Association between psychiatric disorders and iron deficiency anemia among children and adolescents: a nationwide population-based study

• Mu-Hong Chen,
• Tung-Ping Su,
• Ying-Sheue Chen,
• Ju-Wei Hsu,
• Kai-Lin Huang,
• Wen-Han Chang,
• Tzeng-Ji Chen and
• Ya-Mei BaiEmail author

BMC Psychiatry201313:161

https://doi.org/10.1186/1471-244X-13-161

©  Chen et al.; licensee BioMed Central Ltd. 2013

Received: 11 May 2012

Accepted: 28 May 2013

Published: 4 June 2013

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Abstract

Background

A great deal of evidence has shown that iron is an important component in cognitive, sensorimotor, and social-emotional development and functioning, because the development of central nervous system processes is highly dependent on iron-containing enzymes and proteins. Deficiency of iron in early life may increase the risk of psychiatric morbidity.

Methods

Utilizing the National Health Insurance Database from 1996 to 2008, children and adolescents with a diagnosis of IDA were identified and compared with age and gender-matched controls (1:4) in an investigation of the increased risk of psychiatric disorders.

Results

A total of 2957 patients with IDA, with an increased risk of unipolar depressive disorder (OR = 2.34, 95% CI = 1.58 ~ 3.46), bipolar disorder (OR = 5.78, 95% CI = 2.23 ~ 15.05), anxiety disorder (OR = 2.17, 95% CI = 1.49 ~ 3.16), autism spectrum disorder (OR = 3.08, 95% CI = 1.79 ~ 5.28), attention deficit hyperactivity disorder (OR = 1.67, 95% CI = 1.29 ~ 2.17), tic disorder (OR = 1.70, 95% CI = 1.03 ~ 2.78), developmental delay (OR = 2.45, 95% CI = 2.00 ~ 3.00), and mental retardation (OR = 2.70, 95% CI = 2.00 ~ 3.65), were identified. A gender effect was noted, in that only female patients with IDA had an increased OR of bipolar disorder (OR = 5.56, 95% CI = 1.98 ~ 15.70) and tic disorder (OR = 2.95, 95% CI = 1.27 ~ 6.86).

Conclusion

Iron deficiency increased the risk of psychiatric disorders, including mood disorders, autism spectrum disorder, attention deficit hyperactivity disorder, and developmental disorders. Further study is required to clarify the mechanism in the association between IDA and psychiatric disorder.

Keywords

Iron deficiency anemia Psychiatric disorders Comorbidity

Background

According to the World Health Organization, iron deficiency (ID) is the most prevalent nutritional deficiency. A 30% prevalence of iron deficiency anemia (IDA), at a minimum, has been noted among children, adolescents, and women in non-industrialized countries, and ID is also the most prevalent nutritional deficiency in industrialized countries [1, 2, 3, 4]. ID, defined by two or more abnormal measurements (serum ferritin, transferrin saturation, erythrocyte protoporphyrin), is insidious and uneasily detected by patients themselves and may not develop significant clinical symptoms [1, 2, 3, 4]. IDA is characterized by a defect in hemoglobin synthesis owing to significant ID, resulting in the reduced capacity of the red blood cells to deliver oxygen to body cells and tissues, and many clinical symptoms, such as pale conjunctiva, shortness of breath, dizziness, and lethargy [1, 2, 3, 4]. The main risk factors for IDA and ID include a low intake of iron, poor absorption of iron from diets, chronic loss of iron (i.e., ulcer, metrorrhagia), and some specific periods of life when iron requirements are especially high, such as growth and pregnancy [1, 2, 3, 4].

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Mood disorder with mixed, psychotic features due to vitamin b12 deficiency in an adolescent: case report

