| Adam O, Goebel FD.
[Secondary gout and
pseudo-Bartter syndrome in females with laxative abuse].
Klin Wochenschr 1987 Sep 1;65(17):833-9
Abstract: Four females (27-54 y), presenting with a history of long-term laxative abuse, were admitted to the Medizinische Poliklinik for evaluation of generalized weakness. Laboratory
findings revealed signs of Bartter's syndrome, including hypokalemia,
systemic alkalosis and normal blood pressure. Three of the four females showed impaired renal function and
elevated serum uric acid levels, two of them suffered from recurrent gouty attacks. In our patients the incidence of hyperuricemia and impaired renal function, as a consequence of
chronic hypokalemia, was much higher than known from patients with Bartter's syndrome. Hyperuricemia is related to some pathophysiological features of
Pseudo-Bartter's syndrome, (e.g. systemic alkalosis, elevated angiotensin) and combined with additional factors (e.g. catabolism, reduced plasma volume) may lead to gouty attacks. Gallstones
were found in two of the four females. Long term surreptitious laxative ingestion frequently is observed in females. Hypokalemia, induced by the laxatives, causes reduced
intestinal motility and leads to augmented laxative intake. These patients are prone to develop Pseudo-Bartter's syndrome, causing eventually a hyperuricemia and gouty attacks.
| Brimacombe JR, Breen DP.
Anesthesia and Bartter's syndrome: a case report and
review. AANA J. 1993; 61(2):193-7.
Brimioulle S et
al. Hydrochloric Acid Infusion for Treatment of Metabolic
Alkalosis associated with Respiratory Acidosis. Crit
Care Med. 1989; 17: 232-236.
Javaheri S &
Kazemi H. Metabolic Alkalosis and Hypoventilation in
Humans. Am Rev Respir Dis 1987; 136:
| Marik PE, Kussman BD, Lipman J, Kraus P.
Acetazolamide in the treatment of metabolic alkalosis in critically ill
patients. Heart Lung 1991;20(5 Pt 1):455-9
Abstract: Metabolic alkalosis is a common acid-base disturbance in critically ill patients. In many patients correction of fluid and electrolyte status does not fully correct the metabolic
derangement. In this study we examined the effect of 500 mg of intravenous acetazolamide, after correcting for fluid and electrolyte abnormalities, on the acid-base status of 30
ventilated patients. In all patients studied there was a fall of total serum bicarbonate; the mean reduction at 24 hours was 6.4 mmol/L, with a normalization of the base excess
& pH. The onset of action was rapid (within 2 hours), and the maximal effect occurred at a mean of 15.5 hours, although there was wide variation. The effect of acetazolamide was
still apparent at 48 hours. No adverse effects were noted. We conclude that in patients with metabolic alkalosis, once fluid and electrolyte abnormalities have been corrected,
acetazolamide is an effective and safe form of therapy with a quick onset and long duration of action.
J, Pyle R, Eckert E, Hatsukami D, Lentz R. Electrolyte and other physiological abnormalities in patients with bulimia.
Psychol Med 1983 May;13(2):273-8
Abstract: The frequencies of various forms of eating-related behaviour (such as vomiting and laxative abuse) are reported for a series of non-anorectic bulimia patients seen for evaluation
in an eating disorders clinic. The results of serum electrolyte, glucose and other screening tests in these patients are presented. Electrolyte abnormalities were found in 82 of the
168 patients (48.8%) who were diagnosed as having either bulimia or atypical eating disorder. The most common abnormality was
(27.4%); hypochloremia (23.8%) and hypokalemia (13.7%) were also commonly seen. No significant blood sugar abnormalities were encountered. An elevated serum amylase level was found to be
associated with frequent binge-eating and vomiting behaviour. The pathophysiology of electrolyte abnormalities in this patient group is briefly reviewed.
J, Materson B, Rogers A. Laxative abuse syndrome.
