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Severe Orthostatic Hypotension Following Weight Reduction Surgery

Severe Orthostatic Hypotension Following Weight Reduction Surgery Surgical interventions for morbid obesity are common practice in many countries, especially when other treatment options have failed or when rapid weight loss is desired. The association between weight and blood pressure is well established, especially the paradigm of obesity-related hypertension. We describe a 45-year-old obese woman with a medical history of hypertension and type 2 diabetes mellitus who lost 57 kg within a few months after a weight reduction surgery. She suffered from severe orthostatic hypotension, which probably resulted from sympathetic nervous system dysfunction. Our patient's clinical status improved with pharmacological interventions, but her symptoms resolved completely after she gained weight following a surgical reversal of the gastric partitioning owing to a local complication. Autonomic nervous system activity does change with the changes in body weight, but after evaluation of this patient, we believe that rapid weight loss may impair sympathetic function and blood pressure control. Although losing weight is a known treatment option for hypertension, exaggerated reversal of obesity-related hypertension might result in orthostatic hypotension.Postural intolerance is a debilitating disorder that may severely impair the ability to maintain normal daily activities. The pathogenesis of orthostatic hypotension (OH) may involve many factors, eg, hypovolemia, drugs, primary disorders of the autonomic nervous system, or secondary neurogenic causes. The association between weight and blood pressure is well established, especially between hypertension and obesity. We describe an obese hypertensive woman who underwent weight reduction surgery that resulted in rapid weight loss and OH. The patient's workup revealed abnormalities in the functions of the sympathetic nervous system, which were likely related to exaggerated weight loss.REPORT OF A CASEA 45-year-old markedly obese woman (weight, 118 kg; height, 166 cm; and body mass index, 44 kg/m2) with a history of type 2 diabetes mellitus and hypertension tried many weight reduction programs, without success. She underwent vertical banding gastroplasty 8 months prior to admission, which resulted in a weight reduction of 57 kg (to 61 kg). Soon afterward, her hyperglycemia and hypertension resolved. Four weeks prior to admission, she began experiencing dizziness, especially while standing, and recurrent episodes of near syncope. She denied the use of any medications. She was on a diet of 1200 kcal/d, which was based mainly on microwave-heated dishes of crushed potatoes or rice.On admission, her blood pressure readings were 90/40 mm Hg supine, 70/30 mm Hg sitting, and 50 mm Hg systolic standing, with acceleration of the heart rate from 62 to 88 and 105 beats/min, respectively. Besides orthostatism, other findings were a midline abdominal surgical scar and loose skin as a result of extreme weight loss. The results of the rest of the physical and neurological examinations were unremarkable, and there were no overt signs of hypovolemia or extrapyramidal dysfunction. Autonomic functions were assessed: heart rate variation with deep breathing and blood pressure response to Valsalva maneuver were normal. There was no impairment of other autonomic system functions. Yet the exposure to cold water (the cold pressor test, which assesses sympathetic function) induced a decrease of 22 mm Hg in systolic blood pressure. The patient underwent additional diagnostic workup as detailed.The results of the following laboratory investigations were negative or normal: complete blood cell count, serum electrolyte levels, renal and liver function tests, urinalysis, 24-hour urinary sodium levels, markers of collagen-vascular diseases, protein and immune electrophoresis, VDRL, and serological tests for human immunodeficiency virus, cytomegalovirus, Epstein-Barr virus, hepatitis B virus, and hepatitis C virus. The resting plasma renin activity (0.45 µg/L per hour) and aldosterone level (4.14 ng/d [0.11 nmol/L]) were also normal, as were the thyrotropin level (2.63 mU/mL) and the results of a rapid corticotropin stimulation test.Several 24-hour urine samples (including those collected during symptoms) revealed normal levels of catecholamines, serotonin metabolites, and porphyrines. The glycosylated hemoglobin level was 6.3%, and the fasting plasma insulin level was normal (11 µIU/mL [80 pmol/L]). The supine plasma norepinephrine and epinephrine values were 172 and 35 pg/mL (1017 and 191 pmol/L), respectively, and the standing