Eating disorders (II)

You can read my first post about the book, which lead to a brief comment exchange which may be of interest to people curious about diagnostics aspects, here. The book has a lot of stuff; in this post I’ll discuss the immune system, covered in chapter 5 of the book, as well as some ways that eating disorders may affect the skin (many of the remaining chapters of the book cover this topic). This will be my last post about the book.

In chapter 5 the authors start out by noting that adequate nutrition is an important factor in terms of maintaining immunocompetence and that malnutrition increases the risk of infection. Quite a few details are known about how specific aspects of nutritional deficiencies affect specific parts of the immune system. When both energy- and protein intake is insufficient (protein-energy malnutrition, PEM) this state of affairs is associated with atrophy of immune organs such as the thymus and spleen, as well as impairments in T cell populations (likely a natural consequence of thymus atrophy – the ‘T’ in ‘T cell’ stands for thymus…). Cytokine prodution (e.g. IL-1, IL-2, interferon-γ) is down-regulated in PEM, and the ability of T cells to respond appropriately to those cytokines is decreased. Impairments in macrophage phagocytotic function and neutrophils have been observed in malnourished individuals.

The authors note in the coverage that there now “seems to be consensus accepting that, overall, the manifestations of the immunocompromised status of ED patients are less frequent and severe than in PEM [3]. In general, the immune function seems to be better preserved than would be expected, considering the highly defective nutritional status of the patients. […] [some of] the most frequent findings described are leukopenia [white blood cell deficiency] with relative lymphocytosis [increased proportion of lymphocytes in the blood], [and] thrombocytopenia [platelet deficiency] […] immunocompetence and particularly T cell subsets are useful tools to follow-up the nutritional status in patients with ED. This asseveration applies also to BN patients, since T cell subsets seem to reflect their subclinical malnutrition, which is not evident from their weight status. […] Vomiting as a purging strategy is associated with a more deleterious effect on T cells […] Complement-system proteins […] have been found decreased in AN [anorexia nervosa] and BN [bulimia nervosa] [6,79] [and] seem to depend also on white adipose tissue mass. […] These proteins might be useful in the follow-up of AN patients, since C3 and C4 falls seem to occur when treated patients resume their restricting habits increasing their risk of relapse [81].”

Despite eating disorders having significant effects on the immune system, infection risk in people with eating disorders seems surprisingly to not be elevated, at least not until an advanced stage of the disease has been reached. There are multiple explanations offered for this observation, but the answer as to why this is is not completely clear. One reason might be that people with eating disorders tend to maintain relatively high protein and vitamin intake in a manner dissimilar from the intake patterns associated with classic starvation, mediating the effects of energy deficiency. Two other reasons offered both relate to the fact that the immune system does not respond normally to pathogens, and so to the extent that symptoms relate to immune responses to infection people with eating disorders have fewer symptoms; this relates to both down-regulation of memory T-cells and suppressed capacity to mount the classic acute-phase response to infection; a reduced febrile response to bacterial infection has been observed in anorexics. In the context of muted responses to infection, the hormone leptin (‘the satiety hormone’) may also be implicated; “there is a function for leptin as an up-regulator factor of inflammatory immune responses. Moreover, leptin production is acutely increased during infection and inflammation […] an impairment in this acute increase in leptin production in AN patients might be related to the lack of infection symptoms in these patients [26].” Interestingly leptin also seems to be downregulated in BN.

