Expanding the differential diagnosis for transaminitis in patients with anorexia nervosa.

Aminotransferase elevations have been described in patients with anorexia nervosa. Hypothesized etiologies have included ischemic hepatitis, refeeding-induced transaminitis, and the process of autophagy. Supervised enteral nutrition is the mainstay of treatment for severe anorexia, but an increase in aminotransferase levels after initiation of enteral feeding presents clinicians with a diagnostic dilemma. We present a 31-year-old woman with anorexia nervosa (body mass index [BMI] of 13.5 kg/m2) who experienced a worsening of aminotransferase elevations even after the initiation of enteral feeding. Despite nutritional supplementation, the patient's weight continued to fall for 6 days. Peak aminotransferase concentrations correlated with the patient's lowest weight and improved only after an increase in BMI was eventually achieved. Secondary causes of severe transaminitis were investigated, and after no cause was found, a liver biopsy was performed. Pathology was consistent with liver injury secondary to severe malnutrition rather than from refeeding syndrome. This case highlights malnutrition as an important cause of aminotransferase elevations and underscores the need for judicious early weight restoration in patients with anorexia and abnormal liver chemistry.

Adenosina deaminasa: su respuesta ante desequilibrios nutricionales / Adenosine deaminase in malnutrition

It has been previously shown that nutritional produces an increment in the activity of adenosine deaminase (ADA) in thymus, serum and other fluids in immunonocompromised patients. This study analyzed if ADA activity could be used as a biochemical indicator of nutritional status in populations at nutritional risk. Twenty six women with anorexia nervosa (AN) 14-32 years old, and 33 obese children (O) 5-13 years old were studied. ADA activity was determined as described by Giusty and Galante, comparing results with control subjects of the same age. The results (x +/- SD, expressed as IU/L) were AN: 25.7+8.2 and 21.0 +/- 4.6; and 0:27.1+9.1° and 23.0±5.6 in experimental and control individuals, respectively (p<0.02). These findings support the hypothesis that ADA activity in serum can be used as a functional indicator related to the defence mechanism in nutritional studies.

Se ha demostrado que el estrés nutricional provoca incremento en la actividad de adenosina deaminasa en timo de rata y además aumenta su actividad en el suero y otros fluidos biológicos de pacientes inmunocompro-metidos. En este estudio se analizó si la determinación de la actividad de ADA en suero podría considerarse parámetro bioquímico funcional en el seguimiento de poblaciones en riesgo nutricional. Se estudiaron mujeres con anorexia nerviosa (AN, 14-32 años) y niños obesos de ambos sexos (O, 5-13 años). La actividad de ADA se determinó por el método de Giusti y Galante. Los resultados se compararon con controles de igual edad. Los resultados (X +/- DE (UI/L)) fueron AN: 25.7 +/- 8.2 vs. 21.0 +/- 4.6 y O: 27.1 +/- 9.1vs. 23.0 +/- 5.6 (p<0.02). Estos hallazgos, avalarían la hipótesis surgida de estudios previos, de proponer la determinación de la actividad sérica de ADA, como un indicador funcional relacionado con los mecanismos de defensa en los estudios de nutrición.

Eating disorders: a role for dipeptidyl peptidase IV in nutritional control.

Dipeptidyl peptidase IV (DPP IV), a serine protease with broad tissue distribution and known activity in serum, has been postulated to modulate nutrition control by modification or inactivation of peptide hormones operating in the enteroinsular axis. We hypothesized that changes of DPP IV activity in serum are related to the nutrition status of patients with eating disorders. Serum DPP IV activity was measured in 52 patients (28 with anorexia nervosa and 24 with bulimia nervosa) in four consecutive weekly analyses. Simultaneously, the number of CD26 (DPP IV)-positive peripheral blood lymphocytes was counted. The same analyses were carried out in 28 healthy female volunteers. In week 1 and throughout the observation period, DPP IV activity in the sera of patients with anorexia nervosa and, to a lesser extent, those with bulimia nervosa was elevated in comparison to that of healthy controls (week 1: means = 92.8 U/L for anorexia-nervosa patients and 89.3 U/L for bulimia-nervosa patients versus 74.7 U/L for healthy control subjects, P = 0.014; weeks 1-4: 91.8 U/L for anorexia-nervosa patients and 86.2 U/L for bulimia-nervosa patients versus 77.6 U/L for healthy controls, P < 0.001). We assume that the increase in DPP IV serum activity will increase the turnover of distinct peptide hormones with known effects on nutrition control and susceptibility to degradation by DPP IV. The potential impact of an increase in DPP IV activity in serum on satiety and nutrition control contributes to previously reported implications for immune function.