Ali Evren Tufan,^1,5 Rabia Bilici,² Genco Usta,³ and Ayten Erdoğan⁴

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Abstract

Vitamin B12 is one of the essential vitamins affecting various systems of the body. Reports of psychiatric disorders due to its deficiency mostly focus on middle aged and elderly patients. Here we report a case of vitamin B 12 deficiency in a 16-year old, male adolescent who presented with mixed mood disorder symptoms with psychotic features. Chief complaints were “irritability, regressive behavior, apathy, crying and truancy” which lasted for a year. Premorbid personality was unremarkable with no substance use/exposure or infections. No stressors were present. The patient was not vegetarian. Past medical history and family history was normal. Neurological examination revealed glossitis, ataxia, rigidity in both shoulders, cog-wheel rigidity in the left elbow, bilateral problems of coordination in cerebellar examination, reduced swinging of the arms and masked face. Romberg’s sign was present. Laboratory evaluations were normal. Endoscopy and biopsy revealed atrophy of the gastric mucosa with Helicobacter Pylori colonization. Schilling test was suggestive of malabsorbtion. He was diagnosed with Mood disorder with Mixed, Psychotic Features due to Vitamin B12 Deficiency and risperidone 0.5 mg/day and intramuscular vitamin B12 500 mcg/day were started along with referral for treatment of Helicobacter pylori. A visit on the second week revealed no psychotic features. Romberg’s sign was negative and cerebellar tests were normal. Extrapyramidal symptoms were reduced while Vitamin B12 levels were elevated. Risperidone was stopped and parenteral Vitamin B12 treatment was continued with monthly injections for 3 months. Follow-up endoscopy and biopsy at the first month demonstrated eradication of H. pylori. He was followed monthly for another 6 months and psychiatric symptoms did not recur at the time of last evaluation. Despite limitations, this case may underline the observation that mood disorders with psychotic features especially with accompanying extrapyramidal symptoms lacking a clear etiology may be rare manifestation of vitamin B12 and/or folate deficiency in children and adolescents and be potentially amenable to treatment.

Keywords: Vitamin B12, psychosis, mood disorder, extrapyramidal symptoms

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Background

Vitamin B12 is one of the essential vitamins affecting various systems of the body. In case of deficiency; hematologic (megaloblastic, macrocytic anemia), neurologic (demyelinization, paresthesia), gastrointestinal (anorexia, glossitis) as well as psychiatric symptoms arise. The psychiatric symptoms may not be concurrent with symptoms arising from other systems and even may precede them [1–3]. The symptoms may include agitation, irritability, negativism, confusion, disorientation, amnesia, impaired concentration and attention and insomnia; while psychiatric disorders that may be diagnosed in patients having vitamin B12 deficiency include depression, bipolar disorder, panic disorder, psychosis, phobias and dementia [1–6]. In adult patients, the clinical picture may especially involve affective or psychotic symptoms. These observations may be explained by the importance of vitamin B 12, folate and homocysteine in carbon transfer metabolism (methylation) required for the production of serotonin, other monoamine neurotransmitters and catecholamines [1–6]. Up to now, reports of psychiatric disorders due to vitamin B12 deficiency mostly focused on middle aged and elderly patients and pediatric cases are reported to be rare [7–9]. This study aimed to report a case of vitamin B 12 deficiency in an adolescent who presented with mixed mood disorder symptoms with psychotic features.

Case presentation

A sixteen-year old male adolescent was brought to our department with complaints of “irritability, regressive behavior, apathy, crying and truancy”. Upon questioning of his parents it was learned that the complaints have been present for the past year. The patient had started to display anxiety during separation from his mother, wept frequently and complained of vague pains, lethargy, forgetfulness and reduced concentration alternating with racing thoughts, irritability, anhedonia, distractibility, reduced sleep and appetite. Speech was reduced and he became progressively isolated from his peers. He refused to go to school and when sent became truant frequently. His parents reported that he was frequently agitated, spent his free time in front of his computer and that he ran excessive debts on their credit cards buying items on-line. There was no previous history of compulsive shopping or buying sprees. Premorbid personality of the adolescent was described as extrovert, euthymic and active. He was well liked by his friends although the academic staff reported problems in attention starting from the second grade. His teachers also reported fidgetiness and impulsivity which was especially prominent in mathematics lessons.

In the mental status examination, impaired attention, concentration, as well as insomnia, reduced working and short-term memory, elementary auditory (i.e. knocking and ringing), olfactory (i.e. burnt rubber, perfumes and tobacco), and visual hallucinations (i.e. a white, man-like shape, especially present in the evenings), as well as passive suicidal ideation were noted. Judgment, abstract thought and reality testing were impaired. Speech was hypo-phonic, thought process was sluggish. Thought content was found to be impoverished and dominated by somatic complaints, delusions of reference, guilt and thought broadcasting. Mood was blunted and the affect was restricted in range. Psychomotor activity and appetite were reduced.

