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Biomedical subjects

G B Appel

Publications and source records attributed to G B Appel.

88 records · Page 5Linked to original sources
PubMed1977

The anion gap in asymptomatic plasma cell dyscrasias.

The presence of a low anion gap in patients with multiple myeloma has recently been emphasized. This has been related to the retention of chloride and bicarbonate anions to offset the cationic charge of the monoclonal immunoglobulins. We now report the presence of a low anion gap in 50 patients with asymptomatic plasma cell dyscrasias. No correlation was found between the size of the anion gap and the height of the paraprotein "spike" or the size of the anion gap and an index of the net cationic charge of the monoclonal immunoglobulins.

Anions↗
PubMed1977

Primary hyperparathyroidism and benign monoclonal gammopathy.

Three patients had primary hyperparathyroidism and monoclonal serum immunoglobulins. Although multiple myeloma was suspected in each case, subsequent evaluation was consistent with a "benign monoclonal gammopathy". Parathyroid adenomas were removed from two patients. The three patients are presented and compared to the four other cases that have been reported previously. The association between primary hyperparathyroidism and benign monoclonal gammopathy is discussed in terms of possible pathogenetic mechanisms. Primary hyperparathyroidism should be suspected in patients with hypercalcemia and benigh monoclonal gammopathy, as well as in other conditions, like multiple myeloma, that are known to be associated with hypercalcemia.

Adenoma↗
PubMed1976

The syndrome of multiple endocrine gland insufficiency.

Addison's disease, when caused by idiopathic atrophy of the adrenal cortex, is frequently associated with other endocrine abnormalities. Primary hypothyroidism and hypogonadism have been reported in association with adrenal insufficiency; understandably, such cases may lead to diagnostic confusion with respect to possible pituitary disease. This case study concerns a woman who exhibited, in sequence and over a period of 17 years, hypogonadism, hypoadrenalism, diabetes mellitus and, finally, hypothyroidism. Originally misdiagnosed as having Sheehan's syndrome, she eventually became hyperpigmented. The true nature of her illness was then revealed to be primary insufficiency of multiple endocrine glands, with the demonstration of elevated levels of several pituitary hormones. Because multiple endocrine insufficiencies may coexist or develop with time, we suggest that a patient with a single documented endocrine deficiency be investigated initially and serially for additional glandular deficiencies.

Addison Disease↗
PubMed1976

Pharmacokinetics of cefamandole in the presence of renal failure in patients undergoing hemodialysis.

The pharmacology of cefamandole in seven patients with stable renal insufficiency and in eight patients undergoing hemodialysis was determined. All patients had creatinine clearances less than 5 ml/min. The half-life of cefamandole in those patients with stable chronic renal failure was 7.7 +/- 2.2 h. The mean venous level 1 h after intravenous injection of a 1-g dose was 85.3 +/- 32.0 mug/ml. The mean venous half-life of cefamandole during hemodialysis was 6.1 h. The venous serum level after 5.5 of hemodialysis was 50.4 +/- 20.8 mug/ml. The mean coefficient of extraction was 0.155, and the mean clearance was 34.7 ml/min. The time interval between doses of cefamandole administered intravenously should be lengthened to 24 h in the presence of stable renal failure. No major change in dosage schedule is necessary for patients undergoing dialysis.

Adult↗
PubMed1976

Renal vein thrombosis, nephrotic syndrome, and systemic lupus erythematosus: an association in four cases.

We report here four cases of systemic lupus erythematosus associated with the nephrotic syndrome and renal vein thrombosis and review six familiar cases previously noted in the literature. Renal biopsy in each of our cases showed changes consistent with the membranous type of lupus nephropathy. We discuss the exclusive appearance of this pattern in relation to renal vein thrombosis in other forms of renal disease. The occurance of renal vein thrombosis in patients with systemic lupus erythematosus and the nephrotic syndrome supports the evidence that the thrombosis is a complication rather than a cause of the nephrotic syndrome. The presence of pleuritic pain in a patient with systemic lupus erythematosus and the nephrotic syndrome should alert the clinician to the possibility of renal vein thrombosis and pulmonary emboli. With appropriate diagnosis and anticoagulation therapy, our patients had a benign course during 7 to 48 months of follow-up.

