Metabolic Illness Research Articles

The Risks and Benefits of Switching Antipsychotics: A Case Study Approach

Progression of metabolic illness in a patient with schizophrenia who was stabilized on an atypical antipsychotic is described using a case study framework. Risks and benefits of staying on current treatment versus switching to another agent and switching strategies are described. Switching an antipsychotic with more favorable side effects may improve metabolic parameters if other weight loss strategies have failed. Switching or stopping medications too quickly may exacerbate psychiatric symptoms. There is little evidence to support which is the best switching strategy. The psychiatric mental health nurse practitioner carries a significant responsibility of discussing risks and benefits of switching and closely monitoring the patient during a switch of medications. Ensuring that the patient decides and agrees upon the treatment plan will improve the overall outcome.

Medical Monitoring Often Missing From Care of Patients on SGAs

Medical Monitoring Often Missing From Care of Patients on SGAs

Metabolic Syndrome and Psychiatric Illness: Interactions, Pathophysiology, Assessment and Treatment

Metabolic Syndrome and Psychiatric Illness: Interactions, Pathophysiology, Assessment and Treatment

Physical Illness and Schizophrenia: A Review of the Evidence

Back to table of contents Previous article Next article Book ReviewFull AccessPhysical Illness and Schizophrenia: A Review of the EvidenceMarie Hobart M.D.Marie Hobart M.D.Search for more papers by this authorPublished Online:1 Aug 2008https://doi.org/10.1176/ps.2008.59.8.938aAboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail Individuals with schizophrenia die 25 years earlier than the general population—a number now well publicized in this country thanks to the efforts of the National Association of State Mental Health Program Directors and others. Excess mortality is of course true world wide as well. Stefan Leucht and colleagues start with this sobering fact in Physical Illness and Schizophrenia: A Review of the Evidence. They set out to tell us what we know about physical illness as it relates to schizophrenia with the expressed purpose of encouraging recognition and intervention earlier in the course of physical illness. Many individuals with schizophrenia receive very limited medical care, and when they do receive care it is often at a point when physical illness is severe or even life threatening. The authors have done an exhaustive Medline search from 1966 to May 2006 to look at epidemiological studies of the association between schizophrenia and physical illness. They have specifically avoided including mortality studies and studies that focus primarily on the side effects of medications. Some information is grouped by types of illness, such as infectious disease, cancer, hereditary and neonatal diseases, nutritional and metabolic diseases, and immunologic disorders. The rest of the information is organized anatomically, including diseases of the nervous system, urogenital disorders, gynecologic and pregnancy-related disorders, and cardiovascular disease. In each subset the authors point out the number of hits on MEDLINE. This is followed by a brief discussion of how they determined which articles to include. In addition to searching MEDLINE, they routinely examined cited references and sought expert opinion to ensure completeness.Some topics have only a few noteworthy studies that the authors summarize. Other areas, such as HIV infection, cancer, complications of pregnancy, cardiovascular disease, metabolic illness, polydypsia, thyroid disease, and rheumatoid arthritis, have an extensive database. Detailed tables assist the reader in reviewing theses studies chronologically. Tables include location, research questions, the study and control populations, main findings, data source, and conclusions. Tables do not include how the diagnosis of schizophrenia was made in the study populations, and some studies include other psychiatric diagnostic groups. Forty percent of the studies used come from the United States; the rest are from Europe and elsewhere.This book will be particularly useful for those doing research on co-occurring medical illness and those researching schizophrenia both in psychiatry and in general medicine. Those involved in public policy regarding service delivery and research funding will find a wealth of information, as well as an appreciation for the limits of our current knowledge. The book does not address the systems issues of how to improve the quality of medical care and interventions for this population, but it challenges the reader to be part of taking the next step in addressing these critical issues.Dr. Hobart is chief medical director at Community Healthlink, Inc., and assistant professor of psychiatry, University of Massachusetts School of Medicine, Worcester. FiguresReferencesCited byDetailsCited ByNone Volume 59Issue 8 August, 2008Pages 938-939PSYCHIATRIC SERVICES August 2008 Volume 59 Number 8 Metrics PDF download History Published online 1 August 2008 Published in print 1 August 2008