levels were 335 and 32 pg/mL (1980 and 174 pmol/L), respectively, without elevation of the plasma dopamine level. The plasma thiamine diphosphate level was 21 fmol/106red blood cells (reference range, 18-25 fmol/106red blood cells), and the folic acid and vitamin B12levels were also normal.No pathological findings were detected on an x-ray film of the chest or on a computed tomographic scan of the head. Because of the patient's history of an adrenal mass, we performed a computed tomographic scan of the abdomen, which revealed a small left adrenal mass measuring 1.0 × 1.5 × 1.5 cm that was identical in size and shape to a lesion found on a previous scan obtained 20 months earlier. Echocardiography showed good left ventricular function and mild mitral regurgitation. The results of a purified protein derivative skin test were negative, and an abdominal wall fat biopsy specimen was negative for amyloid. The blood volume, determined with chromium 51–labeled red blood cells, was 71 mL/kg, and the calculated red blood cell mass was 24 mL/kg, values that were both within the normal range.Nerve conduction tests revealed a low amplitude of the sympathetic skin response (galvanic), which assesses the sudomotor (sweating) function. This abnormality is suggestive of autonomic involvement. The electrocardiogram showed normal sinus rhythm.Because of suspected hypovolemia, volume expansion with intravenous normal saline was attempted, but had no significant effect on the orthostatic tolerance. Fludrocortisone acetate (0.1-0.4 mg/d) was then added to the patient's regimen, along with supplemental potassium (1.8 g/d) (magnesium levels were normal) and subcutaneous injections of 2000 U of erythropoietin 3 times a week. Supportive measures, such as salty foods, caffeine-rich beverages, muscle maneuvers, and elastic stockings, were also used. The patient's diet was also supplemented with a liquid enteral feeding preparation (Ensure Plus, Abbott Laboratories Inc, Columbus, Ohio), an addition of 750 kcal/d. The result of the combined therapeutic approach was a gradual increase in blood pressure within 3 weeks. At that time, the supine blood pressure was 160/90 mm Hg, and the standing blood pressure was 110/60 mm Hg after 2 minutes. The erythropoietin injections were discontinued.Symptomatic progress was slower, with residual dizziness. Ten weeks later, the patient reported significant improvement, which correlated with the improvement in blood pressure response, to values of 115/80 mm Hg supine and 100/70 mm Hg standing, with only a mild increment in the standing heart rate (71-82 beats/min). She returned to her normal daily activities. Her therapeutic regimen was gradually discontinued, until complete cessation 4 months after admission. Throughout 10 additional months of follow-up, she reported only some episodes of dizziness. One year later, because of severe local stenosis, the gastric band had to be removed. This was followed by a weight gain of 8 kg, which resulted in complete resolution of her symptoms, a condition that lasted throughout an additional 1 year of follow-up.COMMENTOnly partial information is available on changes in autonomic functions after a rapid weight loss, especially after a surgical procedure for morbid obesity. The patient described herein presented with sympathotonic OH (SOH), a syndrome in which the decrease in blood pressure associated with standing is accompanied by tachycardia. To the best of our knowledge, the only case of OH that developed after gastric partitioning was reported by Hoeldtke et al,who described 4 patients with SOH and 1 with postural tachycardia syndrome following rapid weight loss or a viral illness.The pathogenesis and incidence of SOH are still unclear. The condition is characterized by excessive sympathetic discharge characterized by postural tachycardia; however, the standing blood pressure remains low.Hoeldtke and colleagues found that the latencies of the plantar autonomic surface potentials were slightly prolonged in their patients, including 1 patient after gastric partitioning. They suggested the possibility of an autonomic neuropathy, which primarily affects the low thoracic or lumbar sympathetic neurons. The postural tachycardia syndrome was recently shown to result from partial sympathetic denervation, especially in the legs.Our patient's workup revealed the following autonomic nervous system findings: normal cardiac innervation; mild abnormalities on the cold pressor test, suggesting efferent or processing abnormality of the sympathetic vasomotor reflex; and low amplitude of the sympathetic skin response. Also, the plasma epinephrine level failed to increase when the patient stood. In exploring the