The patient reported that those complaints arose in the past year and that hallucinations were added in the past three months. Within the last month, delusions of reference (i.e. thinking that others were looking at and talking about him), delusions of guilt (i.e. that he had sinned and would be punished) arose and the patient reported that his thoughts were broadcast so that others can read and understand his thoughts. No history of psychoactive substance use, encephalitis, use of antipsychotics/antiemetics, exposure to carbon-monoxide or organophosphate compounds or stressors was present. The patient was not vegetarian. Past medical history and family history was unremarkable for both psychopathology and chronic medical disorders. Physical and neurological examination revealed glossitis, ataxia, rigidity in both shoulders, cog-wheel rigidity in the left elbow, bilateral problems of coordination in cerebellar examination, reduced swinging of the arms and masked face. Romberg’s sign was present although no signs or symptoms of peripheral neuropathy could be observed. Evaluation with The Extrapyramidal Symptom Rating Scale (ESRS) yielded a score of 19, with items of bradykinesia and parkinsonism being positive [10].

Electroencephalography, electromyography, somatosensorial evoked potentials, cerebrospinal fluid analysis, cranial MRI, thyroid and liver function tests, pancreatic enzymes, electrolytes, parathormone, ceruloplasmin and whole blood count were within normal limits. HIV (ELISA) was negative. Twenty-four hour urine copper level was within normal ranges. An ophthalmologic examination ruled out the presence of a Kayser Fleischer ring. A peripheral blood smear with Wright’s stain was found to be normal. Endoscopy revealed atrophy of the gastric mucosa while a biopsy sample taken during endoscopy revealed colonization with Helicobacter Pylori. A Schilling test was administered to determine the etiology of Vitamin B12 deficiency and it was observed that radiolabeled Vitamin B12 levels were low both for Stage I and II of the test which was thought to reflect malabsorbtion [11].

Psychometric testing with the Beck Depression (BDI) and Anxiety Inventories (BAI) revealed scores of 35 (Cut-off score = 17, Severe Depressive Symptoms) and 36 (Without a clinically defined cut-off score albeit denoting severe anxiety), respectively [12,13]. An evaluation with the Turkish version of the Young Mania Rating Scale (YMRS), which does not have clinically designated cut-off score, yielded a score of 13 [14]. Psychotic symptoms were evaluated with Positive and Negative Syndrome Scale and the patient scored 20, 23 and 56 for the Positive, Negative and General Psychopathology subscales (Total 99) [15]. Vitamin B 12 levels were found to be 166 ng/mL in two subsequent tests after 6–8 hours of fasting with immunoassay method via Advia Centaur XT^TM (Normal 197–400 ng/mL) while folate and transcobalamine levels were normal. Hemoglobin was found to be 10 g/dL (Normal 14–18 g/dL) and MCV was 98 fL (Normal 80- 100 fL) [16]. Bone marrow examination did not reveal megaloblastic changes.

As a result of the history and evaluations and noting that the psychotic symptoms were superimposed on affective-anxious symptoms, the patient was diagnosed as having Mood disorder with Mixed, Psychotic Features due to Vitamin B12 Deficiency according to DSM-IV-TR criteria and risperidone 0.5 mg/day and intramuscular vitamin B12 500 mcg/day were started for treatment [17]. Risperidone was chosen because of it being one of the most commonly used atypical antipsychotics for management of psychosis, pervasive developmental disorders, mental retardation, mood disorders and disruptive behavior disorders in children and adolescents and having no known interaction with vitamin B12. The usual dose range of risperidone for acute psychosis and mood disorder is reported to be 2–8 mg/day while we have started risperidon at 0.5 mg/day to help stabilize the patient while the medical work-up and treatments were being completed [18]. Vitamin B12 was the only vitamin supplement started.