Physical Illness and Schizophrenia: A Review of the Evidenceby Stefan Leucht, Tonja Burkard, John H. Henderson, Mario Maj, and Norman Sartorius; New York, Cambridge University Press, 2007, 224 pages, $58 softcover

Back to table of contents Previous article Next article Book ReviewFull AccessPhysical Illness and Schizophrenia: A Review of the EvidenceMarie Hobart M.D.Marie Hobart M.D.Search for more papers by this authorPublished Online:1 Aug 2008https://doi.org/10.1176/ps.2008.59.8.938aAboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail Individuals with schizophrenia die 25 years earlier than the general population—a number now well publicized in this country thanks to the efforts of the National Association of State Mental Health Program Directors and others. Excess mortality is of course true world wide as well. Stefan Leucht and colleagues start with this sobering fact in Physical Illness and Schizophrenia: A Review of the Evidence. They set out to tell us what we know about physical illness as it relates to schizophrenia with the expressed purpose of encouraging recognition and intervention earlier in the course of physical illness. Many individuals with schizophrenia receive very limited medical care, and when they do receive care it is often at a point when physical illness is severe or even life threatening. The authors have done an exhaustive Medline search from 1966 to May 2006 to look at epidemiological studies of the association between schizophrenia and physical illness. They have specifically avoided including mortality studies and studies that focus primarily on the side effects of medications. Some information is grouped by types of illness, such as infectious disease, cancer, hereditary and neonatal diseases, nutritional and metabolic diseases, and immunologic disorders. The rest of the information is organized anatomically, including diseases of the nervous system, urogenital disorders, gynecologic and pregnancy-related disorders, and cardiovascular disease. In each subset the authors point out the number of hits on MEDLINE. This is followed by a brief discussion of how they determined which articles to include. In addition to searching MEDLINE, they routinely examined cited references and sought expert opinion to ensure completeness.Some topics have only a few noteworthy studies that the authors summarize. Other areas, such as HIV infection, cancer, complications of pregnancy, cardiovascular disease, metabolic illness, polydypsia, thyroid disease, and rheumatoid arthritis, have an extensive database. Detailed tables assist the reader in reviewing theses studies chronologically. Tables include location, research questions, the study and control populations, main findings, data source, and conclusions. Tables do not include how the diagnosis of schizophrenia was made in the study populations, and some studies include other psychiatric diagnostic groups. Forty percent of the studies used come from the United States; the rest are from Europe and elsewhere.This book will be particularly useful for those doing research on co-occurring medical illness and those researching schizophrenia both in psychiatry and in general medicine. Those involved in public policy regarding service delivery and research funding will find a wealth of information, as well as an appreciation for the limits of our current knowledge. The book does not address the systems issues of how to improve the quality of medical care and interventions for this population, but it challenges the reader to be part of taking the next step in addressing these critical issues.Dr. Hobart is chief medical director at Community Healthlink, Inc., and assistant professor of psychiatry, University of Massachusetts School of Medicine, Worcester. FiguresReferencesCited byDetailsCited byNone Volume 59Issue 8 August, 2008Pages 938-939PSYCHIATRIC SERVICES August 2008 Volume 59 Number 8 Metrics PDF download History Published online 1 August 2008 Published in print 1 August 2008

Peroxisome proliferator-activated receptors: Targets for the treatment of metabolic illnesses (Review)

Peroxisome proliferator-activated receptors (PPARs) belong to a family of transcription factors of which three isotypes, PPARα, PPARδ (β) and PPARγ, are known. These play a central role in regulating intermediate metabolism and in incidences of inflammation. In recent years, a greater understanding of their mechanisms of action and their effects, principally in the management of cardiovascular disease, has been achieved. PPAR agonists, catalysts and agents have been used since the 1990s, when it was confirmed that fibrates possess lipid modifying properties when selectively activating PPARα. In addition, thiazolidinediones, structures analogous to fibrates, showed PPARγ activity with an insulin-sensitizing effect, leading to their use in the control and even prevention of diabetes mellitus type 2. Currently, studies are oriented to the development of agents that activate multiple PPAR isoforms - not only dual (PPARα/γ), but also PPAR panagonists (α/γ/δ). The purpose of this review is to explain the mechanisms of the molecular action and the effects of PPAR agonists, and also to analyze existing and current studies concerning their use in cardiovascular and metabolic illnesses.

