A Case of Gelatinous Transformation of the Bone Marrow and Peripheral Blood Count in a Patient with Anorexia Nervosa.

A 26-year old woman with diagnosis Anorexia Nervosa, restricting type presented to the ED with refusal to eat, weakness and amenorrhea. She weighted 29.2 kg, which at a height of 5 ft made her BMI 12.6 kg/m2. Laboratory data showed a hemoglobin of 9.3/dl, hematocrit of 28.4%, leukocyte count of 8.9 K/ul, platelets count 131 K/ul. Ferritin was 168.4 ng/ml, serum iron 80 mcg/dL, transferin saturation 35.7%. Initial chemistries revealed albumin of 3.5 g/dl, prealbumin 12.4 mg/dl. Following hydration, the hemoglobin level fell to 6.9 g/dl, hematocrit to 22.0%. Remarkably, patient also experienced transient leukopenia (3.0 K/ul) and thrombocytopenia (92 K/ul).

Peripheral blood smear revealed anisocytosis, polychromasia, hypochromia and RBC fragments. The histological examination of bone marrow biopsy and aspirate showed almost complete depletion of hematopoietic tissue with rare erythroid, myeloid cells and occasional megakaryocyte. Fat tissue was completely melted presenting Gelatinous Degeneration, no stainable iron was seen. The flow cytomery did not show abnormal myeloid maturation, increased blast population or lymphoproliferative disorder. Smear prepared from the flow sample contained maturing myeloid and erythroid cells. Reticulocytes were preserved and accounted for 0.7%.

The patient was treated with blood transfusions and nutritional support. After 2 months, all biochemical imbalances and hematological parameters normalized. This is reflected in a hemoglobin level of 10.5g/dL, hematocrit of 31.3%, leukocyte count of 5.7 K/ul and platelet count of 371 K/ul. On the day of discharge to Anorexia Nervosa Clinic patient weighted 32.0 kg.

Although abnormalities in the peripheral blood are common in anorexia nervosa, in the rare cases anorexia may be associated with hypo- and aplasia, variable hypocellularity and complete Gelatinous Degeneration Bone Marrow. GDBM is an extreme condition significantly related to bone marrow necrosis and characterized by reduction of fat spaces and accumulation of material rich in acid mucopolysacharides, what we observed in our patient. The bone marrow fat depletion could adversely affect the local environment and interfere with normal hematopoiesis by way of an alteration in the release cytokines or growth factors.

We have hypothesized that Gelatinous Degeneration Bone Marrow related only to the amount of weight loss; not to other factors such as duration of caloric deprivation, age or clinical type of anorexia.

In most anorexia cases in the literature, alterations of bone marrow were reflected in the peripheral blood as mild or no cytopenia. However, we found that peripheral blood findings do not correlate with bone marrow changes, and are not good predictors of bone marrow involvement in anorexia nervosa. As a result, bone marrow morphology should be reviewed to assess severity of hematologic abnormalities in this instance.

Our findings confirmed that even severe aplastic bone marrow alterations as gelatinous degeneration, as well as abnormalities in the peripheral blood is a reversible process conditioned to weight recovery after establishment of adequate nutrition.

Importantly, clinical significance of the laboratory abnormalities and medical findings in anorexia nervosa patients has not been firmly established. We do not have risk-stratification for treatment, what is crucial for reversing a common, but seems under recognized problem in our ‘obsessed with weight loss’ culture.