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1.
J Formos Med Assoc ; 94(5): 248-54, 1995 May.
Article in English | MEDLINE | ID: mdl-7613258

ABSTRACT

The diagnosis of hypoaldosteronism usually depends upon a combination of abnormal clinical and laboratory findings. The most common abnormality in hypoaldosteronism is hyperkalemia, which may be combined with sodium depletion. In the present study, 5 of 16 patients diagnosed with isolated hypoaldosteronism (IHA) had sodium depletion due to renal salt wasting, and four patients had normokalemia. Of these 16 IHA patients, 70% had subnormal baseline and stimulated plasma renin activity (PRA). Six patients diagnosed with type I pseudohypoaldosteronism (PHA) had normal or high PRA and plasma aldosterone concentrations (PAC). In 11 control subjects, supine PAC correlated positively with serum potassium (SK), and PAC stimulated by furosemide and ambulation correlated with the 24-hour urinary potassium excretion (UK). However, these correlations were not found in IHA and PHA patients. The ratio of UK/UNa+K and UNa/UK correlated with the stimulated PAC when the IHA and control subjects were taken as a whole. However, these electrolyte excretion parameters bore no relationship to the supine PAC. The stimulated PAC/SK ratio was used to discriminate the three groups; all IHA patients had a ratio below 3. The results indicate that stimulated PAC reflects the bioactivity of aldosterone on the collecting tubule, and the stimulated PAC/SK ratio is useful for the diagnosis of hypoaldosteronism and pseudohypoaldosteronism.


Subject(s)
Aldosterone/blood , Hypoaldosteronism/blood , Potassium/blood , Pseudohypoaldosteronism/blood , Adult , Aged , Aged, 80 and over , Case-Control Studies , Diagnosis, Differential , Female , Humans , Male , Middle Aged
2.
Am J Kidney Dis ; 24(6): 932-5, 1994 Dec.
Article in English | MEDLINE | ID: mdl-7985672

ABSTRACT

We report an adult case of asymptomatic Bartter's syndrome with the first presentation of hypokalemic paralysis triggered by gentamicin injection. Marked hypokalemia and hypomagnesemia associated with excessive kaliuresis and magnesiuria were found. Plasma renin activity and aldosterone concentration were high, but blood pressure was normal. Renal biopsy revealed hypercellularity of the renin-producing cell of the juxtaglomerular apparatus. Muscular paralysis subsided after potassium chloride supplementation. Hypokalemia was corrected with potassium and magnesium supplements and the use of diclofenac. To the best of our knowledge, there have been no reports of muscular paralysis associated with gentamicin in Bartter's syndrome.


Subject(s)
Bartter Syndrome/diagnosis , Gentamicins/adverse effects , Muscular Diseases/chemically induced , Paralysis/chemically induced , Acute Disease , Adult , Bartter Syndrome/therapy , Female , Gentamicins/therapeutic use , Humans
3.
J Formos Med Assoc ; 93(4): 324-7, 1994 Apr.
Article in English | MEDLINE | ID: mdl-7914775

ABSTRACT

We report a classical case of Prader-Willi syndrome (PWS) in an adult with typical interstitial deletion of chromosome 15, and emphasize the study of hormonal change. This 21-year-old female had PWS face characteristics, small hands and feet, marked obesity, mental retardation, growth retardation, absence of puberty and amenorrhea. She also had the characteristic history of infantile hypotonia, poor feeding, failure to thrive and then improved appetite, followed by obesity from the age of four years. She had compulsive hyperphagia, to the extent of stealing and lying to take food. Chromosome study with high resolution banding technique revealed a small interstitial deletion at band q12 of chromosome 15, which is characteristically found in a majority of patients with PWS. Hormonal study revealed hypogonadism and growth hormone deficiency of supposed hypothalamic origin. She also had non-insulin-dependent diabetes mellitus with decreased pancreatic insulin reserve.


Subject(s)
Hormones/metabolism , Prader-Willi Syndrome/metabolism , Adult , Chromosome Deletion , Chromosomes, Human, Pair 15 , Female , Humans , Prader-Willi Syndrome/genetics , Prader-Willi Syndrome/pathology
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