Polaprezinc (Zinc-L-Carnosine Complex) as an Add-on Therapy for Binge Eating Disorder and Bulimia Nervosa, and the Possible Involvement of Zinc Deficiency in These Conditions: A Pilot Study.

BACKGROUND: Zinc plays an important role in appetite regulation. L-Carnosine, an endogenous dipeptide, may also regulate eating behavior via its histaminergic and antiglutamatergic properties. Polaprezinc (zinc-L-carnosine complex) is a medication for gastric ulcers. A small case series reported successful treatment of binge eating with add-on polaprezinc. METHODS: This was an open trial of add-on polaprezinc in patients with binge eating disorder (BED; n = 22) or bulimia nervosa (BN; n = 7) receiving antidepressants. A 4-week baseline period was followed by a 16-week polaprezinc treatment at 150 mg/d (containing 34 mg zinc and 116 mg L-carnosine) in addition to ongoing psychotropic medications. We also assessed their zinc status via a laboratory index and zinc deficiency-related symptoms. RESULTS: At the study end, both conditions showed a significant reduction in the 4-week frequency of combined objective and subjective binge eating episodes, the 4-week frequency of days when at least 1 such episode occurred (only in BED), several aspects of eating disorder psychopathology (rated by the Eating Disorder Examination-Questionnaire), and comorbid depressive symptoms (rated by the 16-item Quick Inventory of Depressive Symptomatology [Self-Report]). Serum copper/zinc ratio decreased from 1.4 to 1.1 on average in both conditions. All patients had multiple zinc deficiency-related symptoms at baseline that substantially improved after polaprezinc treatment. Overall, the effectiveness of polaprezinc was greater in BED patients than in BN patients, with minor adverse effects. CONCLUSIONS: These findings offer preliminary evidence for the effectiveness of polaprezinc in treating BED and BN and suggest the involvement of zinc deficiency in these conditions.

Oral treatment of pressure ulcers with polaprezinc (zinc L-carnosine complex): 8-week open-label trial.

Polaprezinc (zinc L-carnosine complex) is a tablet commonly prescribed for gastric ulcers in Japan. Recently, we reported the effects of polaprezinc on pressure ulcer healing at 4-week follow-up. We aimed to further evaluate the efficacy and safety of polaprezinc in 8-week treatment for chronic pressure ulcers. Patients with stage II-IV pressure ulcers for ≥ 8 weeks received 150 mg/day polaprezinc (containing 116 mg L-carnosine and 34 mg zinc) per os for a maximum of 8 weeks. We measured the severity of pressure ulcers weekly using the Pressure Ulcer Scale for Healing (PUSH) score and monitored blood biochemistry. Fourteen patients (nine men; 68.4 ± 11.8 years) were enrolled. Pressure ulcer stages were II (one patient; 7 %), III (nine; 64 %), and IV (four; 29 %). The PUSH score improved significantly from 8.1 [95 % CI, 6.0-10.3] at baseline to -1.4 [-4.0 to 1.1] after 8 weeks (P < 0.001). Differences from baseline were significant after 1 week (P < 0.05). The mean weekly improvement in PUSH score was 2.0. Eleven patients healed within 8 weeks and none dropped out. Serum zinc levels increased significantly (P < 0.001), whereas serum copper levels (P = 0.001) and copper/zinc ratios (P < 0.001) decreased significantly. In one patient, preexisting copper deficiency deteriorated. These preliminary data suggest that polaprezinc may be effective and well-tolerated in 8-week treatment of pressure ulcers and could be a candidate for their oral treatment.

Effects of L-carnosine and its zinc complex (Polaprezinc) on pressure ulcer healing.