Dipeptidyl peptidase IV (DPP IV, CD26) in patients with mental eating disorders.

The notion that patients with eating disorders maintain a functional immunosurveillance in spite of severe malnutrition has attracted researchers for years. Dipeptidyl Peptidase IV (DPP IV), a serine protease with broad tissue distribution and known activity in serum, operates in the cascade of immune responses. Membrane-bound DPP IV expressed on lymphocytes, also known as the leukocyte antigen CD26, is considered to participate in T cell activation. We hypothesized that the activity of DPP IV in serum and expression of CD26 in lymphocytes may be altered in patients with eating disorders. Serum DPP IV activity and the number of CD26 (DPP IV)-positive peripheral blood lymphocytes were measured in 44 patients (anorexia nervosa (AN): n = 21, bulimia (B): n = 23) in four consecutive weekly analyses. The analysis of CD26-positive cells included the characterization of CD26-bright and CD26-dim positive subsets. Additionally, the expression of CD25 (IL-2 Receptor alpha chain) was evaluated to estimate the degree of T cell activation. The same analyses were carried out in healthy female volunteers (HC, n = 20). CD26-positive cells were reduced in patients as compared to healthy controls (mean 40.2% (AN) and 41.1% (B) vs. 47.4% (HC), p < 0.01), while the DPP IV activity in serum was elevated (mean 108.4 U/l (AN) and 91.1 U/l (B) vs. 80.3 U/l (HC), p < 0.01). The potential implications of changes in DPP IV expression and serum activity on--and beyond--immune function are discussed.

Alterations in expression and in serum activity of dipeptidyl peptidase IV (DPP IV, CD26) in patients with hyporectic eating disorders.

The notion that patients with eating disorders maintain a functional immunosurveillance in spite of severe malnutrition has attracted researchers for years. Dipeptidyl peptidase IV (DPP IV), a serine protease with broad tissue distribution and known activity in serum, operates in the cascade of immune responses. Membrane-bound DPP IV expressed on lymphocytes, also known as the leucocyte antigen CD26, is considered to participate in T-cell activation. We hypothesized that the activity of DPP IV in serum and expression of CD26 in lymphocytes may be altered in patients with eating disorders. Serum DPP IV activity and the number of CD26 (DPP IV)-positive peripheral blood lymphocytes were measured in 34 patients [anorexia nervosa (AN): n = 11, bulimia (B): n = 23] in four consecutive weekly analyses. In addition, the expression of CD25 (interleukin-2 receptor alpha chain) was evaluated to estimate the degree of T-cell activation. The same analyses were carried out in healthy female volunteers (HC, n = 20). CD2-CD26-positive cells were reduced in patients compared with healthy controls [mean 40.2% (AN) and 41.1% (B) versus 47.4% (HC), P < 0.01], while the DPP IV activity in serum was elevated [mean 108.4 U/l (AN) versus 91.1 U/l (B) and 80.3 U/l (HC), P < 0.01]. The potential implications of our observations on, and beyond, immune function are discussed.

Case of the month. June 1996--anorexia nervosa.

