Sydney Benchetrit MD, Jacques Bernheim MD and Eduardo Podjarny MD
Background: Primary aldosteronism is a common cause of non-renal secondary hypertension. A correct diagnosis results in curing the hypertension or targeting appropriate pharmacotherapy. In patients with low renin resistant hypertension (after treatment with three or more different anti-hypertensive drugs the blood pressure remains above 140/90 mmHg), screening for aldosteronism is mandatory.
Objectives: To demonstrate that normal blood levels of potassium in resistant hypertensive patients do not exclude the possible presence of hyperaldosteronism, and to suggest the use of the plasma aldosterone concentration (ng/dl)/plasma renin activity (ng/ml/hour) ratio in screening for hyperaldosteronism.
Methods: Blood tests, suppression and stimulation tests (2 L normal saline IV/4 hours and 20 mg furosemide IV for 60 minutes in a standing position) were systematically performed in 20 low renin normokalemic resistant hypertensive patients. None had renal disorders, known endocrine abnormalities or heart failure. They did not receive anti-hypertensive drugs affecting PAC[1] or PRA[2]. Basal PRA and PAC were measured twice: PAC after saline infusion and PAC/PRA after stimulation.
Results:. PAC/PRA above 50 was used to denote hyperaldosteronism. Serum K was 4 ± 0.07 mM/L, PAC 22.8 ± 1.8 ng/dl, PRA 0.13 ± 0.02 ng/ml/hour, PAC/PRA 190 ± 22 (above 100 in 17). After suppression PAC decreased from 25 ± 1.8 to 11 ± 1 ng/dl (normal <5 ng/dl). Stimulation did not affect PRA and PAC/PRA. Abdominal computed tomography scan revealed normal adrenal glands in 15 patients. Spironolactone (116 ± 60 mg/day) normalized blood pressure in all patients; it was used as a single therapy in 8, and in association with only one anti-hypertensive drug in the remaining 12 patients. In one patient the treatment was discontinued due to the presence of hyperkalemia.
Conclusions: Low renin resistant hypertension associated with normokalemia may be due to hyperaldosteronism. Normal aldosterone levels in the basal condition do not exclude the possibility of hyperaldosteronism. Using a PAC/PRA ratio above 50 as a screening test can aid the physician in deciding when to perform dynamic tests, thus increasing the sensitivity of the diagnosis of hyperaldosteronism. CT scan is frequently normal. Targeted pharmacotherapy leads to a normalization of blood values.
[1] PAC = plasma aldosterone concentration
[2] PRA = plasma renin activity
Rasmi Magadle MD, Paltiel Weiner MD, Marinella Rabner MD, Miri Mizrahi-Reuveni MD and Avi Davidovich MD
Background: The association between coronary and/or other arterial aneurysms and polycystic kidney disease is well known. While myocardial infarction is a possible complication of atheroscletotic coronary aneurysms, it is reasonable to assume that CA[1] in patients with PKD[2] may make them prone them for a similar complication.
Objective: To evaluate the possible occurrence of CA and MI[3] in first relatives of a patient with PKD, CA and MI.
Patients: We studied 12 family members: 2 parents, 8 sisters and 2 brothers of a young woman who was incidentally diagnosed as having a MI, while her mother was known to have PKD. We used electrocardiogram, thallium-image test, and transthoracic echocardiography to determine MI, ultrasonography of the kidney to determine PKD, and coronary angiography and ventriculography to determine CA and MI, respectively.
Results: PKD was detected in seven family members, while CA and MI were found in five and three of them, respectively.
Conclusions: In a family with PKD we detected a high prevalence of CA, with MI as a complication of the latter.
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[1] CA = coronary aneurysms
[2] PKD = polcystic kidney disease
[3] MI = myocardial infarction
Haim Shirin MD, Yaron Davidovitz MD, Yona Avni MD, Paulina Petchenko MD, Zipora Krepel MSc, Rafael Bruck MD and Dina Meytes MD
Background: Epidemiological studies in different parts of the world have revealed controversial results on the association between hepatitis C virus infection and non-Hodgkin’s lymphoma. This discrepancy suggests that HCV[1] lymphotropism or its effect on host lymphocytes may be influenced by regional and racial factors, as well as by genomic variations.