possibility of lower extremity neuropathies in this case, we considered an unintended surgical sympathectomy. In this regard, OH has been reported to occur after a sympathectomy, but to the best of our knowledge, it has not yet been described as a complication of vertical banding gastroplasty.Our patient also could have suffered from diabetic autonomic neuropathy. Glycosylated hemoglobin levels were found to be higher in diabetic patients with OH than in those without OH, and vagal dysfunction has been suggested in obese diabetic patients.However, our patient did not have other symptoms of autonomic failure, and her hyperglycemia, which she had had for 8 years, resolved while she lost weight. Another possibility that was considered was a Guillian-Barré–like syndrome with incomplete autonomic involvement following a viral illness. Cases of SOH that developed after viral illnesses have been reported previously.The rapid resolution of our patient's symptoms could support this hypothesis, but the unusual presentation makes this possibility unlikely. Also, her medical history revealed that 20 months earlier she had a left adrenal mass that was identical in size, but the normal levels of catecholamines in her urine samples and the reversibility of the SOH indicate that this was an incidental finding. We believe that her symptoms were related to her rapid weight loss.A direct effect of weight loss on autonomic function could underlie the clinical presentation. However, data to support this suggestion are as yet largely unavailable. In this regard, it should be mentioned that observations in cases of anorexia nervosa support the claim that there is a minimum of caloric intake that is required to maintain sufficient blood pressure.Another important possibility to consider is a "reverse course" of ORH.There are at least 2 theories regarding ORH: one claims that sympathetic nervous system underactivity is the metabolic basis for obesity; the other claims that sympathetic nervous system overactivity occurs with chronic overeating. A recent description of enhanced renal noradrenaline spillover rate in obese individuals supports the second hypothesis.Insulin-mediated vasodilatation (which is possibly nitric oxide dependent) is impaired by insulin resistance in ORH as well. Insulin resistance also increases sensitivity to noradrenaline in obese subjects.It is suggested that the rapid reversal of obesity-related effects on blood pressure could underlie our patient's hypotension. Some evidence to support a "reverse model" already exists: weight gain or increased salt intake may be associated with elevated levels or increased sensitivity to norepinephrine in some patients,but the opposite is also true. Restriction of sodium and calories has been shown to reduce sympathetic activity and the circulating levels of norepinephrine; a decrease in intra-abdominal fat may reduce blood pressure; and a low-calorie diet, especially a protein diet, has been shown to reduce sympathetic activity and has produced OH in obese patients.In another study, 28 obese patients who underwent weight reduction surgery had increased sympathetic activity and low vagal activity before surgery, both of which improved after weight loss.Thus, the net effect of surgery in our patient could result from a rapid weight loss.Combination therapies in cases of OH are efficacious and are recommended.Many cases involving autonomic neuropathies can be managed with a combination of an α-adrenergic agonist (eg, midodrine hydrochloride) and erythropoietin (which may interfere with endothelial-derived vasorelaxation and enhance endothelin release).The combined therapeutic approach yielded significant symptomatic relief in our patient, but only the gradual weight gain abolished all her orthostatic symptoms. This finding may strengthen the suggested association between weight loss and hypotension or the "over-reversal" of ORH.RDHoeldtkeGEDworkinSRGasperBCIsraelSympathotonic orthostatic hypotension: a report of four cases.Neurology.1989;39:34-40.IJSchatzOrthostatic hypotension, I: functional and neurogenic causes.Arch Intern Med.1984;144:773-777.GJacobFCostaJRShannonThe neuropathic postural tachycardia syndrome.N Engl J Med.2000;343:1008-1014.JJVan LieshoutWWeilingKHWesselingEEndertJMKaremakerOrthostatic hypotension caused by sympathectomies performed for hyperhidrosis.Neth J Med.1990;36:53-57.NTsutsuKNunoiYYokomizoMKikuchiMFujishimaRelationship between glycemic control and orthostatic hypotension in type 2 diabetes mellitus: a survey by the Fukuoka Diabetes Clinic Group.Diabetes Res Clin Pract.1990;8:115-123.HSasakiMNagulesparanADuboisHypergastrinemia in obese noninsulin-dependent diabetes: a possible reflection