Okay, let’s move on and talk a little bit about how eating disorders may affect the skin. The book has a lot of stuff about this so this will not be an exhaustive review of the material covered in the book – but I did think I ought to talk a little bit about this stuff. Skin signs are important in a diagnostic context: “As most patients with eating disorders tend to minimize or even deny their disorder, the skin changes are sometimes the only indication that the patient has an eating disorder.” Some of the skin signs described in the book relate quite directly to specific behaviours (e.g. vomiting in purging subtypes), whereas others are of a more generalized nature and are rather due to the fact that the body does not get enough energy/micronutrients/etc. to handle all the tasks it’s supposed to handle. Some skin signs are considered ‘guiding signs’ of eating disorders, in the sense that they’re signs often found in an eating disorder context but are not usually found in the differential diagnoses natural to consider in the given clinical context, so they can be used as guiding tools in a diagnostic context. Examples of guiding signs include “lanugo-like body hair [very fine, soft, and usually unpigmented, downy hair] due to starvation, Russell’s sign [calluses on the knuckles or back of the hand] and [tooth] enamel erosions due to self-induced vomiting, and self-induced dermatoses due to psychiatric comorbidity.”

Frequent skin signs in eating disorders include dry, scaly skin; orange discolouration of the skin due to excessive consumption of beta carotene (carrots); the aforementioned lanugo-like body hair; coldness of the extremities (feet, toes) and bluish/purplish colouring of the hands and feet, caused by slow circulation (acrocyanosis); hair loss; inflammation of the lips and nail changes. “With a BMI between 17.5 and 16, the skin is usually pale or yellowish and cold, but no specific signs are found.” They note in the book that “Russell sign, dental enamel erosion, and salivary gland enlargement [elsewhere in the coverage they also dub this phenomenon ‘“chipmunk” cheeks of the bulimic’] are pathognomonic of purging behavior”. Dry skin is reported in 70% of people with anorexia nervosa (-AN), and acne is reported in 47–59% of patients – these are very common symptoms/consequences of AN. The same is the case for lanugo; in one study of AN patients (n=62), 77% had lanugo. In one study, alopecia was present in 67% of bulimics (n=122) and 61% of anorexics (n=62).

Observing the hands may be important: “Strumia [1], observing the hand of the patients with anorexia nervosa (AN), noticed that many peculiar skin signs, such as xerosis, acrocyanosis, carotenoderma, evident blood vessels due to decreased subcutaneous tissue, cold hand, nail dystrophy [“Brittle nails affect approximately 30% of patients with anorexia nervosa and bulimia nervosa”], Russell’s sign and artefacta, were located on the hands. Strumia used the term “anorectic’s hand” and suggested that, by examining the hand of a young patient, one can reasonably suspect an eating disorder. Only Russell’s sign is pathognomonic of eating disorders, but at least three signs, excluding Russell’s sign, are required for the diagnosis of “anorectic’s hand”, for example, xerosis, carotenoderma and cold hand. A perspicacious dermatologist should pay attention to this important sign when it appears in young females that show signs of reduced self-esteem and distorted perception of body weight.”

It is noted in the book that classical deficiency syndromes such as scurvy are very rare in AN because “AN is not commonly associated with vitamin deficiencies” – rather it’s the case that many anorectics over-supplement on vitamin supplements, which can paradoxically induce or worsen some skin complaints, such as e.g. xerosis (dry skin).

“the progression of anorexic pathology is accompanied by changing patterns in dietary habits [5]. These patterns include periods of low or no carbohydrate intake and an avoidance of dietary fats. They can also include patterns in which the primary foods consumed are fruits and vegetables. During this period, meat is often avoided. Changes in relative amounts of heavy to light isotopes [of nitrogen] in the hair indicate changes in the body’s metabolic state and dietary intake. […] By definition, individuals with anorexia or anorexia and bulimia are losing weight and do not get adequate nutrition. These individuals get their nitrogen largely from plants, and/or do not get sufficient nitrogen in their diet and are in nitrogen imbalance. By contrast, individuals diagnosed with only bulimia are maintaining their weight, and therefore get adequate nutrition and are likely not to be in nitrogen imbalance. […] Hatch et al. […] suggest that a distinction may be possible between anorexia and bulimia nervosa using 15N/14N and 13C/12C ratios in hair.”

“A reduced pain sensitivity has been found in eating disorder (ED) patients, but it is unclear what physiological and psychological factors are associated with this abnormality.”

January 26, 2016 - Posted by | books, medicine

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