Adipocitocinas: implicaciones en el pronóstico y tratamiento farmacológico de patología cardiovascular

Adipocytokines, fat tissue derived factors with regulatory properties, are involved in the pathophysiology of atheromatous and metabolic illnesses such as: ischemic heart disease, insulin resistance, obesity, dyslipidemia and diabetes mellitus. Enlargement of visceral adipose tissue depots determines a worse evolution for those complaints. Drugs as angiotensin converting enzyme inhibitors (ACEI), thiazolidinediones (glitazones) or angiotensin-II receptor antagonists, generally associated with the adequate hypolipidemic (statins, fibrates) or antiobesity (orlistat, sibutramine, rimonabant) medication, would increase those adipocytokines with anti-inflammatory and insulin-sensitizing properties (i.e. adiponectin or visfatin), while reducing pro-inflammatory and thrombogenic cytokines (as leptin, tumor necrosis factor [TNF]-alpha, plasminogen activator inhibitor 1 [PAI-1]). Thus, these pharmacologic therapeutic approaches would have a beneficial effect in order to diminish morbidity-mortality and improve the prognosis of patients with said diseases, all of them related to high cardiovascular risk.

Weight gain and metabolic issues of medicines used for bipolar disorder

Patients with bipolar disorder are at high risk of gaining weight and developing metabolic illnesses, and pharmacologic treatment for the disorder may significantly increase this risk. This paper reviews the literature on the metabolic consequences of the medications used in bipolar disorder and describes the possible strategies to prevent, monitor, and treat the common metabolic illnesses that patients with bipolar disorder may develop during treatment.

`Gentleman' genius: Inside The Clinic for Special Children in Lancaster County, Pa., the beloved pediatrician-geneticist who cares for Amish and Mennonite children also is attracting international attention for his research on the genetic causes of metabolic illness

One wouldn't expect to find a world-class research physician practicing medicine at the edge of an Amish farm, but that is precisely where D. Holmes Morton, M.D., FAAP, has set up shop. ![][1] Photo courtesy of Max Aguilera-Hellweg Improving treatment and outcomes of

The potential dangers of treating head injury patients with corticosteroids

In the past, corticosteroids were given to head-injured patients in order to prevent secondary brain damage, even if clinical trials had been inconclusive and potential risks of complications were of concern. Recently, CRASH, a large, multi-centre study on short-term, high-dose corticosteroid treatment in head trauma, was interrupted after enrolling > 10,000 patients because corticosteroid treatment was associated with significantly higher mortality within two weeks. Participating clinicians were not requested to judge the causes of death, but rates of infections and gastrointestinal haemorrhages did not differ between treated patients and controls. Other potential corticosteroid complications include metabolic derangements (particularly hyperglycaemia), adrenal insufficiency and critical illness myopathy. Furthermore, experimental data suggest that corticosteroids may have some harmful effects on neural tissue. In this review, the potential risks of treating head-injured patients with corticosteroids are examined.

Agreement between bicarbonate measured on arterial and venous blood gases

This study aims to determine the extent of agreement between venous and arterial bicarbonate for a group of emergency department patients with respiratory or metabolic illness requiring blood gas analysis as part of their evaluation. This prospective study of patients who were deemed by their treating doctor to require an arterial blood gas analysis to determine their ventilatory or acid-base status, compared bicarbonate on an arterial and a venous sample taken as close to simultaneously as possible. Data were analysed using bias (Bland-Altman) methods. Subgroup analyses were performed for the metabolic, respiratory, chronic obstructive airways disease and acidotic subgroups. Two hundred and forty-six patients were entered into the study; 195 with acute respiratory disease and 51 with suspected metabolic derangement. The values of bicarbonate on arterial and venous samples showed close agreement with an average difference between the samples of 1.20 mmol/L (95% limits of agreement being -2.73 to +5.13 mmol/L). Similar agreement was found for all subgroups. Venous bicarbonate estimation shows a high level of agreement with the arterial value, with acceptably narrow 95% limits of agreement. These results suggest that venous bicarbonate estimation may be an acceptable substitute for arterial measurement.

