Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Clozapine is approved by the US Food and Drug Administration for treatment-resistant schizophrenia and mitigation of suicidality in patients with schizophrenia or schizoaffective disorder. Clozapine requires monitoring of adverse events, such as hypotension, myocarditis, cardiomyopathy, seizures, severe neutropenia, and gastrointestinal hypomotility. Sialorrhea is another adverse event that can be bothersome for patients and result in nonadherence or the development of aspiration pneumonia. Clonidine, an α_2A adrenergic receptor agonist, is one medication option that can reduce or eliminate sialorrhea. Clonidine is generally well tolerated but can contribute to hypotension and sedation. One adverse event associated with clonidine not described in the literature is thrombocytopenia. Reported is a case of clonidine-associated thrombocytopenia when used for the treatment of clozapine-induced sialorrhea.

Abstract

Vitamin D deficiency has been correlated with non-scarring alopecia including alopecia areata or female pattern hair loss. It was theorized that hair loss secondary to vitamin D deficiency in patients susceptible to trichotillomania may exacerbate this obsessive-compulsive disorder. Though vitamin D deficiency is common, especially among patients suffering from neuropsychiatric disorders, its correlation with trichotillomania is not well reported. Two female patients suffering from trichotillomania defined by noticeable hair loss on the scalp through the Massachusetts General Hospital Hair Pulling Scale were treated to promote hair growth. Treatment included dietary supplementation with vitamin D3 1000 IU every day. It was found that in both patients treated with vitamin D3, marked improvements occurred over the span of 3 to 4 months. These included a reduction in obsessive compulsive disorder related hair loss as measured using the Massachusetts General Hospital Hair Pulling Scale, which correlated to their serum 25-hydroxyvitamin D levels. Experimental and clinical evidence is available to explain the underlying physiology and its probable relationship to trichotillomania's pathophysiology.