Objective: To determine the prevalence of HCV infection in patients with lymphoproliferative disorders diagnosed and treated in our institute in Israel.
Methods: A total of 212 consecutive patients (95 males and 117 females) treated in our hematology outpatient clinic between August 1997 and September 1999 was screened for anti-HCV antibodies and hepatitis B surface antigen. HCV infection was confirmed by the presence of HCV RNA in the serum. The prevalence of HCV in patients with lymphoproliferative disorders was compared to a control group of patients with myeloproliferative disorders and myelodysplastic syndromes.
Results: HCV infection was more prevalent in the group of LPD] patients than in the control group, but this finding was not statistically significant. The prevalence of HCV among LPD patients was 7.8%, while that in the group with myeloproliferative and myelodysplastic disorders was 1.19% and in the general population 0.64%. Among the different classes of LPD, a significant association with HCV infection was established only in patients with diffuse large B cell lymphoma. Furthermore, HCV infection was significantly more prevalent than HBV infection in the LPD group, but not in the myeloproliferative and myelodysplastic disorders group.
Conclusions: Our finding of a significant association between HCV infection and diffuse large B cell lymphoma leads us to suggest that anti-HCV antibodies be performed routinely in such subjects.
Bianca Raikhlin-Eisenkraft PhD and Yedidia Bentur MD
Background: Ciguatera poisoning is the commonest fish-borne seafood intoxication. It is endemic to warm water tropical areas and is caused by consumption of bottom-dwelling shore reef fish, mostly during spring and summer. The causative agent, ciguatoxin, is a heat-stable ester complex that becomes concentrated in fish feeding on toxic dinoflagellates. The common clinical manifestations are a combination of gastrointestinal and neurologic symptoms. Severe poisoning may be associated with seizures and respiratory paralysis.
Objective: To describe a series of patients who sustained ciguatera poisoning from an uncommon region and an unexpected source.
Patients: Two families complained of a sensation of “electrical currents,” tremors, muscle cramps, nightmares, hallucinations, agitation, anxiety and nausea of varying severity several hours after consuming rabbitfish (“aras”). These symptoms lasted between 12 and 30 hours and resolved completely. The temporal relationship to a summer fish meal, the typical clinical manifestations along with the known feeding pattern of the rabbitfish suggested ciguatera poisoning.
Conclusions: The Eastern Mediterranean basin is an unusual region and the rabbitfish an unusual source for ciguatera poisoning. There are no readily available and reliable means for detecting ciguatoxin in humans. A high index of suspicion is needed for diagnosis and a thorough differential diagnosis is essential to eliminate other poisonings, decompression sickness and encephalitis. Supportive therapy is the mainstay of treatment.
Marina Shargorodsky, MD and Reuven Zimlichman, MD
David Ergas, MD, Eran Eilat, MD, PhD, Shlomo Mendlovic, MD, PhD and Zeev M. Sthoeger, MD
Philip J. Hashkes, MD, MSc, Orit Friedland, MD and Yosef Uziel, MD, MSc
Kosta Y. Mumcuoglu, PhD, Avi Keysary, PhD and Leon Gilead, MD
Alain Fischer, MD, Salima Hacein-Bey, MD, Franeoise Le Deist, MD, Geneviove De Saint Basile, MD and Marina Cavazzana-Calvo
Ronen Rubinshtein, MD, Eran Bar-Meir, MD, Ahuva Grubstein, MD and Haim Bitterman, MD
Nirit Lev, MD, Shalom Michowiz, MD, Edna Inbar, MD, Claire I. Coire, MD, Silvio Pitlik, MD and Eldad Melamed, MD
Alex Palatnik, MD and Jonathan Benjamin, MD
David G. Mendes, MD, Gilad Barak and Emanuel Mendes
Mahmoud Abu-Shakra, MD and Dan Buskila, MD