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Biomedical subjects

M A Perazella

Publications and source records attributed to M A Perazella.

At least 55 records · Page 3Linked to original sources
PubMed1997

Hypertension and hypokalemia: unusual syndromes.

Secondary hypertension accounts for a minority of all cases of hypertension. Certain clues in the patient's medical history and laboratory parameters may help identify the rare patient with secondary hypertension. The association of hypertension with hypokalemia and renal potassium wasting should raise one's suspicion for a state of mineralocorticoid excess. The clinical syndrome of hypertension and hypokalemia may be related either to a high renin state, such as renovascular disease, or to a low renin state, such as primary hyperaldosteronism, adrenal enzyme defects, certain familial syndromes, and licorice ingestion. Over the past decade, a genetic basis has been identified for apparent mineralocorticoid excess (AME) syndrome, Liddle's syndrome, and glucocorticoid remediable aldosteronism (GRA). This brief review focuses on a few of the unusual conditions which cause a true or apparent mineralocorticoid excess state, and summarizes the clinical presentation, pathogenetic mechanism, and treatment of these diseases.

Animals↗
PubMed1997

Hyperkalemia and trimethoprim-sulfamethoxazole: a new problem emerges 25 years later.

Trimethoprim-sulfamethoxazole is a frequently prescribed antibiotic with a wide spectrum of antimicrobial activity. A previously unreported and potentially lethal adverse reaction associated with "high dose" trimethoprim-sulfamethoxazole therapy, hyperkalemia, was described. Subsequent to the descriptions of hyperkalemia with "high dose" trimethoprim-sulfamethoxazole, a handful of cases noted the development of hyperkalemia with "standard dose" trimethoprim-sulfamethoxazole in elderly patients without evidence of an obvious defect in potassium homeostasis. A surveillance study of patients treated with "standard dose" trimethoprim-sulfamethoxazole as compared to similar controls treated with other antibiotics confirmed the rise in potassium associated with trimethoprim-sulfamethoxazole therapy. Recognition of this potassium disorder led to investigation and description of the mechanism by which trimethoprim-sulfamethoxazole-induced hyperkalemia. Trimethoprim was found to act like the potassium-sparing diuretic amiloride and reduce renal potassium excretion. Hence, trimethoprim-sulfamethoxazole therapy was found to be associated with a new adverse reaction, hyperkalemia, nearly 25 years after its introduction into clinical practice as an antimicrobial agent.

Animals↗
PubMed1996

A middle-aged woman with back and flank pain.

Xanthogranulomatous pyelonephritis is an uncommon variant of chronic pyelonephritis that predominantly affects middle-aged women. Patients usually present with fever, back or flank pain, flank mass, and the constitutional symptoms of fatigue, malaise, weight loss, and anorexia. Rarely, they may present with a draining sinus. There is usually a history of urinary tract infection, obstruction, or instrumentation. Other abnormalities include anemia, leukocytosis, abnormal liver enzymes, pyuria, and hematuria. Mild azotemia may be present, but frank renal failure is rare. Urine and renal tissue cultures are frequently positive. The most commonly isolated bacterial pathogens are P. mirabilis and E. coli, but other organisms have also been implicated. A CT scan is the best radiologic imaging technique to discover the extent of inflammation as well as any involvement of adjacent structures. Lipid-laden macrophages called xanthoma cells characterize the disease at the microscopic level. Nephrectomy is curative. Careful preoperative evaluation will guide surgical planning in choosing an approach that provides adequate exposure of the affected tissue and facilitates subsequent care of the patient.

Back Pain↗
PubMed1996

Hyperkalemia in hospitalized patients treated with trimethoprim-sulfamethoxazole.