Hiperparatireoidismo primário em paciente com lúpus eritematoso sistêmico

Primary hyperparathyroidism (PHP) is a metabolic illness that results from autonomous secretion of parathyroid hormone and is one of the most common causes of hypercalcemia. We present the case of a 47-year-old female with a previous diagnosis of systemic lupus erythematosus (SLE) in whom clinical (diffuse bone pain, emotional lability, jaw tumor) and laboratory features (calcium= 13.5 mg/dL, phosphate= 1.8 mg/dL, alkaline phosphatase= 3028 U/L, PTH intact= 1472 pg/dL) prompted the diagnosis of PHP secondary to parathyroid adenoma as demonstrated by the anatomopathology. After treatment with calcitonin spray 400 UI per day, IV pamidronate 90 mg/week, and subtotal parathyroidectomy, the patient status improved with normal laboratory tests. This is the second report to describe the coexistence of these two disorders in a single patient. Although the pathophysiology of the association of PHP and SLE is not known, the recognition of this association has a practical implication since the therapeutical strategy is completely different.

A Clinical Guide to Inherited Metabolic Diseases

Whenever the possibility of an inherited metabolic disease is broached on the ward round, I shudder. These children are usually very sick and young, offering few diagnostic clues. My first instinct is to seek advice from my esteemed colleagues in the biochemistry laboratory, hoping that annual leave or travel to a congress will not rob me of salvation from this source. But Dr Clarke's concise yet inclusive book has made me feel less dependent on such help. The number of disorders that have been attributed to inherited point defects in metabolism now exceeds 500. These are individually rare but collectively account for a substantial proportion of illness, especially in children. I had often asked myself how the non-expert clinician could ever get a grip on this complex topic. ‘Had’ because Clarke offers a problem-oriented approach that includes the investigations required and exhaustive tabulation of differential diagnoses. After an introductory chapter on disease mechanisms he groups the syndromes by clinical presentation—neurological (chronic and acute encephalopathy, stroke, movement disorder, myopathy and psychiatric); metabolic acidosis; hepatic (jaundice, hepatomegaly, hypoglycaemia, hepatocellular dysfunction); cardiac (cardiomyopathy, arrhythmias, coronary artery disease); storage syndromes; and dysmorphism. Then follow chapters on acute metabolic illness in the newborn, newborn screening, laboratory investigations and treatment. So that is the scope, but what about the content. Does the text lead the perplexed clinician towards the right conclusion? Take metabolic acidosis—a common presentation that has the ability to mystify and deceive when it may be no more than severe shock with poor perfusion and lactic acidosis. It is also a common presenting or coincident feature of many inherited metabolic diseases. Clarke elegantly guides the reader towards timely diagnostic decisions. Some of his clinical ‘pearls’ are: that metabolic acidosis may be ‘so mild that the generally recognized clinical signs, such as tachypnea, are absent or so subtle that they are missed’; that ‘In other cases, the patient presents with an episode of acute, severe, even life-threatening, acidosis, and the underlying persistence of the condition is only recognised after resolution of the acute episode’; and that ‘the most frustrating presentation is infrequent bouts of recurrent, acute acidosis separated by long intervals of apparent good health during which diagnostic tests show no significant abnormality’. In his approach to metabolic acidosis, Clarke first asks whether it is a result of abnormal losses of bicarbonate or accumulation of acid; in other words, is the anion gap normal or expanded? This division is crucial as it is the latter in which inherited metabolic diseases reside, so the reader learns at an early stage the direction of the investigation. Accumulated acids are lactic acids, ketoacids or organic acids. The differential diagnosis and description of these is exhaustive; a three-page table of the organic acidurias is just one example. There is not space here to offer accounts of the other chapters, all of which are just as impressive. If your clinical work brings you into contact with patients who may be hiding an inherited metabolic disease, Clarke's Guide is for you. Clearly it will be of greatest help to paediatricians. My friends in the biochemistry laboratory will be allowed to borrow my copy, on the understanding that I get it back before they go away.