BACKGROUND: L-carnosine (CAR) is an endogenous dipeptide. We aimed to determine the effects of CAR and its zinc complex polaprezinc (PLZ) on pressure ulcer healing in institutionalized long-term care patients. METHODS: This study was a nonrandomized controlled trial with a maximum 4-week follow-up. Forty-two patients with stage II-IV pressure ulcers for 4 or more weeks were allocated to 1 of 3 groups in order of recruitment: the control group (n = 14) was untreated, the PLZ group (n = 10) orally received 150 mg/d PLZ (containing 116 mg CAR and 34 mg zinc), and the CAR group (n = 18) orally received 116 mg/d CAR. Pressure ulcer severity was measured weekly using the Pressure Ulcer Scale for Healing (PUSH) score. RESULTS: At baseline, no significant differences were found among groups in demographic and nutrition parameters and pressure ulcer characteristics (severity, size, and staging). After 4 weeks, the rate of pressure ulcer healing, assessed by the mean weekly improvement in PUSH score, was significantly greater in the CAR (1.6 ± 0.2, P = .02) and PLZ groups (1.8 ± 0.2, P = .009) than in the control group (0.8 ± 0.2). The difference between the CAR and PLZ groups was not significant (P = .73). Actual dietary intakes over this period did not differ significantly among groups. CONCLUSIONS: Our results suggest that CAR and PLZ may almost equally accelerate pressure ulcer healing during 4 weeks. The results need confirmation by randomized controlled trials with larger sample sizes.

Long-term intake of a high zinc diet causes iron deficiency anemia accompanied by reticulocytosis and extra-medullary erythropoiesis.

To elucidate the pathophysiology of zinc (Zn)-induced iron (Fe) deficiency anemia (IDA), we examined hemoglobin (Hb) concentrations, hematocrit (Ht) levels, numbers of circulating red blood cells (RBC) and reticulocytes, values of mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC), serum Zn, Fe and erythropoietin (EPO) concentrations and histopathological changes in the bone marrow, spleen and liver using rats fed with a standard or high Zn diet for 20 weeks. Rats fed with the high Zn diet exhibited a significant decrease in Hb concentrations, Ht levels and MCV, MCH and MCHC values, indicating microcytic hypochromic anemia characterized by Fe deficiency. Also, a marked decrease in serum Fe concentrations was seen in rats fed with the high Zn diet relative to rats fed with the standard diet. Interestingly, the number of RBC was comparable in both groups of rats, although a decrease in the number of RBC is ordinarily seen in IDA. There were reticulocytosis and extra-medullary erythropoiesis in the spleen and an increase in serum EPO concentrations in rats fed with the high Zn diet vs. those on the standard diet. These observations suggest that both reticulocytosis and extra-medullary erythropoiesis in the spleen played a role in maintaining the number of RBC in rats fed with the high Zn diet, preventing further progression of anemia. Further, increased production of EPO may be involved in the induction of reticulocytosis and extra-medullary erythropoiesis in the spleen.

Microinjection of dihydrotestosterone into the medial preoptic area produces male-like pattern of growth hormone secretion in ovariectomized female rats.

The pattern of growth hormone (GH) secretion is sexually dimorphic in rats. We have previously shown that the secretory pattern in adult ovariectomized (OVX) female rats is masculinized by the administration of a single dose of dihydrotestosterone (DHT), a nonaromatizable androgen. To investigate the primary site of action of DHT in the brain, a small amount of DHT was injected directly into a defined area of the brain, and the blood GH profile was observed for 18 h in conscious adult OVX female rats. The bilateral direct injection of 1 microg DHT into the medial preoptic area (MPA) produced a male-like secretory pattern of GH in OVX rats. The masculinizing effects became apparent at 9 h after injection, from which time the episodic GH secretion was produced regularly at intervals of about 150 min, the amplitude of the peak increased and baseline levels were lowered. These parameters, analyzed during 9-18 h after DHT injection, were not different from those in adult male rats. On the contrary, microinjection of DHT into the bed nucleus of the stria terminalis, the hypothalamic periventricular nucleus, or the hypothalamic arcuate-ventromedial nucleus did not affect the secretory pattern of GH. The data indicate that DHT primarily acts on cells in the MPA through androgen receptors and modulates the secretion of somatostatin and/or GH-releasing hormone secondarily to masculinize the GH secretory pattern in OVX rats.