OBJECTIVE: To determine the effect of standard-dose trimethoprim-sulfamethoxazole on serum potassium concentration in hospitalized patients. DESIGN: Prospective chart review. SETTING: Community-based teaching hospital. PATIENTS: 105 patients with various infections were hospitalized and treated. Eighty patients treated with standard-dose trimethoprim-sulfamethoxazole (trimethoprim, < or = 320 mg/d; sulfamethoxazole, < or = 1600 mg/d) composed the treatment group; 25 patients treated with other antibiotic agents served as the control group. MEASUREMENTS: Serum sodium, potassium, and chloride concentrations; serum carbon dioxide content; anion gap; blood urea nitrogen level; and serum creatinine level. RESULTS: The serum potassium concentration in the treatment group (mean +/- SD) was 3.89 +/- 0.46 mmol/L (95% CI, 3.79 to 3.99 mmol/L), and it increased by 1.21 mmol/L (CI, 1.09 to 1.32 mmol/L) 4.6 +/- 2.2 days after trimethoprim-sulfamethoxazole therapy was initiated. Blood urea nitrogen levels increased from 7.92 +/- 5.7 mmol/L (CI, 6.67 to 9.16 mmol/L) to 9.2 +/- 5.8 mmol/L (CI, 7.9 to 10.5 mmol/L), and serum creatinine levels increased from 102.5 +/- 49.5 mumol/L (CI, 91.4 to 113.6 mumol/L) to 126.1 +/- 70.7 mumol/L (CI, 110.3 to 141.9 mumol/L). Patients with a serum creatinine level of 106 mumol/L (1.2 mg/dL) or more developed a higher peak potassium concentration (5.37 +/- 0.59 mmol/L [CI, 5.15 to 5.59 mmol/L]) than patients with a serum creatinine level of less than 106 mumol/L (4.95 +/- 0.48 mmol/L [CI, 4.80 to 5.08 mmol/L]). Patients with diabetes had a slightly higher peak potassium concentration (5.14 +/- 0.45 mmol/L [CI, 4.93 to 5.39 mmol/L]) than did patients without diabetes (5.08 +/- 0.59 mmol/L [CI, 4.93 to 5.23 mmol/L]), but the difference was not statistically significant. The serum potassium concentration in the control group was 4.33 +/- 0.45 mmol/L (CI, 4.15 to 4.51 mmol/L), and it decreased nonsignificantly over 5 days of therapy. CONCLUSIONS: Standard-dose trimethoprim-sulfamethoxazole therapy used to treat various infections leads to an increase in serum potassium concentration. A peak serum potassium concentration greater than 5.0 mmol/L developed in 62.5% of patients; severe hyperkalemia (peak serum potassium concentration > or = 5.5 mmol/L) occurred in 21.2% of patients. Patients treated with standard-dose trimethoprim-sulfamethoxazole should be monitored closely for the development of hyperkalemia, especially if they have concurrent renal insufficiency (serum creatinine level > or = 106 mumol/L).

Adult↗
PubMed1996

Angiotensin-converting enzyme inhibitor therapy in chronic hemodialysis patients: any evidence of erythropoietin resistance?

Exacerbation of anemia associated with angiotensin-converting enzyme (ACE) inhibitor therapy has been noted to occur in patients with chronic renal failure, end-stage renal disease, and renal transplantation. Angiotensin-converting enzyme inhibitors appear to cause anemia through induction of decreased red blood cell production. There are data suggesting that ACE inhibitors may impair erythropoiesis via either suppression of angiotensin-mediated erythropoietin (EPO) production or bone marrow response to EPO. Patients on chronic hemodialysis receive recombinant human EPO (rHuEPO) for therapy of anemia and may also receive an ACE inhibitor for hypertension or congestive heart failure. We undertook a retrospective study to evaluate whether patients treated with ACE inhibitors developed a more severe anemia or required a higher dose of rHuEPO to maintain a similar hematocrit. Ninety-five of 108 chronic hemodialysis patients met study criteria (hemodialysis for 4 months and no treatment with an ACE inhibitor for at least 4 months = group 1; therapy with an ACE inhibitor for at least 4 months = group 2). Forty-eight patients (group 1, n = 24; group 2, n = 24) were available for analysis after exclusion for a variety of factors. There was no difference between the two groups in terms of baseline characteristics, number of blood transfusions or hospital days, or other laboratory parameters. There was no statistically significant difference in average hematocrit between group 1 (33.5% +/- 3.9%) and group 2 (32.6% +/- 1.6%). Similarly, no significant difference was observed for the average rHuEPO dose/treatment between group 1 (3,272 +/- 1,532 IU/treatment; 50.69 +/- 26.94 IU/kg/treatment) and group 2 (3,401 +/- 1,009 IU/treatment; 52.87 +/- 19.38 IU/kg/treatment). These results suggest that ACE inhibitors do not significantly induce more severe anemia or alter rHuEPO response in chronic hemodialysis patients.

Anemia↗
PubMed1996

Hyperkalemia in the elderly: a group at high risk.

Hyperkalemia is a serious electrolyte disorder which appears to develop more commonly in the aged patient. The elderly may be predisposed to hyperkalemia as a result of underlying abnormalities in potassium homeostasis. These include inapparent renal insufficiency, tubulointerstitial disease in the kidney, disturbed aldosterone production, and abnormal salt and water balance. Several commonly prescribed medications may further disrupt potassium balance and promote the development of hyperkalemia in these patients. Trimethoprim-sulfamethoxazole, a commonly used antimicrobial agent, has recently been noted to cause hyperkalemia in the elderly, even with standard dosage. The elderly should be considered at high risk to develop hyperkalemia, especially when they are using certain medications. Potassium concentration should be monitored closely when these patients are hospitalized and/or treated with potassium-altering medications.