Diagnosis and treatment of maple syrup disease: a study of 36 patients.

To evaluate an approach to the diagnosis and treatment of maple syrup disease (MSD). Family histories and molecular testing for the Y393N mutation of the E1alpha subunit of the branched-chain alpha-ketoacid dehydrogenase allow us to identify infants who were at high risk for MSD. Amino acid concentrations were measured in blood specimens from these at-risk infants between 12 and 24 hours of age. An additional 18 infants with MSD were diagnosed between 4 and 16 days of age because of metabolic illness. A treatment protocol for MSD was designed to 1) inhibit endogenous protein catabolism, 2) sustain protein synthesis, 3) prevent deficiencies of essential amino acids, and 4) maintain normal serum osmolarity. Our protocol emphasizes the enhancement of protein anabolism and dietary correction of imbalances in plasma amino acids rather than removal of leucine by dialysis or hemofiltration. During acute illnesses, the rate of decrease of the plasma leucine level was monitored as an index of net protein synthesis. The treatment protocol for acute illnesses included the use of mannitol, furosemide, and hypertonic saline to maintain or reestablish normal serum sodium and extracellular osmolarity and thereby prevent or reverse life-threatening cerebral edema. Similar principles were followed for both sick and well outpatient management, especially during the first year, when careful matching of branched-chain amino acid intake with rapidly changing growth rates was necessary. Branched-chain ketoacid excretion was monitored frequently at home and branched-chain amino acid levels were measured within the time of a routine clinic visit, allowing immediate diagnosis and treatment of metabolic derangements. 1) Eighteen neonates with MSD were identified in the high-risk group (n = 39) between 12 and 24 hours of age using amino acid analysis of plasma or whole blood collected on filter paper. The molar ratio of leucine to alanine in plasma ranged from 1.3 to 12.4, compared with a control range of 0.12 to 0.53. None of the infants identified before 3 days of age and managed by our treatment protocol became ill during the neonatal period, and 16 of the 18 were managed without hospitalization. 2) Using our treatment protocol, 18 additional infants who were biochemically intoxicated at the time of diagnosis recovered rapidly. In all infants, plasma leucine levels decreased to <400 micromol/L between 2 to 4 days after diagnosis. Rates of decrease of the plasma leucine level using a combination of enteral and parenteral nutrition were consistently higher than those reported for dialysis or hemoperfusion. Prevention of acute isoleucine, valine, and other plasma amino acid deficiencies by appropriate supplements allowed a sustained decrease of plasma leucine levels to the therapeutic range of 100 to 300 micromol/L, at which point dietary leucine was introduced. 3) Follow-up of the 36 infants over >219 patient years showed that, although common infections frequently cause loss of metabolic control, the overall rate of hospitalization after the neonatal period was only 0.56 days per patient per year of follow-up, and developmental outcomes were uniformly good. Four patients developed life-threatening cerebral edema as a consequence of metabolic intoxication induced by infection, but all recovered. These 4 patients each showed evidence that acutely decreased serum sodium concentration and decreased serum osmolarity were associated with rapid progression of cerebral edema during their acute illnesses. Classical MSD can be managed to allow a benign neonatal course, normal growth and development, and low hospitalization rates. However, neurologic function may deteriorate rapidly at any age because of metabolic intoxication provoked by common infections and injuries. Effective management of the complex pathophysiology of this biochemical disorder requires integrated management of general medical care and nutrition, as well as control of several variables that influence endogenous protein anabolism and catabolism, plasma amino acid concentrations, and serum osmolarity.

Phosphoinositide metabolism, lithium and manic depressive illness

Physiology underlying manic depressive illness and treating effects of its most commonly used remedy – “lithium” is yet to be elucidated. Recent years of psychopharmacology research witnessed sparkling developments in our understanding of the mechanisms underlying lithium’s mood stabilizing effects. Recent data on molecular biology and in vivo magnetic resonance spectroscopy suggest that some of the initial actions of lithium may occur through the inhibition of the enzyme inositol monophosphatase (IMPase) and reduction of myo–inositol, which in turn initiate a cascade of events at different levels of signal transduction process and gene expression in brain; such as the effects on protein kinase C, myristoylated alenine rich C kinase substrate protein, glycogen synthase kinase 3β, B cell lymphoma–2 protein, and activator protein–I. It is likely that the enzyme IMPase other that being the key point in initiating lithium’s therapeutic effects, may also play a critical role in the physiology underlying manic depressive illness.