of high prevalence of vagal dysfunction.J Clin Endocrinol Metab.1983;56:744-750.SHLimCBTanKMChanHTTjiaAcute sympathotonic orthostatic hypotension with recovery.Ann Acad Med Singapore.1990;19:404-406.lFohlinBFreyschussBBjarkeCTDaviesCThorenFunction and dimensions of the circulatory system in anorexia nervosa.Acta Paediatr-Scand.1978;67:11-16.MSRumantirMVazGLJenningsNeural mechanisms in human obesity-related hypertension.J Hypertens.1999;17:1125-1133.ADBaronHemodynamic actions of insulin.Am J Physiol.1994;267:E187-E202.KMasuoHMikamiTOgiharaMLTuckWeight gain–induced blood pressure elevation.Hypertension.2000;35:1135-1140.MIKoolenPBrummelenAdrenergic activity and peripheral hemodynamics in relation to sodium sensitivity in patients with essential hypertension.Hypertension.1984;6:820-825.VMCampeseFKarubianIChervuMPariseNSarkiesRBigazziPressor reactivity to norepinephrine and angiotensin in salt-sensitive hypertensive patients.Hypertension.1993;21:301-307.OKAnderssonBFagerbergTHednerHaemodynamic adjustment to weight reduction-separate effects of energy versus salt restriction.J Hypertens Suppl.1983;1:35-37.HKanaiKTokunagaSFujiokaKKKameda-TakemuraYMatsuzawaDecrease in intra-abdominal visceral fat may reduce blood pressure in obese hypertensive women.Hypertension.1996;27:125-129.JDeHavenRSherwinRHendlerPFeligNitrogen and sodium balance and sympathetic nervous system activity in obese subjects treated with low-calorie protein or mixed diet.N Engl J Med.1980;302:477-482.KKarasonHMolgaardJWikstrandLSjostromHeart rate variability in obesity and the effect of weight loss.Am J Cardiol.1999;83:1242-1247.DRobertsonTLDavisRecent advances in the treatment of orthostatic hypotension.Neurology.1995;45(suppl 5):S26-S32.NDVaziriMechanism of erythropoietin-induced hypertension.Am J Kidney Dis.1999;33:821-828.Accepted for publication February 22, 2001.Presented in part at the Spring Meeting of the Israel Society of Internal Medicine, Ramat Gan, Israel, March 7, 2000.Corresponding author and reprints: Haim Bitterman, MD, Department of Internal Medicine A, Carmel Medical Center, 7 Michal St, Haifa 34362, Israel (e-mail: haimb@tx.technion.ac.il). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Internal Medicine American Medical Association

Severe Orthostatic Hypotension Following Weight Reduction Surgery

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Publisher
American Medical Association
Copyright
Copyright 2001 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.
ISSN
2168-6106
eISSN
2168-6114
DOI
10.1001/archinte.161.17.2145
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Abstract

Surgical interventions for morbid obesity are common practice in many countries, especially when other treatment options have failed or when rapid weight loss is desired. The association between weight and blood pressure is well established, especially the paradigm of obesity-related hypertension. We describe a 45-year-old obese woman with a medical history of hypertension and type 2 diabetes mellitus who lost 57 kg within a few months after a weight reduction surgery. She suffered from severe orthostatic hypotension, which probably resulted from sympathetic nervous system dysfunction. Our patient's clinical status improved with pharmacological interventions, but her symptoms resolved completely after she gained weight following a surgical reversal of the gastric partitioning owing to a local complication. Autonomic nervous system activity does change with the changes in body weight, but after evaluation of this patient, we believe that rapid weight loss may impair sympathetic function and blood pressure control. Although losing weight is a known treatment option for hypertension, exaggerated reversal of obesity-related hypertension might result in orthostatic hypotension.Postural intolerance is a debilitating disorder that may severely impair the ability to maintain normal daily activities. The pathogenesis of orthostatic hypotension (OH) may involve many factors, eg, hypovolemia, drugs, primary disorders of the autonomic nervous system, or secondary neurogenic causes. The association between weight and blood pressure is well established, especially between hypertension and obesity. We describe an obese hypertensive woman who underwent weight reduction surgery that resulted in rapid weight loss and OH. The patient's workup revealed abnormalities in the functions of the sympathetic nervous system, which were likely related to exaggerated weight loss.REPORT OF A CASEA 45-year-old markedly obese woman (weight, 118 kg; height, 166 cm; and body mass index, 44 kg/m2) with a history of type 2 diabetes mellitus and hypertension tried many weight reduction programs, without