Alexander Haubenstock

Ascorbic acid aggravates secondary hyperoxalemia in patients on chronic hemodialysis.

Excerpt A deficiency in ascorbic acid is found in many patients having chronic hemodialysis treatment, and supplementation is commonly recommended. Ascorbic acid is a metabolic precursor of oxalic ...

Upper gastrointestinal endoscopy findings in patients with long-standing bulimia nervosa

Bulimia nervosa, an eating disorder now recognized with increasing frequency, is receiving growing attention because of purported complications. Recent claims of a high frequency of erosions, ulceration, and bleeding in the esophagus, ascribed to repeated, self-induced vomiting, prompted us to investigate by endoscopy the upper gastrointestinal mucosa in 37 consecutive patients with long-standing bulimia nervosa. The endoscopic appearance of esophageal and gastric mucosa was normal in 23 patients. Signs of mild esophagitis observed in eight patients were not related to the duration or severity of bulimic behavior or to symptoms of gastroesophageal reflux; two of these eight patients had sliding hiatal hernias. The remaining six patients were found to have superficial mucosal erythema in the stomach or duodenum, but none showed actual erosions, ulcers, or bleeding. Our observations suggest that, in contrast to reports by others, mucosal injury consequent to chronic, self-induced vomiting in patients with bulimia nervosa is relatively infrequent and limited.

Baclofen (LioresalR) Intoxication Report of 4 Cases and Review of the Literature

4 cases of baclofen intoxication were reported to the Vienna Poison Information Center during the years 1974-1982. These cases are presented and are discussed along with previously published cases of baclofen intoxication. A review of symptomatology and therapy is given.

Malignant histiocytosis with unusual features. Disseminated intravascular coagulation with severe hyperfibrinolysis, acute polyneuroradiculitis Guillain‐Barré, and a unique chromosome abnormality

The case of a 25‐year‐old man with the characteristic features of malignant histiocytosis (proliferation of abnormal histiocytic cells with erythrophagocytosis, hepatosplenomegaly, increased serum acid phosphatase, hypercalcemia, and bone pain) is reported. Chromosome studies revealed a near tetraploid karyotype with a pair of marker chromosomes. A few hours after initiation of chemotherapy with cyclophosphamide, Adriamycin (doxorubicin), vincristine, and prednisolone (CHOP regimen), the patient developed an acute ascending paralysis. Cerebrospinal fluid (CSF) findings were consistent with a diagnosis of Guillain‐Barré Syndrome. On the next day, disseminated intravascular coagulation (DIC) with severe hyperfibrinolysis occurred. After intensive chemotherapy, complete remission could be achieved.

Indium 111‐labeled platelet kinetic studies and platelet‐ associated igg in hairy cell leukemia

In order to study the pathogenesis of thrombocytopenia in patients with hairy cell leukemia (HCL), levels of platelet‐associated IgG (PAIgG), platelet life span (MLS), and the sequestration site of autologous 111In‐labeled platelets were measured in nine patients with HCL. Splenectomized patients (n = 4) had a higher platelet count (x = 122.5 × 109/1; range, 80–190 × 109/1) as well as higher levels of PAIgG (x = 10.7%; range, 5.8–16.9%), than nonsplenectomized patients (platelets x = 76 × 109/1, range 40–100 X 109/1; PAIgG x = 3.2%, range 2.2–4.2%). A normal recovery of 111in‐labeled platelets was found in Splenectomized patients, whereas a very low recovery was observed in the nonsplenectomized group (x = 70.2%, range, 50–82.5%, versus x = 22.4%, range, 15–28.2%). The MLS was borderline normal in all patients. The site of sequestration was the spleen in nonsplenectomized patients. The low recovery of 111In‐labeled platelets in nonsplenectomized patients suggests “hypersplenism” with pooling as a major cause of thrombocytopenia, in addition to impaired thrombocytopoiesis and possible immune‐mediated platelet destruction. Cancer 58:234–237, 1986.

Lack of association between HLA antigens and bulimia

Bulimia is an eating disorder characterized by binge eating that is associated with behavior intended to promote weight loss, such as selfinduced vomiting, laxative abuse, excessive exercise, and prolonged fasting. The lifetime prevalence of major affective disorders in bulimic patients is high (Hudson et al. 1987), and a relatively frequent occurrence of affective disorders in patients’ families has been described (Stem et al. 1984). Recently, a monozygotic twin pair with both bulimia and major depressive disorder has been reported (Brewerton et al. 1986), and a high concordance of bulimia in monozygotic twins and a low concordance in dizygotic twins has been observed (Fichter and Nogel 1988). Thus, family and twin studies suggest a genetic predisposition for affective disorders and bulimia, respectively. One method of demonstrating such a genetic factor is to show an association between a disease and the human leukocyte antigen (HLA) system (see review, Gershon et al. 1987). In patients with the classic eating disorder anorexia nervosa, a high frequency of the antigen HLA-B16 (B38 + B39) and the haplotype HLA-A26,B38 has been described by Biederman et al. (1984), however, their finding could not be reproduced by a more recent study (Kiss et al. 1988). To our knowledge, an association between HLA and bulimia has not been investigated to date.