The influence of a high-oxalate/low-calcium diet on calcium oxalate renal stone risk factors in non-stone-forming black and white South African subjects.

To evaluate the influence of a high-oxalate/low-calcium diet on calcium oxalate stone risk factors in both black South Africans (who are largely immune to kidney stones) and white South Africans (in whom stones are more common). Urinary and dietary variables were examined in 11 black and 11 white South African men. None of the subjects had had a kidney stone or any metabolic illness. Their normal domestic food intake was assessed using a semiquantitative food frequency questionnaire. Subjects were given a standardized high-oxalate/low-calcium diet for 3 days; 24-h urine samples were collected before the protocol and during the final day. The samples were analysed using routine modern laboratory techniques. The urine analysis data were used to calculate the Tiselius risk index and the relative urinary supersaturations of calcium oxalate, uric acid and calcium phosphate. Urine analysis showed an intriguing anomaly; black subjects had significantly higher urinary pH and oxalate values than whites (6.50 vs 6.21 and 0.23 vs 0.14 mmol/24 h, respectively), while their urinary citrate was lower (1.47 vs 3.69 mmol/24 h). In addition, the Tiselius risk index and relative supersaturation of calcium oxalate were higher in black subjects. These results are contrary to those which might have been reasonably expected when comparing stone-free and stone-prone groups. After the dietary protocol, the only urinary variable which changed significantly was urinary oxalate, which increased by 57% in whites. Factors which are conventionally used to assess stone risk (pH, oxaluria, citraturia, relative supersaturation) are not helpful in identifying why South African blacks are relatively immune to stones. We suggest that relatively lower oxalate absorption rates may be a physiological feature of this racial group.

Critical care provided in an urban emergency department

The emergency department (ED) provides a substantial amount of critical care. The purpose of this study was to quantitate the critical care provided in an urban ED. The study was performed at a large urban hospital with an annual ED volume of 70,000 patients. All patients requiring critical care in the ED or hospital were prospectively observed between September 1 and November 30, 1993. Patients requiring recovery room care or neonatal intensive care were excluded. Data collected included age, disposition, length of stay, triage acuity assignment in the ED, primary diagnosis, and critical care procedures. During the study, 11,989 patients were examined in the ED with 500 (5%) requiring admission, 340 (3%) requiring a critical care intervention, and 96 (1%) being admitted to an intensive care unit (ICU). Ten percent of patients receiving critical care in the ED were admitted to the floor for lack of bed space. Triage assignment of emergent life-threatening or urgent potentially life-threatening condition predicted critical care need and waiting time to examination. The spectrum of critical care procedures performed in the ED and ICU were similar except for advanced life support intervention, which was more common in the ED (17 versus 3), and arterial line placement, which was more common in the ICU (14 versus 1). The spectrum of diagnoses reflected the age of patients with cardiovascular illnesses (33%), metabolic illnesses (18%), and trauma (16%) common in adults (age ≥17) and infectious illnesses (46%) or metabolic illnesses (21%) more common in pediatric patients. Overall, 14% of adult critical care, 23% of pediatric critical care, and 15% of all critical care provided in the areas studied occurred in the ED. A significant proportion of critical care is provided in the ED, and triage acuity assignment reflects this need. A significant proportion of critically ill patients was admitted to the floor for lack of bed space, which highlights the financial constraints in urban hospitals such as the one studied.