Adult↗
PubMed1975

Methyl iodide intoxication. A case report.

A 41-year-old chemist developed methyl iodide intoxication. His case is presented with a review of pertinent literature. Characteristics of the poisoning include a delay between exposure and onset of symptoms; early systemic toxicity with congestive changes in the lungs and oliguric renal failure; prominent cerebellar and Parkinsonian neurologic symptoms as well as seizures and coma in severe cases; and psychiatric disturbances that can last from months to years. Although methyl iodide is a rare form of intoxicant, its manifestations are similar to that of poisoning with the other monohalomethanes that are not uncommon.

Adult↗
PubMedDate not supplied

Membranous glomerulopathy associated with graft-versus-host disease following allogeneic stem cell transplantation. Report of 2 cases and review of the literature.

We report two cases of nephrotic syndrome presenting 18 and 20 months after allogeneic stem cell transplantation (alloSCT) with chronic myelogenous leukemia. Both patients had acute and chronic graft-versus-host disease (GVHD) and renal biopsy findings of membranous glomerulopathy (MG). A review of the literature revealed 10 additional cases of immune-complex-mediated glomerular disease following alloSCT, 8 of which were diagnostic of MG. All patients showed evidence of acute or chronic GVHD. Patients typically presented with preserved renal function (mean creatinine 1.2 mg/dl) and full nephrotic syndrome including heavy proteinuria (mean 9.2 g/24 h), edema, hypoalbuminemia (mean 2.1 g/dl) and hypercholesterolemia (mean 472 mg/dl). Most patients showed stabilization of renal function and significant decreases in proteinuria when treated with steroids and/or cyclosporine. The close temporal association as well as evidence from murine models of GVHD support a pathogenetic association between GVHD and the development of MG.

Acute Disease↗
PubMedDate not supplied

COX-2 inhibitors and the kidney.

Cyclooxygenase-2 (COX-2) selective inhibitors are now extensively used for their anti-inflammatory and analgesic efficacy. Several large controlled trials provide evidence to support the proposition that they cause fewer major gastro-intestinal side effects and less toxicity than routine nonsteroidal anti-inflammatory drugs (NSAIDs). In view of the documented different localizations of the cyclooxygenase-1 and COX-2 enzymes in the kidney, it was initially hoped that COX-2 inhibitors would be associated with fewer renal side effects than other NSAIDs. This has not been borne out by subsequent studies. Like other NSAIDs, COX-2 inhibitors can cause salt and water retention, leading to edema and worsening hypertension. They can also cause acute declines in renal function and glomerular filtration rate. These events are, however, uncommon in large rheumatology populations and infrequently lead to discontinuation of the medications. Judicious use of COX-2 inhibitors in high-risk patients (such as those with chronic renal insufficiency, diabetes or congestive heart failure) will lead to a decreased incidence of adverse renal events.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Studies on the mechanism of non-oliguric experimental acute renal failure.

Although acute renal failure, caused either by renal ischemia or nephrotoxic agents, is usually characterized by oliguria, a severe fall in glomerular filtration rate, and a fall in renal blood flow, some patients and experimental models display a non-oliguric pattern of renal injury. The present study was designed to evaluate the mechanism of preservation of high urinary flow rate under this condition. Following the administration of the aminoglycoside gentamicin to rats for five days, a decrease in concentrating ability was demonstrated, caused by impaired vasopressin-mediated water transport. Further treatment resulted in a fall in Cin to 15 percent of control, although RBF was reduced to only 67 percent of control, and urine flow rate rose above control levels. Induction of acute and renal failure with dichromate was associated with variable high or low urinary flow rates according to pre-injury intake of sodium. Urine volume correlated directly with cortical blood flow. These data suggest that the non-oliguric pattern of acute renal injury is caused by preservation of cortical perfusion in the setting of severe tubular injury.

Acute Kidney Injury↗