A Qlomerular lesion identical to that of IQA nephropathy was demonstrated unexpectedly in a 17 year old boy who presented with clinical manifestations of pulmonary hemosiderosis and no evidence of renal disease. This subclinical glomerular lesion would have remained undetected in this patient unless kidney tissue was obtained and examined by immunofluorescence or electron microscopy. It is unknown if the glomerular lesion in this case is causally related to pulmonary hemosiderosis.
Yum MN, Lampton LM. Bloom PM, Edwards JL: Asymptomatic IQA nephropathy associated with pulmonary hemosiderosis. Am J Med 64: 1056-1060, 1978.
IgA nephropathy Idiopathic pulmonary hemosiderosis pulmonary-renal syndrome
Eight hypertensive patients treated with the usual doses of various antihypertensive agents were admitted with severe symptomatic sinus bradycardia. The mean beat-t rate on admission (38 f 5 beatsjmin, mean f standard deviation) increased to a mean of 60 f 7 beats/min, and symptoms disappeared after cessation of the antihypertensive agent. Results of electrophysiologic studies were abnormal in four patients tested. Three patients were challenged with propranolol(o.l mg/kQ body weight) and mean spontaneous cycle length (28.33 and 2.5 per cent) and maximal sinus node recovery time (412,48 and 44 per cent) increased after challenge. After a mean follow-up time of 15 f 3 months, six were managed successfully by manipulation of their medical regimen, whereas two required permanent ventricular pacing. It is concluded that symptomatic severe bradyarrhythmias may be precipitated by sympatholytic agents in patients with suspected sinus node disease, and that electrophysiologic testing may be of value in predicting adverse responses to these drugs.
Scheinman MM. Strauss HC, Evans GT. Ryan C. Massie B. Wallace A: Adverse effects of sympatholytic agents in patients with hypertension and sinus node dysfunction. Am J Med 64: 1013-1020, 1978.
Sick slnus syndrome Hypertension Methyldopa Propranolol Clonidine Guanethidine
Sickle cell anemla AS hemoglobinopathy Hematuria High altitude hypoxia
Cellular immunologic studies were performed on leukemic cells of a 59 year old patient with monocytic leukemia. Morphologically, most circulating leukocytes were monocytes. They demonstrated Fc and C3 (third component of complement) receptors, phagocytized latex particles, showed in vitro cytoplasmic spreading and lysed antibody-coated chicken erythrocytes. Phagocytosis of, as well as resetting with, C3-coated erthrocytes and very rapid cytoplasmic spreading suggested in vivo monocyte “activation.” The cells were easily maintained in primary culture for up to 13 weeks, with acquisition of typical macrophage morphology. In add&km, nearly all cells demonstrated surface immunogtobulin (Slg) which upon further study was shown to probably be Fc-receptor bound with unusually high affinity and with greater representation of IgG (kappa) than IgG (lambda). These studies suggest that apparent “monoclonal” Slg does not necessarily indicate a truly clonal proliferation of B cell origin.
Ackerman SK, Bumol TF, Kay NE, Douglas SD: Celluar immunologic studies of a patient with monocytic leukemia. Am J Med 64: 1061-1068, 1978.
The extensive literature describing abnormalities associated with sickle cell trait is reviewed. It is weighted with uncontrolled series and anecdotal reports, and the frequency of complications of sickle trait is, with few exceptions, undefined. Many early reports suffered from imprecise identification of the sickle hemoglobinopathies and probable inclusion of patients with doubly heterozygous disorders or even homozygous sickle cell anemia. There is evidence that sickle cell trait does not impair survival, and controversy exists as to whether certain occupations. such as those involving flying, diving or extreme exertion, are unduly hazardous for people with AS hemoglobinopathy. There is convincing evidence that certain abnormalities, such as hyposthenuria, renal hematuria, bacteriuria and pyelonephritis in pregnancy, and splenic infarction with high altitude hypoxia, do occur with increased frequency in sickle cell trait. Other real hazards may exist, but these await convincing demonstration by properly controlled studies.
Sears DA: The morbidity of sickle cell trait. A review of the literature. Am J Med 64: 1021-1036, 1978.
Sickle cell trait Hyposthenuria