A 52-year-old man presented with severe neck immobility and radiographic osteosclerosis. Elevated fluoride levels in serum, urine, and iliac crest bone revealed skeletal fluorosis. Nearly a decade of detailed follow-up documented considerable correction of the disorder after removal of the putative source of fluoride (toothpaste).Introduction: Skeletal fluorosis, a crippling bone disorder, is rare in the United States, but affects millions worldwide. There are no data regarding its reversibility. Materials and Methods: A white man presented in 1996 with neck immobility and worsening joint pains of 7-year duration. Radiographs revealed axial osteosclerosis. Bone markers were distinctly elevated. DXA of lumbar spine (LS), femoral neck (FN), and distal one-third radius showed Z scores of +14.3, +6.6, and −0.6, respectively. Transiliac crest biopsy revealed cancellous volume 4.5 times the reference mean, cortical width 3.2 times the reference mean, osteoid thickness 25 times the reference mean, and wide and diffuse tetracycline uptake documenting osteomalacia. Tap and bottled water were negative for F. Surreptitious ingestion of toothpaste was the most plausible F source. Results: Monitoring for a decade showed that within 3 months of removal of F toothpaste, urine F dropped from 26 to 16 mg/liter (reference range: 0.2-1.1 mg/liter), to 3.9 at 14 months, and was normal (1.2 mg/liter) after 9 years. Serum F normalized within 8 months. Markers corrected by 14 months. Serum creatinine increased gradually from 1.0 (1997) to 1.3 mg/dl (2006; reference range: 0.5-1.4 mg/dl). Radiographs, after 9 years, showed decreased sclerosis of trabeculae and some decrease of sacrospinous ligament ossification. DXA, after 9 years, revealed 23.6% and 15.1% reduction in LS and FN BMD with Z scores of +9.3 and +4.8, respectively. Iliac crest, after 8.5 years, had normal osteoid surface and thickness with distinct double labels. Bone F, after 8.5 years, was 1.15% (reference range, <0.1), which was a 36% reduction (still 10 times the reference value). All arthralgias resolved within 2 years, and he never fractured, but new-onset nephrolithiasis occurred within 9 months and became a chronic problem. Conclusions: With removal of F exposure, skeletal fluorosis is reversible, but likely impacts for decades. Patients should be monitored for impending nephrolithiasis.

Technological innovations in the ICU have led to artificially prolonged life, with an associated cost. Chronic critical illness (CCI) occurs in patients with prolonged mechanical ventilation and allostatic overload, and is associated with a discrete and consistent metabolic syndrome. Metabolic interventions are extrapolated from clinical critical care research, scientific theory, and years of CCI patient care experience. Intensive metabolic support (IMS) is a multi-targeted approach consisting of tight glycemic control with intensive insulin therapy, early and adequate nutrition therapy, nutritional pharmacology, management of metabolic bone disease, and meticulous attention to other endocrine/metabolic derangements. Ideally, IMS should be under the supervision of a metabolic support consultative team. Further research specifically focused on the CCI population is needed to validate this current approach.

Osteoporosis, a condition associated with significant morbidity and mortality, is prevalent in the growing elderly population. Aging is associated with characteristic changes in the complex pathways of bone remodeling and in patterns of food intake. Whereas the traditional focus of nutritional supplementation for protection of bone health has centered around calcium and vitamin D, a multitude of nutrients have been identified with effects on bone, both individually and in combination. An integrative physiology approach can assist in formulating a deeper understanding of the complex interactions of nutrition and aging with bone, with the goal of identifying modifiable risk factors for the prevention of bone loss.

Objective Anorexia nervosa (AN) is a serious disorder with associated morbidity and mortality, most commonly diagnosed in females. Existing literature on male anorexia is sparse, and a review of the endocrine effects of AN in males has not previously been published. Our objective is to highlight the clinical characteristics of AN in males as a routinely overlooked cause of multiple endocrinopathies and systemic illness in hospitalized patients. Methods We present 4 cases (2 cases at The Mount Sinai Hospital; 2 cases at Long Island Jewish Hospital) of young men with hormonal dysfunction due to underlying AN. Pertinent de-identified data were collected from a chart review of cases seen on the endocrinology consult service at both hospitals. Institutional Review Board approval was not required for an observational report of the cases presented. Results Four young men with AN demonstrated evidence of multiple systemic complications from severe caloric and protein malnutrition. Varying degrees of endocrinopathies were present, including hypogonadotropic hypogonadism, hypercortisolemia, and nonthyroidal illness syndrome, resulting in bradycardia, gastroparesis, hypothermia, acute systolic heart failure, and erectile dysfunction. Ages at diagnosis were 20, 24, 23, and 20 years, with mean age 21.75 years. Most of the clinical effects from these endocrinopathies resolved with improved caloric intake and nutrition, although symptoms of hypogonadism persisted. Conclusion This small case series highlights the importance of AN as a potential cause of multiple endocrinopathies in males. The heterogeneous presentations and varying degrees of clinical manifestations in our cohort emphasize the challenge in diagnosis. Increased awareness of AN in males is vital, as its prevalence is likely underestimated and appropriate diagnosis and treatment can ameliorate the metabolic dysfunction in a majority of cases. Further studies on males with eating disorders are needed to help guide diagnostic and therapeutic decisions.

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After exposure to a low and high dose dexamethasone regime, 11 of 34 acute psychiatric inpatients demonstrated abnormal dexamethasone suppression characterized by morning and/or mid-afternoon escape from suppression. This abnormality of suppression was found in primary depression, in mania, and in acute schizophrenia. In primary depression, the presence of abnormal dexamethasone suppression failed to discriminate “endogenous” depressed from “other depressed” subjects. Because nonsuppression to a high dose of dexamethasone is also found in patients with ectopic ACTH secretion and in patients with autonomous adrenal tumors, caution is necessary in the interpretation of nonsuppression which persists after recovery from psychiatric illness. As patients with Cushing's syndrome of uncertain etiology may be referred to a psychiatrist for a diagnostic evaluation, the psychological correlates of abnormal dexamethasone suppression need to be established with greater certainty.

Malnutrition, following critical illness-related metabolic and immune neuroendocrine derangements, is exacerbated by energy and protein deficits beginning early in the intensive care unit (ICU) stay. While nutrition support is an important component of ICU care, adverse effects can occur. Underfeeding, due to insufficient energy and/or protein is associated with poor patient outcomes. Overfeeding carbohydrates, lipids, and/or protein can result in hyperglycemia, hypertriglyceridemia, hepatic dysfunction, and/or azotemia. Individualization of the nutritional prescription with clinical monitoring and repeated adjustment is necessary to avoid harm. Appropriate use of tight glycemic control protocols in combination with nutrition support can prevent hyperglycemia, while minimizing glycemic variability and hypoglycemic events. While the enteral route is favored for nutrition support, early supplemental parenteral nutrition should be considered in selected high-risk patients. Thus, risk stratification of patients upon admission to the ICU can be helpful to design individualized nutritional prescriptions maximizing benefit while avoiding potential interference with recovery.