At the same time the patient was referred for treatment of Helicobacter pylori and was prescribed clarithromycin 1000 mg/day, lansoprazole 60 mg/day and amoxicillin 2000 mg/day. A follow-up visit on the second week revealed that no psychotic features were present, Romberg’s sign was negative and that cerebellar tests were within normal limits. Extrapyramidal symptoms were reduced. Both the patient and his mother reported that apathy, crying, regressive behavior and truancy were reduced. An evaluation with BDI and BAI revealed scores of 9 and 15, respectively while Evaluation with ESRS and YMRS yielded a score of 3 for both. PANSS scores for positive, negative and general psychopathology subscales were 13, 15 and 36 respectively (Total 64). Vitamin B12 levels were measured at this visit as 595 ng/mL. At the scond week, risperidone was stopped and parenteral Vitamin B12 treatment was continued with monthly injections for 3 months. The time course of changes in BDI, BAI, PANSS and its subscales, YMRS and ESRS according to Vitamin B12 levels is illustrated in Figure ​Figure11.

 

read more here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404901/

Aleukemic leukemia presenting with paranoid psychosis.

Conn Med. 2013 Oct;77(9):537-9.

Dasanu CA¹, Davis LK, Bauer F.

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Abstract

Mast cells not only synthesize and release serotonin, but also express and are activated through multiple serotonin receptors. Low blood serotonin level might define a specific subset of patients with systemic mastocytosis (SM) who are more likely to present with neurologic and gastrointestinal complaints. Mast cell leukemia (MCL) is a rare and aggressive type of systemic mastocytosis, and psychiatric manifestations in its course have not been well-characterized. We describe herein a unique patient with a KIT D816V mutation positive a leukemic leukemia variant of systemic mastocytosis with gastrointestinal involvement, presenting with a severe and sustained paranoid delusional illness. While diarrhea improved with the use of histamine H1 and H2 receptor antagonists, the psychosis did not, and the disease followed a dramatic course with a rapidly fatal outcome. As there is paucity of literature, diagnosis of MCL presenting with psychiatric symptoms remains a diagnostic challenge and warrants clinicians to be alert of this rare possibility

 

 

 

https://www.ncbi.nlm.nih.gov/pubmed/24266131

Adult-Onset Case of Undiagnosed Neurodegeneration with Brain Iron Accumulation with Psychotic Symptoms

Luigi Attademo,¹ Enrico Paolini,¹ Francesco Bernardini,¹ Roberto Quartesan,^1,2 and Patrizia Moretti^1,2

¹School of Psychiatry, University of Perugia, 06156 Perugia, Italy
²Division of Psychiatry, Clinical Psychology and Psychiatric Rehabilitation, Department of Clinical and Experimental Medicine, Santa Maria della Misericordia Hospital, University of Perugia, 06156 Perugia, Italy

Received 14 April 2014; Accepted 11 May 2014; Published 20 May 2014

Academic Editor: Volker Arolt

Copyright © 2014 Luigi Attademo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Neurodegeneration with brain iron accumulation (NBIA) is a collective term to indicate a group of neurodegenerative diseases presenting accumulation of iron in the basal ganglia. These disorders can result in progressive dystonia, spasticity, parkinsonism, neuropsychiatric abnormalities, and optic atrophy or retinal degeneration. Onset age ranges from infancy to late adulthood and the rate of progression is very variable. So far, the genetic bases of nine types of NBIA have been identified, pantothenate-kinase-associated neurodegeneration (PKAN) being the most frequent type. The brain MRI “eye-of-the-tiger” sign, T2-weighted hypointense signal in the globus pallidus with a central region of hyperintensity, has been considered virtually pathognomonic for PKAN but recently several reports have denied this. A significant percentage of individuals with clinical and radiographic evidence of NBIA do not have an alternate diagnosis or mutation of one of the nine known NBIA-associated genes (idiopathic NBIA). Here we present an adult-onset case of “undiagnosed” NBIA with the brain MRI “eye-of-the-tiger” sign, and with psychotic symptoms which were successfully treated with antipsychotic and mood stabilizer medications. Here, the term “undiagnosed” is used because the patient has not been screened for all known NBIA genes, but only for two of them.

 

read more here https://www.hindawi.com/journals/crips/2014/742042/

Hemochromatosis-induced bipolar disorder: a case report.

Gen Hosp Psychiatry. 2012 Jan-Feb;34(1):101.e1-3. doi: 10.1016/j.genhosppsych.2011.04.013. Epub 2011 May 31.

Serata D¹, Del Casale A, Rapinesi C, Mancinelli I, Pompili P, Kotzalidis GD, Aimati L, Savoja V, Sani G, Simmaco M, Tatarelli R, Girardi P.