success. She underwent vertical banding gastroplasty 8 months prior to admission, which resulted in a weight reduction of 57 kg (to 61 kg). Soon afterward, her hyperglycemia and hypertension resolved. Four weeks prior to admission, she began experiencing dizziness, especially while standing, and recurrent episodes of near syncope. She denied the use of any medications. She was on a diet of 1200 kcal/d, which was based mainly on microwave-heated dishes of crushed potatoes or rice.On admission, her blood pressure readings were 90/40 mm Hg supine, 70/30 mm Hg sitting, and 50 mm Hg systolic standing, with acceleration of the heart rate from 62 to 88 and 105 beats/min, respectively. Besides orthostatism, other findings were a midline abdominal surgical scar and loose skin as a result of extreme weight loss. The results of the rest of the physical and neurological examinations were unremarkable, and there were no overt signs of hypovolemia or extrapyramidal dysfunction. Autonomic functions were assessed: heart rate variation with deep breathing and blood pressure response to Valsalva maneuver were normal. There was no impairment of other autonomic system functions. Yet the exposure to cold water (the cold pressor test, which assesses sympathetic function) induced a decrease of 22 mm Hg in systolic blood pressure. The patient underwent additional diagnostic workup as detailed.The results of the following laboratory investigations were negative or normal: complete blood cell count, serum electrolyte levels, renal and liver function tests, urinalysis, 24-hour urinary sodium levels, markers of collagen-vascular diseases, protein and immune electrophoresis, VDRL, and serological tests for human immunodeficiency virus, cytomegalovirus, Epstein-Barr virus, hepatitis B virus, and hepatitis C virus. The resting plasma renin activity (0.45 µg/L per hour) and aldosterone level (4.14 ng/d [0.11 nmol/L]) were also normal, as were the thyrotropin level (2.63 mU/mL) and the results of a rapid corticotropin stimulation test.Several 24-hour urine samples (including those collected during symptoms) revealed normal levels of catecholamines, serotonin metabolites, and porphyrines. The glycosylated hemoglobin level was 6.3%, and the fasting plasma insulin level was normal (11 µIU/mL [80 pmol/L]). The supine plasma norepinephrine and epinephrine values were 172 and 35 pg/mL (1017 and 191 pmol/L), respectively, and the standing levels were 335 and 32 pg/mL (1980 and 174 pmol/L), respectively, without elevation of the plasma dopamine level. The plasma thiamine diphosphate level was 21 fmol/106red blood cells (reference range, 18-25 fmol/106red blood cells), and the folic acid and vitamin B12levels were also normal.No pathological findings were detected on an x-ray film of the chest or on a computed tomographic scan of the head. Because of the patient's history of an adrenal mass, we performed a computed tomographic scan of the abdomen, which revealed a small left adrenal mass measuring 1.0 × 1.5 × 1.5 cm that was identical in size and shape to a lesion found on a previous scan obtained 20 months earlier. Echocardiography showed good left ventricular function and mild mitral regurgitation. The results of a purified protein derivative skin test were negative, and an abdominal wall fat biopsy specimen was negative for amyloid. The blood volume, determined with chromium 51–labeled red blood cells, was 71 mL/kg, and the calculated red blood cell mass was 24 mL/kg, values that were both within the normal range.Nerve conduction tests revealed a low amplitude of the sympathetic skin response (galvanic), which assesses the sudomotor (sweating) function. This abnormality is suggestive of autonomic involvement. The electrocardiogram showed normal sinus rhythm.Because of suspected hypovolemia, volume expansion with intravenous normal saline was attempted, but had no significant effect on the orthostatic tolerance. Fludrocortisone acetate (0.1-0.4 mg/d) was then added to the patient's regimen, along with supplemental potassium (1.8 g/d) (magnesium levels were normal) and subcutaneous injections of 2000 U of erythropoietin 3 times a week. Supportive measures, such as salty foods, caffeine-rich beverages, muscle maneuvers, and elastic stockings, were also used. The patient's diet was also supplemented with a liquid enteral feeding preparation (Ensure Plus, Abbott Laboratories Inc, Columbus, Ohio), an addition of 750 kcal/d. The result of the combined therapeutic approach was a gradual increase in blood pressure within 3 weeks. At that time, the supine blood pressure was 160/90 mm Hg, and the standing blood pressure was 110/60 mm Hg after 2 minutes. The erythropoietin injections were