A 32 year old woman with a history of anorexia nervosa began experiencing severe muscle weakness. Proximal weakness was worse than distal and she became unable to walk. Serum creatine kinase was elevated 15-fold and EMG was consistent with a myopathic process. Muscle biopsy showed focal areas of absent staining using NADH and ATPase enzyme histochemistry. Gomori trichrome revealed many positive inclusions which were positive using immunohistochemistry for actin. Electron microscopy revealed these areas to contain cytoid bodies with Z-band streaming and disorganization of the myofibrillar network. These findings are consistent with the myopathy associated with ipecac (emetine) toxicity. A urine toxicology screen demonstrated evidence of emetine abuse, which was later admitted by the patient. Following discontinuation of the drug, the patient recovered normal muscle strength.

Adaptation of coenzyme stimulation assays for the nutritional assessment of vitamins B1, B2 and B6 using the Cobas Bio centrifugal analyser.

Adaptation of coenzyme stimulation assays for the nutritional assessment of thiamine, riboflavin and pyridoxine on the Cobas Bio centrifugal analyser are described. Whole blood was collected into acid-citrate dextrose, which preserves the erythrocytes, prior to assay for several days. Washed erythrocytes stored at -70 degrees C and subsequently thawed, showed altered enzyme activities. The methods offer improved precision over existing procedures and take advantage of the high throughput capabilities of the instrumentation.

Platelet alpha 2-adrenoceptor and adenylate cyclase in patients with anorexia nervosa and bulimia.

Platelets alpha 2-adrenoceptors were studied in 24 patients with anorexia nervosa shortly after admission to the hospital and after 10% weight gain. Twenty patients with bulimia and 24 healthy age- and sex-matched normal subjects also were studied. Receptor number was significantly increased in patients with bulimia and anorexia nervosa. After 10% weight gain, the receptor number almost normalized in anorexia nervosa patients. Kd values were increased in all patients groups at all times of study. In patients with bulimia or anorexia nervosa, both initially and after weight gain, the maximal effect of prostaglandin E1 (PGE1) on platelet cAMP production was greatly increased, while the half-maximally effective dose was unchanged. Also, the maximal inhibitory effects of epinephrine and clonidine on PGE1-stimulated platelet cAMP production were greater, while the half-maximal dose of both alpha 2-agonists was unchanged. Metabolic and endocrine indicators of starvation were present in both bulimic and anorexia nervosa patients initially. Blood beta-hydroxybutyric acid was elevated, and plasma T3 values and the orthostatic response of plasma norepinephrine (delta NA) were reduced, while cortisol was elevated (only in anorexia nervosa patients). Among these parameters, only delta NA significantly correlated with the actions of PGE1 and epinephrine on cAMP production. In conclusion, the activity of the sympathetic nervous system was reduced in patients with anorexia nervosa and bulimia. This reduction was accompanied by an increased capacity and a decreased affinity of platelet alpha 2-receptors and an increased PGE1 stimulatory and epinephrine inhibitory effects on cAMP production.

Changes in skeletal muscles of young women with anorexia nervosa. An enzyme histochemical study.

Biopsies from four young women with advanced anorexia nervosa were examined to investigate the effect of malnutrition on skeletal muscles. None of the patients showed signs of neuromuscular disease and all were physically active at the time of examination. Cryostat sections from the vastus lateralis muscle were stained with hematoxylin-azophloxin-safran and with stains for myofibrillar ATP-ase activity. In addition to routine examination of the sections, the size and distribution of the type 1 and type 2 fibres were calculated by means of a Kontron Digiplan MOP 02. Routine stained sections showed a small grouped atrophy in three cases and a more diffuse atrophy in the fourth. Enzyme histochemical stains revealed a distinct type 2 atrophy, a finding which should serve to distinguish the changes of pure malnutrition from those of conventional denervation. Exact measurements confirmed the predominant type 2 atrophy but showed definite atrophy also of the type 1 fibres. Compared with normal controls the type 1 fibres were reduced by 46% and the type 2 fibres by 75%. These findings are largely in agreement with the recent observations by Essén et al. (1981) on anorexia nervosa. However, in contrast to Essén et al. we did not find any change in the numerical distribution of the fibre types, especially no increase in type 1 fibres. Thus, we could not confirm the hypotheses of a conversion of the fibre types in cachexia.