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Abstract

OBJECTIVE:

A patient presenting with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, bipolar disorder was found to be affected by high iron hemochromatosis. This prompted us to explore the relation between bipolar disorder and iron overload.

METHOD:

We report the case and review the peer-reviewed literature focusing on mood symptoms in patients with hemochromatosis or iron overload. Animal studies of brain effects of iron overload are summarized. High iron hemochromatosis was confirmed by genetic testing, and treatment was instituted to address iron overload.

RESULTS:

Patient’s bipolar symptoms completely subsided after phlebotomic reduction of iron overload.

CONCLUSION:

Clinicians should explore the possibility of iron overload and seek genetic confirmation of hemochromatosis in resistant bipolar disorder to avoid unnecessary medication.

Copyright © 2012 Elsevier Inc. All rights reserved.

Schizophrenia-like psychosis and aceruloplasminemia

Mark Walterfang, Evrim March, Daniel Varghese, Kathryn Miller, Leonie Simpson, Bruce Tomlinson, and Dennis Velakoulis

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Abstract

Schizophrenia-like illnesses occur in a variety of medical and neurological conditions but to date have not been described in association with aceruloplasminemia. Aceruloplasminemia is an autosomal recessive disorder of iron metabolism which leads to iron deposition in the basal ganglia, thalamus, cerebellum and hippocampus and which usually presents in middle age with extrapyramidal symptoms and dementia. We describe a 21-year-old woman on treatment for aceruloplasminemia who presented with schizophrenia-like psychosis and declining function in the absence of neurological signs. Neuropsychological testing showed significant dominant hemisphere deficits. Magnetic resonance imaging showed bilateral iron deposition in the cerebellar dentate nuclei and thalami, frontal atrophy, and periventricular white matter hyperintensities. Functional imaging suggested global hypoperfusion. The clinical, cognitive and imaging findings were not typical for either aceruloplasminemia or schizophrenia alone and the possible relationship between the two disorders is discussed with particular reference to implications for our understanding of schizophrenia.

Keywords: aceruloplasminemia, schizophrenia, psychosis

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Introduction

Numerous medical conditions are known to produce psychotic symptoms that resemble schizophrenia, including metabolic and neurological disorders (Cummings 1996). We describe a young woman with schizophrenia-like psychotic symptoms and functional decline in the context of diagnosed aceruloplasminemia, a disorder which has not been previously associated with psychosis.

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Case history

BB was a 21-year-old woman referred for neuropsychiatric assessment on the background of a psychotic illness and a confirmed diagnosis of aceruloplasminemia. BB’s family had noticed an initial 18-month period of functional and social deterioration, poor school performance, social withdrawal, and periods of verbal aggression. She was initially treated by her general practitioner with fluvoxamine, but later deteriorated with frank persecutory delusions, auditory hallucinations, aggression and poor self-care over the subsequent 6 months. The local mental health team began risperidone 3 mg/day, which treated the positive symptoms but did not arrest her functional decline. BB completely avoided all social contact, only watched television and was unable to manage her activities of daily living. She was referred for neuropsychiatric assessment to further elucidate the contribution of the aceruloplasminemia to her cognitive and functional abilities.

 

BB had no formal psychiatric history. She had mild learning difficulties as a child, but attended mainstream schooling. At age 15 she had seen a school psychologist after telling other students she was going to be reborn as a prince. BB had been diagnosed with aceruloplasminemia at age 20, after detection of abnormal liver function and hyperferritinemia of 1700 μg/L (15–200). Liver biopsy confirmed significant iron overload without fibrosis, and desferrioxamine 20 g thrice weekly was initiated. The diagnosis of aceruloplasminemia was highly suspected because a paternal uncle had been diagnosed with the disorder. The patient and her maternal uncle share a common, unique mutation for this disorder. BB’s uncle had been described by the family as suffering long-standing behavioral problems but had never been given a psychiatric diagnosis. There was a history of consanguinity, with her parents’ grandparents being first cousins.

BB’s delivery was normal but for a prolonged rupture of membranes. She walked at 12 and talked at 15 months. She was a shy and clingy child at school who had verbal and social difficulties. She left school in Year 11 and attended a technical college where she also struggled. She had not worked or attended school since the age of 18. There was no history of substance abuse.