discontinued.Symptomatic progress was slower, with residual dizziness. Ten weeks later, the patient reported significant improvement, which correlated with the improvement in blood pressure response, to values of 115/80 mm Hg supine and 100/70 mm Hg standing, with only a mild increment in the standing heart rate (71-82 beats/min). She returned to her normal daily activities. Her therapeutic regimen was gradually discontinued, until complete cessation 4 months after admission. Throughout 10 additional months of follow-up, she reported only some episodes of dizziness. One year later, because of severe local stenosis, the gastric band had to be removed. This was followed by a weight gain of 8 kg, which resulted in complete resolution of her symptoms, a condition that lasted throughout an additional 1 year of follow-up.COMMENTOnly partial information is available on changes in autonomic functions after a rapid weight loss, especially after a surgical procedure for morbid obesity. The patient described herein presented with sympathotonic OH (SOH), a syndrome in which the decrease in blood pressure associated with standing is accompanied by tachycardia. To the best of our knowledge, the only case of OH that developed after gastric partitioning was reported by Hoeldtke et al,who described 4 patients with SOH and 1 with postural tachycardia syndrome following rapid weight loss or a viral illness.The pathogenesis and incidence of SOH are still unclear. The condition is characterized by excessive sympathetic discharge characterized by postural tachycardia; however, the standing blood pressure remains low.Hoeldtke and colleagues found that the latencies of the plantar autonomic surface potentials were slightly prolonged in their patients, including 1 patient after gastric partitioning. They suggested the possibility of an autonomic neuropathy, which primarily affects the low thoracic or lumbar sympathetic neurons. The postural tachycardia syndrome was recently shown to result from partial sympathetic denervation, especially in the legs.Our patient's workup revealed the following autonomic nervous system findings: normal cardiac innervation; mild abnormalities on the cold pressor test, suggesting efferent or processing abnormality of the sympathetic vasomotor reflex; and low amplitude of the sympathetic skin response. Also, the plasma epinephrine level failed to increase when the patient stood. In exploring the possibility of lower extremity neuropathies in this case, we considered an unintended surgical sympathectomy. In this regard, OH has been reported to occur after a sympathectomy, but to the best of our knowledge, it has not yet been described as a complication of vertical banding gastroplasty.Our patient also could have suffered from diabetic autonomic neuropathy. Glycosylated hemoglobin levels were found to be higher in diabetic patients with OH than in those without OH, and vagal dysfunction has been suggested in obese diabetic patients.However, our patient did not have other symptoms of autonomic failure, and her hyperglycemia, which she had had for 8 years, resolved while she lost weight. Another possibility that was considered was a Guillian-Barré–like syndrome with incomplete autonomic involvement following a viral illness. Cases of SOH that developed after viral illnesses have been reported previously.The rapid resolution of our patient's symptoms could support this hypothesis, but the unusual presentation makes this possibility unlikely. Also, her medical history revealed that 20 months earlier she had a left adrenal mass that was identical in size, but the normal levels of catecholamines in her urine samples and the reversibility of the SOH indicate that this was an incidental finding. We believe that her symptoms were related to her rapid weight loss.A direct effect of weight loss on autonomic function could underlie the clinical presentation. However, data to support this suggestion are as yet largely unavailable. In this regard, it should be mentioned that observations in cases of anorexia nervosa support the claim that there is a minimum of caloric intake that is required to maintain sufficient blood pressure.Another important possibility to consider is a "reverse course" of ORH.There are at least 2 theories regarding ORH: one claims that sympathetic nervous system underactivity is the metabolic basis for obesity; the other claims that sympathetic nervous system overactivity occurs with chronic overeating. A recent description of enhanced renal noradrenaline spillover rate in obese individuals supports the second hypothesis.Insulin-mediated vasodilatation (which is possibly nitric oxide dependent) is impaired by insulin resistance in ORH