Syetollc time intervals L-thyroxine Respiration Water-electrotyte balance
lmmunoregulatlon
lmmunoregulation was studied in 11 patients who developed autoantibodies while taking procainamide. Patients taking procainamide had normal suppressor cell function. However, lymphocytes from the prccainarnide group secreted significantly more immunoglobulinG (IgG) than did either normal subjects or patients with spontaneous systemic lupus erythematosus. There was a positive correlation between the circulating anti-SS DNA antibody tfer and the synthesis of IgG. In mixing studies, the T cell fraction obtained from these patients enhanced PWM-stimulated IgG synthesis by normal lymphocytes but did not effect unstimulated B cells or Con A activated suppressor cells. Procainamide may act by directly stimulating helper T cells. This defect is fundamentally different from the suppressor cell dysfunction demonstrated in spontaneous systemic lupus erythematosus. However, as in systemic lupus erythematosus, the development of clinical disease requires the participation of additional genetic or immunologic factors.
Miller KB, Salem D: Immune regulatory abnormalities produced by procainamide. Am J Med 1982; 73: 487-492.
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Gonadal function was examined in 19 young men with Hodgkin’s disease before therapy and compared with that of 11 men with other malignancies, 13 men with primary testicular failure, and 19 normal men of similar age. Total (p
Vigersky RA, Chapman RM, Berenberg J. Glass AR: Testicular dysfunction in untreated Hodgkin’s disease. Am J Med 1982; 73: 482-486.
Suppressor cells Au&antibodies
Procalnamide Helper ceils
TestiS
Hodgkin’s disease
The role of the renal kallikrein-kinin system in the pathogenesis of hypertension and various forms of renal dysfunction after human renal transplantation was assessed by measurement of urinary kallikrein activftyin 41 renal transplantrecipients. The urinarykallikrein in these patiits appeared to originate from the transplanted kidney and not their own diseased kidneys. Twenty-three recipients had hypertensionand excreted less kallikrein than their 18 nonnOtenSive counterparts. Subjects with renal complications of transplantation (acute tubular necrosis, nine patients, or acute rejection, eight patients) also excreted less kallikrein than the 28 subjects without such complications. Among those with acute renal complications, subjects with acute tubular necrosis excreted less kallikrein than those wlth acute rejection. The kallikrein-kinin system may be involvedin the pathogenesisof hypertensionand some forms of renal dysfunction after renal transplantation.
The metabolic, cardiovascular, renal, and pulmonary responses of IO hypothyroid patients were studiedduring the first week of therapy with intravenous levothyroxine (L-thyroxine), 100 pg per day. f&an serum thyroxine, trikxfothyronine,and reverse trifcdothwonine coilcenbatiorls were normalized within four days. Significant decreases in serum tftyrotropin, creatine phosphokinase, and cholesterol levels, and an increasa in the basal metabolic rate, were observed. An early cardiovascular response was demonstrated by serial measurement of the mean preejection period (138 to 134 msec. p (0.05). its ratio to left ventricular ejection time (0.49 to 0.46, p (0.02). and pulse-wave arrival time (236 to 224 msec. p <0.05). The mean renal excretion of a water load (four hours) increased (54 to 77 percent, p X0.02) by the fourth day. The bluntedventilatuy responses to hype&apnea seen in two patii were improved. We conclude that a physiologicreplacement dose of fntravenousL-thyroxinefor one week produces significant responses in organ systems responsible for the common clinical complications of myxedema.
Hypertension Dlabetes mellltus
O’Connor DT, Barg AP, Amend W, Vincenti F: Urinary kallikrein excretion after renal transplantation. Relationship to hypertension, graft source, and renal function. Am J Med 1982; 73: 475-481.
Kalllkrein Renal traneplantation Acute tubular necrosis Acute rejection
Ladenson PW, Goldenheim PD. Cooper DS, Miller MA, Riway EC: Early peripheral responses to intravenous L-thyroxine in primary hypothyroidism. Am J Med 1982: 73: 467-474.
Hypothyroidism