Aged↗
PubMed1996

Mechanical mitral valve prosthesis dysfunction from thrombus: transesophageal echocardiography has limitations.

Transesophageal echocardiography (TEE) is a useful clinical tool for the evaluation of a variety of cardiovascular lesions. In particular, TEE has been demonstrated to be a better diagnostic modality in the visualization of mechanical prosthetic heart valves than transthoracic echo-cardiography (TTE). Furthermore, TEE is noted to be particularly useful to evaluate the atrial surface of mitral prostheses, the usual location of thrombi or vegetations. We herein describe a patient with a dysfunctional St. Jude's mitral prosthesis resulting from an organized thrombus who underwent both TTE and TEE without visualization of the thrombus.

Echocardiography, Doppler↗
PubMed1996

Trimethoprim-sulfamethoxazole: hyperkalemia is an important complication regardless of dose.

Trimethoprim-sulfamethoxazole is a frequently prescribed antibiotic with a wide spectrum of antimicrobial activity. As a result of the increasing number of AIDS patients requiring therapy for Pneumocystis carinii pneumonia, high dose trimethoprim-sulfamethoxazole use had dramatically increased. A previously unreported and potentially lethal adverse reaction associated with high dose trimethoprim-sulfamethoxazole therapy, hyperkalemia, subsequently developed. Recognition of this potassium disorder led to investigation and description of the mechanism by which trimethoprim-sulfamethoxazole induced hyperkalemia. Trimethoprim was found to act like the potassium-sparing diuretic amiloride and reduce renal potassium excretion. Subsequent to this work, a handful of cases noted the development of hyperkalemia with standard dose trimethoprim-sulfamethoxazole in elderly patients without evidence of an obvious defect in potassium homeostasis. A prospective surveillance study of patients treated with standard dose trimethoprim-sulfamethoxazole as compared to similar controls treated with other antibiotics confirmed the rise in potassium concentration associated with trimethoprim-sulfamethoxazole therapy. Patients with mild renal insufficiency were the only group at significant risk for more severe hyperkalemia. Hence, trimethoprim-sulfamethoxazole therapy can be complicated by hyperkalemia regardless of the dose employed.

AIDS-Related Opportunistic Infections↗
PubMed1996

Lead and the kidney: nephropathy, hypertension, and gout.

Lead intoxication in human beings has been documented since the second century B.C. Renal disease, hypertension, and gout have all been linked to lead by strong circumstantial evidence. Both acute and chronic nephropathy can occur as a result of lead poisoning. Acute renal failure develops following acute lead intoxication and is often associated with gastrointestinal, neurologic, and hematologic disorders. Both blood and urinary laboratory abnormalities are associated with acute intoxication and are often diagnostic. Chronic lead nephropathy, a chronic tubulointerstitial nephritis on biopsy, occurs in the setting of long-term lead exposure and is often associated with hypertension and gout. Diagnosis of chronic lead nephropathy is more difficult since the laboratory abnormalities seen with acute lead intoxication are not present with chronic lead exposure. The typical clinical picture and the exclusion of other causes of renal disease allow the diagnosis of chronic lead nephropathy to be made. Evaluation of lead stores by either the calcium disodium edetate (EDTA) mobilization test or K-x-ray fluorescence are helpful in clinching the diagnosis. Treatment with EDTA lead mobilization is effective for acute lead poisoning while avoidance of further lead exposure prevents recurrence of lead intoxication. Treatment of chronic lead nephropathy with EDTA lead mobilization is useful if renal failure is modest; however, EDTA mobilization is of no benefit in patients with more severe renal insufficiency.

Environmental Exposure↗
PubMed1995

Severe hepatocellular disease as an unusual presentation of metastatic melanoma.

Melanoma is a cutaneous malignancy with an incidence that is rising. Surgery is curative if performed prior to metastasis. Liver metastasis is common and is often associated with an elevation in lactic dehydrogenase. A rise in transaminases is unusual; typically it is low in these patients. We describe a case of metastatic melanoma which presented as severe hepatocellular disease.

Female↗
PubMed1994

Electrolyte and acid-base disorders associated with AIDS: an etiologic review.

In summary, patients with HIV infection may develop a bewildering variety of electrolyte and acid-base disturbances. Hyponatremia from many causes is common and associated with an increased mortality. Potassium disorders are frequent, with hyperkalemia, even to life-threatening levels, more common than hypokalemia. Disturbances in calcium and uric acid homeostasis are less frequent. Acid-base disorders also complicate the clinical course of AIDS and, as with the electrolyte perturbations, may result from HIV infection itself, the illnesses associated with AIDS, or medications.

Acid-Base Imbalance↗