as well. Insulin resistance also increases sensitivity to noradrenaline in obese subjects.It is suggested that the rapid reversal of obesity-related effects on blood pressure could underlie our patient's hypotension. Some evidence to support a "reverse model" already exists: weight gain or increased salt intake may be associated with elevated levels or increased sensitivity to norepinephrine in some patients,but the opposite is also true. Restriction of sodium and calories has been shown to reduce sympathetic activity and the circulating levels of norepinephrine; a decrease in intra-abdominal fat may reduce blood pressure; and a low-calorie diet, especially a protein diet, has been shown to reduce sympathetic activity and has produced OH in obese patients.In another study, 28 obese patients who underwent weight reduction surgery had increased sympathetic activity and low vagal activity before surgery, both of which improved after weight loss.Thus, the net effect of surgery in our patient could result from a rapid weight loss.Combination therapies in cases of OH are efficacious and are recommended.Many cases involving autonomic neuropathies can be managed with a combination of an α-adrenergic agonist (eg, midodrine hydrochloride) and erythropoietin (which may interfere with endothelial-derived vasorelaxation and enhance endothelin release).The combined therapeutic approach yielded significant symptomatic relief in our patient, but only the gradual weight gain abolished all her orthostatic symptoms. This finding may strengthen the suggested association between weight loss and hypotension or the "over-reversal" of ORH.RDHoeldtkeGEDworkinSRGasperBCIsraelSympathotonic orthostatic hypotension: a report of four cases.Neurology.1989;39:34-40.IJSchatzOrthostatic hypotension, I: functional and neurogenic causes.Arch Intern Med.1984;144:773-777.GJacobFCostaJRShannonThe neuropathic postural tachycardia syndrome.N Engl J Med.2000;343:1008-1014.JJVan LieshoutWWeilingKHWesselingEEndertJMKaremakerOrthostatic hypotension caused by sympathectomies performed for hyperhidrosis.Neth J Med.1990;36:53-57.NTsutsuKNunoiYYokomizoMKikuchiMFujishimaRelationship between glycemic control and orthostatic hypotension in type 2 diabetes mellitus: a survey by the Fukuoka Diabetes Clinic Group.Diabetes Res Clin Pract.1990;8:115-123.HSasakiMNagulesparanADuboisHypergastrinemia in obese noninsulin-dependent diabetes: a possible reflection of high prevalence of vagal dysfunction.J Clin Endocrinol Metab.1983;56:744-750.SHLimCBTanKMChanHTTjiaAcute sympathotonic orthostatic hypotension with recovery.Ann Acad Med Singapore.1990;19:404-406.lFohlinBFreyschussBBjarkeCTDaviesCThorenFunction and dimensions of the circulatory system in anorexia nervosa.Acta Paediatr-Scand.1978;67:11-16.MSRumantirMVazGLJenningsNeural mechanisms in human obesity-related hypertension.J Hypertens.1999;17:1125-1133.ADBaronHemodynamic actions of insulin.Am J Physiol.1994;267:E187-E202.KMasuoHMikamiTOgiharaMLTuckWeight gain–induced blood pressure elevation.Hypertension.2000;35:1135-1140.MIKoolenPBrummelenAdrenergic activity and peripheral hemodynamics in relation to sodium sensitivity in patients with essential hypertension.Hypertension.1984;6:820-825.VMCampeseFKarubianIChervuMPariseNSarkiesRBigazziPressor reactivity to norepinephrine and angiotensin in salt-sensitive hypertensive patients.Hypertension.1993;21:301-307.OKAnderssonBFagerbergTHednerHaemodynamic adjustment to weight reduction-separate effects of energy versus salt restriction.J Hypertens Suppl.1983;1:35-37.HKanaiKTokunagaSFujiokaKKKameda-TakemuraYMatsuzawaDecrease in intra-abdominal visceral fat may reduce blood pressure in obese hypertensive women.Hypertension.1996;27:125-129.JDeHavenRSherwinRHendlerPFeligNitrogen and sodium balance and sympathetic nervous system activity in obese subjects treated with low-calorie protein or mixed diet.N Engl J Med.1980;302:477-482.KKarasonHMolgaardJWikstrandLSjostromHeart rate variability in obesity and the effect of weight loss.Am J Cardiol.1999;83:1242-1247.DRobertsonTLDavisRecent advances in the treatment of orthostatic hypotension.Neurology.1995;45(suppl 5):S26-S32.NDVaziriMechanism of erythropoietin-induced hypertension.Am J Kidney Dis.1999;33:821-828.Accepted for publication February 22, 2001.Presented in part at the Spring Meeting of the Israel Society of Internal Medicine, Ramat Gan, Israel, March 7, 2000.Corresponding author and reprints: Haim Bitterman, MD, Department of Internal Medicine A, Carmel Medical Center, 7 Michal St, Haifa 34362, Israel (e-mail: haimb@tx.technion.ac.il).

Journal

JAMA Internal MedicineAmerican Medical Association

Published: Sep 24, 2001

There are no references for this article.