Am J Gastroenterol 1980 Nov;74(5):451-8
Abstract: Laxative abuse syndrome (LAS) is a type of Munchausen syndrome characterized by surreptitious abuse of purgatives. Clinical findings are often perplexing and may mimic
inflammatory bowel disease or malabsorption syndromes. Patients frequently complain of diarrhea alternating with constipation and may have nausea, vomiting and weight loss.
Psychiatric disturbances are common and may include anorexia nervosa. Melanosis coli and cathartic colon, acid-base disturbances (usually
metabolic alkalosis), sodium, potassium and water depletion, hyperuricemia, hyperaldosteronism and other electrolyte changes are possible complications. Diagnosis may be extremely difficult and may
require special chemical analysis of urine and feces and search of the patient's possessions. Treatment is frustrating because the patient is rarely willing to admit to laxative abuse
let alone cooperate in attempting to stop it. Physicians must be aware of the LAS in order to avoid harming the patient with extensive, expensive and often invasive (including
R, Julian B et al. On the mechanism by which chloride corrects metabolic alkalosis in
man. Am J Med 1988 Mar;84(3 Pt 1):449-58
Abstract: To determine whether administration of chloride corrects chloride-depletion metabolic alkalosis (CDA) by correction of plasma volume contraction and restoration of glomerular
filtration rate or by an independent effect of chloride repletion, CDA was produced in normal men by the administration of furosemide and maintained by restriction of dietary
sodium chloride intake. Negative sodium balance (-112 +/- 16 meq) and reduced plasma volume (2.53 versus 2.93 liters, p less than 0.05) developed. The cumulative chloride
deficit of 271 +/- 16 meq was then repleted by oral potassium chloride (267 +/- 19 meq) over 36 hours with continued serial measurements of glomerular filtration rate, effective
renal plasma flow, plasma volume, body weight, and plasma renin and aldosterone levels. CDA was corrected, even though body weight, plasma volume, glomerular filtration
rate, and renal plasma flow all remained reduced and plasma aldosterone was elevated; urinary bicarbonate excretion increased during correction. Administration of an identical
potassium chloride load to similarly sodium-depleted but not chloride-depleted normal subjects produced no change in acid-base status. It is concluded that chloride repletion
can correct CDA by a renal mechanism without restoring plasma volume or glomerular filtration rate or by altering sodium avidity.
M, Douillard C, Binaut R, Provot F.
Bartter's syndromes. Ann Endocrinol (Paris) 1999;60(6):465-72
Abstract: Bartter syndromes are defined as a family of inherited recessive autosomal
tubulopathies. They are characterized by hypochloremia,
hypokalemia, metabolic alkalosis associated with potassium renal leakage and normal blood pressure despite increased plasma renin activity. Three forms of the disease are identified as followed:
1) Gitelman syndrome or hypocalciuria hypomagnesemia syndrome is a mild form often discovered in childhood or teenagers in reason of
tetany. It is an homogeneous disorder related to mutations of the genes encoding the
thiazide-sensitive Na-Cl cotransporter located in the distal convoluted tubule.
2) Antenatal Bartter syndrome with hypercalciuria and nephrocalcinosis or hyperprostaglandin E syndrome is a severe form, often revealed by
hydramnios, prematurity and growth delay. It is related to mutations of two types of genes encoding for transporters of Henle's loop: the
bumetanide-sensitive cotransporter Na-K-2Cl (NKCC2) [type I] or the inwardly-rectifying potassium channel
(ROMK) [type II]. 3) the classical form or type III Bartter
syndrome, often revealed by dehydration in the first year of life, is associated with hypomagnesemia in 20% of cases and normal or increased
calciuria. This form is related to mutations of CLCNKB gene encoding for a chloride channel in Henle's loop. This classification, in part related to the demonstration of mutations in the genes encoding for tubular chloride or potassium channels, does not fit all cases, overlapping syndromes are frequent. Moreover some endocrinological (diabetes) and neurological (deafness) abnormalities are sometimes associated with Bartter syndromes. Both phenotypic and genetic approach must help to the diagnosis of these
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