On mental state examination, she was cooperative but only established superficial rapport. Speech was of normal rate and volume with limited spontaneity. Mood was euthymic and affect reactive, although blunted. At the time of assessment there were no psychotic or depressive symptoms and no insight into her previous symptoms or functional impairment.

On bedside cognitive testing, she scored 25/30 on the Mini-Mental State Examination (Folstein et al 1975), and 75/100 on the Neuropsychiatry Unit Cognitive screening tool (NUCOG) (Walterfang et al 2006), each significantly below expected age norms. Hence, the patient was referred for a neuropsychological review, and information from an earlier assessment was obtained as a baseline. Physical examination was unremarkable. She had some mild conjunctival pallor but no Kaiser-Fleischer rings. She had no abdominal organomegaly. There were no abnormal movements, primitive reflexes or other neurological signs.

BB had normal electrolytes, hepatic, renal and thyroid function. Hemoglobin was low at 101 g/L” (115–150) with normal platelet and white cell counts and B12 and folate levels. Serum ferritin was still elevated at 688 μg/L (15–200).

Magnetic resonance imaging (MRI) showed global atrophy, most marked over the frontal lobes. She had a greater-than-expected load of periventricular white matter hyperintensities, and a thin anterior callosum. Iron deposition was evident in the dentate nucleus of the cerebellum and the thalamus, and to a lesser degree throughout the whole cerebral cortex, but not in the basal ganglia (Figure 1). Single-photon emission computed tomography (SPECT) showed global hypoperfusion. MRI of the abdomen showed no evidence of ovarian iron deposition. EEG was normal. A screen for lysosomal and other storage disorders on peripheral blood lymphocytes and cultured fibroblasts was normal.

Case Report: Psychosis in an adolescent with sickle cell disease

Abstract

Anxiety and depression are well documented complications of adjustment in sickle cell disease (SCD), but psychosis as a direct complication of or adjustment in SCD is uncommon. This article reports a case of psychosis in an adolescent with SCD. It advocates for further study on the relationship between psychosis and brain tissue silent-infarcts in these patients and the urge for alertness on the part of health care professionals regarding a holistic approach to the management of these children and adolescents with SCD.

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Case presentation

Reasons for evaluation

O.J, a seventeen year old male adolescent presented at the psychiatric outpatient facility of Federal Psychiatric Hospital, Calabar, Nigeria with a second episode of mental illness. He is a known sickle cell disease (SCD) patient with Hemoglobin genotype Hb.SS from South-south region of Nigeria. He was single and of Christian faith. He had just completed his high school education. He was brought by the father and an elder sister to the psychiatric out-patient facility on account of being talkative, verbal and physical aggression, poor sleep, accusing house help of witchcraft and refusal to eat his meals, believing they had been poisoned.

 

History of psychiatric and general medical illness

He was apparently well until 4 weeks prior to presentation when he was noticed to be talkative and often talked out of the theme of discussion. He was easily provoked and agitated. He had physically fought the house-help on account of “discovering” her to be a witch and shouting “blood of Jesus”. He had seen so many small children who were alien to the family members in their apartment, this O.J attributed to mean other members of the witchcraft society. He also saw other members of the family as being small in size in his perception while he was growing taller in size in comparison to them. He had not been sleeping adequately most part of the night. When not asleep he would be found talking to himself, praying excessively and reading the Bible. He complained that people around him knew what he was thinking without telling them. He admitted to hearing his thoughts being spoken aloud. He refused to eat the meals prepared at home, believing that the meals were poisoned and that he might be inflicted with witchcraft on eating. There were no associated depressive symptoms but he had expressed suicidal ideation in the past usually during periods of bone pain crises, however there was no definitive suicidal plan. The first episode of mental illness occurred at age fifteen and was characterized by poor sleep, visual hallucination, persecutory belief and easy irritability. It lasted only three weeks following treatment in a private hospital of which details could not be ascertained because of poor record keeping.

He was diagnosed with SCD for the first time at the age of two during a bone pain crisis. He had had blood transfusion thrice at ages four, nine and twelve years following hemolytic crises with packed cell volume (PCV) lower than eighteen percent on each occasion. He had been stable after the last blood transfusion except for intermittent episodes of bone pain crises occurring about four times a year.