Role of cytokines in psychopathology: Therapeutic implications

Cytokines can influence physiological functions such as sleep and food intake; they also interact with a number of neurotransmitters and second messengers in the brain. Cytokines are involved in a number of infectious, inflammatory, neoplastic, metabolic and degenerative illnesses. They also have been implicated in some psychiatric disorders, including 1) depressive and anxiety disorders; 2) schizophrenic disorders (chronic and acute); 3) autistic disorder; 4) eating disorders; and 5) obsessive-compulsive disorder. Alterations in cytokine peptide/receptor production or function in major psychiatric disorders are of special interest to researchers in the field. Exogenous administration of cytokines may be of therapeutic value in disorders in which the cytokine system may be disturbed. In some brain disorders of defined neuropathology, some cytokines have been found clinically useful. Such a development has yet to occur in the treatment of psychiatric disorders; however, some limited and very preliminary observations suggest that manipulation of the cytokine network may be of potential value in the treatment of some psychiatric disorders. Considering the human and economic costs of major psychiatric disorders, alteration of the cytokine network as a potential therapeutic tool is worthy of consideration and investigation.

A Clinical Guide to Inherited Metabolic Diseases. By J.T.R. Clarke

As books on metabolic disease become more comprehensive and weightier, it is refreshing to find this user-friendly clinical guide which should suit most pockets both in size and cost. For those in training or at the fringes of metabolic disease, the standard texts that we know so well may seem rather daunting. This volume takes us through the labyrinth of metabolic diseases without assuming a prior knowledge of their biochemical classification. The author draws very much on his own extensive experience to produce a succinct and readable text. The book opens with some basic genetics and general metabolic principles, highlighting a number of common diagnostic confusions. There follow seven chapters dealing with the presenting features or ‘syndromes’ commonly seen in patients with inherited metabolic diseases. These include: neurological syndrome (encephalopathies, myopathies etc.), metabolic acidosis, hepatic syndrome, cardiac syndromes, storage syndrome and dysmorphism, acute metabolic illness in the neonate and, somewhat surprisingly, PKU (justified on historical grounds and as an exemplar for screening and treatment). The final chapters deal with laboratory diagnosis from simple screening tests to specific and specialized tests, and finally treatment, from dietary manipulation through to gene therapy. The book is well illustrated, and contains many clear tables with a surprising amount of information, as well as a comprehensive index. In short, this is an excellent guide to metabolic disease; it represents good value for money and, I suspect, will be more likely found in the owner’s pocket rather than on the shelf. It is recommended not only to the ‘busy physician’ and trainee, but to all those with an interest in metabolic disease.

Suboptimal Outcome of Management of Metabolic Cardiovascular Risk Factors in Hispanic Patients With Essential Hypertension

We studied outcome of management of metabolic cardiovascular risk factors in 155 randomly chosen Hispanic hypertensive patients (mean age, 63 +/- 1 years; 79% female) screened for dyslipidemia. Hypertriglyceridemia (n = 12) or high risk-adjusted low-density lipoprotein cholesterol (LDL-C) (n = 89) was found in 65%. Triglycerides did not change (6.16 +/- 0.58 to 7.44 +/- 2.34 mmol/L; P = NS) over 2.2 +/- 0.5 years. Only 58 patients with high LDL-C were treated, and 8 had no follow-up lipid tests. In the other 50, LDL-C decreased by 10 +/- 3% (P < .001) over 2.8 +/- 0.2 years but attained goal in only 12. In a subset of 24 patients with extended follow-up (3.8 +/- 0.2 years), there was an initial marked decline in LDL-C, followed by a rebound to baseline levels. In 29 of 54 patients with normal LDL-C, lipid testing was markedly overused compared with recommendations. Obesity (n = 94, 61%) did not improve in those with repeated data (+0.6 +/- 0.8 kg; P = NS; n = 40) over 2.7 +/- 0.3 years. Forty-four of 63 patients with type II diabetes had repeated measurement of glycosylated hemoglobin, with no change (10.5 +/- 0.5% to 11.2 +/- 0.5%; P = NS) over 2.2 +/- 0.3 years. Ten-year risk of coronary events (Framingham cohort parametric regression) calculated for 61 patients with known untreated blood pressures (169 +/- 3/98 +/- 1 mm Hg) was 21.0 +/- 1.7%, with a skewed distribution reaching high values (66%) and attributable in large part (72%) to modifiable risk factors.(ABSTRACT TRUNCATED AT 250 WORDS)