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Objective To describe the case of two siblings with severe protein-calorie malnutrition due to abuse by starvation. Cases description The two patients were simultaneously referred to the Hospital Municipal, where they were admitted to the Pediatric Gastroenterology clinic of a university hospital for diagnostic investigation of the cause of severe malnutrition and screening tests for Celiac Disease, Cystic Fibrosis and Environmental enteropathy among others. The exams were all normal, and after detailed research on the interactions of this family, we reached the conclusion that the malnutrition was due to abuse by starvation. The children spent approximately two months in the hospital, receiving a high-protein and high-calorie diet, with significant nutritional recovery. Comments Abuse by starvation, although rare, should always be considered of as one of the causes of child malnutrition and pediatrician should be aware of the child's development, as well as the family interactions, to prevent more severe nutritional and emotional consequences in the future.

Background: One anastomosis (mini) gastric bypass (OAGB) is believed to be more malabsorptive than Roux-en-Y gastric bypass. A number of patients undergoing this procedure suffer from severe protein–calorie malnutrition requiring revisional surgery. The purpose of this study was to find the magnitude of severe protein–calorie malnutrition requiring revisional surgery after OAGB and any potential relationship with biliopancreatic limb (BPL) length. Methods: A questionnaire-based survey was carried out on the surgeons performing OAGB. Data were further corroborated with the published scientific literature. Results: A total of 118 surgeons from thirty countries reported experience with 47,364 OAGB procedures. Overall, 0.37% (138/36,952) of patients needed revisional surgery for malnutrition. The highest percentage of 0.51% (120/23,277) was recorded with formulae using >200 cm of BPL for some patients, and lowest rate of 0% was seen with 150 cm BPL. These data were corroborated by published scientific literature, which has a record of 50 (0.56%) patients needing surgical revision for severe malnutrition after OAGB. Conclusions: A very small number of OAGB patients need surgical correction for severe protein–calorie malnutrition. Highest rates of 0.6% were seen in the hands of surgeons using BPL length of >250 cm for some of their patients, and the lowest rate of 0% was seen with BPL of 150 cm. Future studies are needed to examine the efficacy of a standardised BPL length of 150 cm with OAGB.

Neurologic complications are not uncommon following bariatric surgery. Hyperammonemic encephalopathy (HAE) due to an acquired or unmasked urea cycle deficit is among the rarest of these. Pediatric nutrition support specialists are familiar with recognizing urea cycle deficits, but adult specialists may not be. Here we present a case of a patient initially misdiagnosed with cirrhosis who presented with recurrent HAE 4 years after Roux-en-Y gastric bypass. She was diagnosed with a proximal urea cycle deficit and severe protein calorie malnutrition. The patient recovered with specialized nutrition and medical support targeting this condition. A literature review indicates multiple fatalities from this condition, indicating the importance of early diagnosis and appropriate nutrition support.

Background.Experimental undernutrition in animals, during the critical brain development period, produces retardation of brain growth as well as a number of different morphologic and functional abnormalities in neurons, mainly in the dendritic synaptic apparatus. These alterations are the cause of the poor neurointegrative development that occurs in experimental malnutrition. Severe malnutrition during early postnatal life in humans is known to produce similar neurointegrative disorders as well as mental retardation, but there are very few studies describing the morphology of the dendritic apparatus in infants suffering from this condition.Objective.To study the dendritic spine density and morphology in dendrites from cortical neurons in infants dying from severe malnutrition.Methodology.Brain sections from the somestesic, motor, and occipital cortical areas of 13 infants who died of severe malnutrition and 7 eutrophic infants who died of other causes were studied by means of the rapid Golgi method. Apical dendritic spines from neurons of the fifth cortical layer were studied and counted in all sections.Results.Apical dendrites were significantly shorter in malnourished infants than in the control group (581.54 ± 54.32 μm in severe malnutrition vs 846.3 μm in normal infants). The number of dendritic spines per dendrite was also significantly diminished (185.3 ± 36.1 in malnourished vs 374.3 ± 41.6 in eutrophic infants). There were marked morphologic abnormalities in the dendritic spines of infants dying of severe malnutrition that were classified as dysplastic.Conclusions.Short apical dendrites, fewer spines, and dendritic spine abnormalities occur in severe infant malnutrition. These anatomic anomalies might be related to the neuropsychological deficits that occur in these children.

Serum concentrations of 3,3′,5′-triiodothyronine (reverse T3, rT3) were measured in adult patients with several systemic illnesses whose serum total and/or free T3 were low, serum total T4 was low or normal, and free T4 was either normal or elevated. The mean serum rT3 was 76, 46, and 77 ng per 100 ml in patients with hepatic cirrhosis, chronic renal failure, and acute febrile illnesses, respectively; the values in patients with hepatic cirrhosis and acute febrile illness were significantly higher than, and values in patients with renal failure did not differ significantly from, the mean serum rT3 (41 ng per 100 ml) in normal subjects. The mean serum rT3 in another group of patients from Calcutta, India, who had severe protein calorie malnutrition (PCM), was 53 ng per 100 ml; it was significantly higher than the corresponding value, 22 ng per 100 ml, in the same patients after feeding treatment. Mean serum rT3 in patients with systemic illnesses was not so high as that (151 ng per 100 ml) in the normal ne...

THERE is evidence that DNA replication and protein synthesis are affected when animals are subjected to nutritional deficiency comparable with severe malnutrition in humans1–7. There is some evidence of similar abnormalities in children with advanced protein–calorie malnutrition1–3,8–11, which suggests that in these circumstances cell division would fail and chromosomes would become structurally abnormal, either spontaneously or as an exaggerated response to environmental factors such as radiation12,13, chemical agents14 or viral infection15–17. We have investigated this possibility with a longitudinal study of chromosome structure in five infants and five preschool children aged 1–60 months with advanced protein–calorie malnutrition (Table 1).

The deficiency of calories and proteins in Kwashiorkor disease (KWO) affects tissue protein and fat throughout the body with pronounced loss of depot fat and wasting of skeletal muscles [1]. This has led to consideration that the heart muscle might also be wasted, with subsequent disturbance of cardiac function [2].

Publisher Summary This chapter discusses the clinical description of the anemia of protein calorie malnutrition (PCM). PCM of various degrees is the most prevalent disease of nutritional deficiency in the world. It affects primarily the young child, although older children and adults of both sexes are not spared. PCM remains one of the major killers in children even when treated in the hospital. Pallor and anemia are among the chief signs of PCM. The present understanding of the anemia of protein calorie malnutrition in children stems from clinical observation, human experimental work, and animal research. The hematological changes observed in children with severe protein calorie malnutrition are primarily an adaptation phenomenon to decrease lean body mass to which various deficiencies and disease states could add their own characteristic changes. The hematological alterations in protein calorie malnutrition must be viewed as a dynamic phenomenon of balance between body composition and the erythron.

Serum cholinesterase levels in 17 healthy children and 56 cases of severe protein calorie malnutrition were studied on admission and after 3 weeks of nutritional rehabilitation. Liver histopathology was studied on admission. Serum cholinesterase was significantly reduced in malnourished children and levels returned to nortmal after treatment for three weeks. Plant cell appearance in the liver and cell necrosis were associated with a greater reduction in serum cholinesterase levels.