Family, development and social history

He was born to a monogamous family, third of three children of the parents. The mother died from complications of breast cancer when O.J was twelve years old. He said he missed the mother because she was most time his source of comfort during episodes of SCD crises. O.J and his two elder siblings lived with their father, a female house-help and their step-mother, whom the father married a year after O.J mother’s death. O.J’s siblings were well adjusted. Cordial relationships existed among the family members except for frequent frictions between O.J and the step-mother which revolved around O.J’s refusals to join siblings and house-help in various house-hold chores. The father was a middle class income earner and rarely stayed around with the children because his insurance work required frequent traveling. O.J and his siblings spent most part of their time with the house-help and their step-mother. None of the patient’s siblings suffered from SCD, but the father had sickle cell trait with Hemoglobin genotype (Hb.AS). There was no positive history of mental illness in the family.

Pregnancy, birth, neonatal and childhood history were uneventful except for periods of SCD crises. Developmental mile stones were within normal. He completed high school education a year prior to this episode of mental illness, made good grades and was planning further studies.

O.J was described as reserved with few friends, often kept to himself, did not like group activities and occupied his time with reading.

Mental state evaluation

O.J was found to be frightened and agitated but well dressed and groomed. There was loosening of association in his speech and he had abnormality of thought possession. He had paranoid beliefs directed at the house-help and step-mother and experienced visual hallucinations. Orientation in place, person and time was good. Immediate and long term memory were good but short term memory was impaired and he could not concentrate. O.J had a fair judgment and insight into his clinical problem as he thought he needed some help and medications to calm his “nerves”.

Physical examination and laboratory investigations

Physical examination revealed a pale young man with a tinge of jaundice and slight dehydration. He had about four centimeter below the right costal margin hepatomegaly. Neurological Examination revealed no gross abnormality. Examinations of other systems were essentially normal. Magnetic Resonance Imaging (MRI), though recommended, could not be done on this patient because of non-availability of facility for this procedure in the geographical region where the patient was managed. Packed Cell Volume (PCV) was twenty two percent. Blood film showed reticulocytosis and one plus of malaria parasite (Plasmodium Falciparum). Total and differential white blood cell (WBC) counts were within normal range. Electrolytes and urea were essentially normal. Liver Function Test (LFT) did not reveal any abnormality.

Diagnosis and treatment

The working diagnosis made on initial assessment was that of paranoid schizophrenia (F-20) and co-morbid sickle cell disease (SCD) (D-57) and malaria (B-50) based on World Health Organization (W.H.O) International Classification of Diseases, 10^th edition (ICD-10). Narrowing down on the diagnosis of paranoid schizophrenia without considering organic delusional (Schizophrenia-like) disorder (F 06.2) secondary to brain tissue silent-infarcts was not possible because of the limitation of in-exhaustive neurological investigation of the patient through MRI. Psychotic symptoms were treated with Risperidone 2 mg daily and he had family therapy sessions. Psychotic symptoms resolved completely after four weeks of in-patient treatment. He was encouraged to join the sickle cell club in his environment to improve his social activities and to share his experience and “pains” with other SCD patients and their parents. He was referred to a Hematologist and advised on regular hematinics and prophylactic anti-malaria intake. He was maintained on Riperidone 2 mg daily which he took for another four weeks before it was tailed off following his discharge to the psychiatric outpatient facility. Liaison service had been developed with the Hematologist in form of periodic feed back report on O.J and he had been completely stable and without psychotic symptoms in four months of follow-up.

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Discussion

Factors associated with the second episode of mental illness in O.J were identified as adjustment to coping with SCD crises, pre-morbid schizoid trait, and loss of mother through death to complications of breast cancer at the age of twelve.

Sickle cell disease (SCD) is found prevalent in black race, Arabians and the Caribbean [1]. It is a hereditary and chronic medical condition that encompasses sickle cell anemia (SCA) (Hb. SS), sickle cell hemoglobin C disease (Hb. SC) and sickle cell B thalassaemia (SB. Thal.) and the condition is characterized by red blood cell sickling patho-physiology that results in anemia, chronic organ damage, acute episodes of pain crises, infection, splenic sequestration, acute chest syndrome, stroke among others [1]. SCA (Hb. SS) is the most common of SCD and carries the most debilitating prognosis [1]. SCD occurs in about two percent of Nigerian population [2].

