate (20 mm Hg) V wave in the pulmonary artery wedge pressure (PAWP) trace. As the PAP trace is displayed continuously, attention to its contour may allow for early detection of changes to the underlying PAWP trace.FC Anaesth     

In vivo and in vitro binding of C4 molecules on red cells: a correlation of numbers of molecules and agglutination

The fourth component of human complement (C4) is one that is essential to the antibody-mediated classical activation pathway. C4d, present on all normal and most patient red cells (RBCs), may be detected by the human antisera anti-Rodgers (Rg) and -Chido (Ch). A study has been made of the Rg/Ch antigens on normal and patient RBCs in an attempt to understand the mechanism by which C4 is bound to normal RBCs in the absence of RBC antibodies (Abs). Because RBCs from C1q-deficient patients express Rg/Ch, it seems that C1q is not essential for C4 binding. Treatment of normal RBCs with proteolytic enzymes, including trypsin, eliminated positive reactions with anti-Rg/Ch even though the C4d fragment is considered to be resistant to cleavage by trypsin. By correlating agglutination reactions with numbers of bound C4d and C3d molecules, it is evident that both C4d and C3d were affected by trypsin treatment and that anti-Rg/Ch were not capable of agglutinating RBCs with less than 50 molecules of bound C4d. It is concluded that trypsin-sensitive and -insensitive RBC membrane structures may both act as acceptors for C4. RBCs with null phenotypes of the major blood group systems all expressed Rg/Ch antigens, so none of the structures that carry these antigens act preferentially as acceptors for C4.     

Trichinella infection and clinical disease

Trichinellosis is caused by ingestion of insufficiently cooked meat contaminated with infective larvae of <it>Trichinella</it> species. The clinical course is highly variable, ranging from no apparent infection to severe and even fatal disease. We report two illustrative cases of trichinellosis. Returning to Denmark a few days after having eaten roasted pork in the Republic of Serbia, a female patient suffered from severe vomiting, epigastric pain, diarrhoea, and later myalgia, generalized oedema, and prostration. A biopsy showed heavy infestation with <it>Trichinella spiralis</it>, 2000 larvae/g of muscle. Life-threatening cardiopulmonary, renal and central nervous system complications developed. The patient recovered after several months. Her husband, who also ate the pork, did not have clinical symptoms, but an increased eosinophil count and a single larva in a muscle biopsy confirmed infection. The epidemiology, clinical manifestations, diagnosis, treatment and prevention of trichinellosis are reviewed.