Adjustment difficulties have been documented among children and adolescents with chronic medical conditions like SCD [3–5]. Anxiety and depression are well documented complications of adjustment in SCD [6–9]. However, psychosis as a direct complication of SCD or of adjustment in SCD among children and adolescents is infrequently reported. Health care professionals need to be alerted on the possibility of psychosis complicating SCD among affected children and adolescents.

Considering the diagnostic limitation imposed by the in-exhaustive neurological investigation of this adolescent through MRI, the co-morbidity of psychosis and SCD in this adolescent would be discussed in light of the three possible dimensions:

Two completely independent disease conditions co-existing

It is possible that the psychotic symptoms and SCD in this patient co-existed completely independent of each other.

Organic psychosis complicating brain tissue silent-infarcts

Brain tissue silent infarcts are not uncommon among SCD patients [10]. Statius van Eps et al [11] reported transient psychosis in association with cerebral infarction in a thirty five year old patient with Sickle cell Hemoglobin C disease (Hb. SC). That psychosis in this patient was complicating brain tissue silent infarcts cannot be ruled out in view of the acute and transient nature of the two psychotic episodes experienced by this adolescent. Future investigation of brain tissue silent infarcts and psychosis among SCD patients is desirable because of the red blood cell sickling patho-physiologic process of the condition. Isolating brain tissue silent-infarcts as etiological factor of psychosis in SCD patients would obviously pose further treatment challenge in tackling the co-morbidity.

Psychosocial adjustment to SCD and other life events precipitating psychosis in an adolescent with ongoing schizophrenia

Stressful life events had been associated with the onset of schizophrenia in individuals predisposed [12]. This adolescent, aside facing the psychosocial problem of adjusting to SCD lost his mother whom was his confidant to complications of breast cancer when he was twelve year old. Therefore, another explanation of the co-morbidity in this adolescent might be that adjustment to SCD and other life stressors precipitated psychotic episodes in the course of ongoing schizophrenia.

Differential diagnosis and treatment response in this adolescent

This adolescent had experienced two episodes of acute and transient psychosis. The first episode at age fifteen lasted only three weeks and completely resolved as evidenced by the patient ability to re-focus on his academics and completing his high school education with good grades. This present episode which resolved following short duration of anti-psychotic medication had also been acute and transient, though the duration being longer than the first episode. The acute and transient nature of psychotic symptoms in this adolescent would point to a fleeting precipitating factor.

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Conclusion

Putting into consideration the three possible dimensions of co-morbidity in this adolescent each of which pose its own treatment challenges, there is need for increased awareness and collaboration using the models of consultation and liaison services among psychiatrists and other health care professionals in managing children and adolescents with SCD.

Treating psychotic symptoms in this group of patients should be with caution regarding the choice of anti-psychotics. Anti-psychotic like Clozapine that had been documented to cause agranulocytosis should be avoided in these patients that are more predisposed to bacteria infections and aplastic anemia crises.

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Acknowledgements

I thank the patient and the parent for the permission given to report this case. I am indebted to Dr. O.B. Kuteyi, Child and Adolescent Unit, Federal Psychiatric Hospital, Calabar, Nigeria for his encouragement and for reading and criticizing the initial draft of this manuscript.

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References

• Serjeant GR. Sickle Cell Disease. Oxford University Press, London; 1985.
• Fleming AF, Storey JL, Molineaus E, Iroko A, Atai ED. Abnormal Hemoglobins in the Sudan Savannah of Nigeria. Ann Trop Med Parasit. 1979;73:161–168. [PubMed]
• Barlow JH, Ellard DR. The psychosocial well-being of children with chronic disease, their parents and siblings: an overview of the research evidence base. Child Care Health Dev. 2006;32:19–31. doi: 10.1111/j.1365-2214.2006.00591.x. [PubMed] [Cross Ref]
• Midence K, Fuggle P, Davies SC. Psychosocial aspects of sickle cell disease (SCD) in childhood and adolescence: a review. Br J Clin Psychol. 1993;32:271–80. [PubMed]
• Gortmaker SL, Walker DK, Weitzman Metal. Chronic conditions, social-economic risks and behavior problems in children and adolescents. Paediatrics. 1990;85:267–276. [PubMed]
• Morin C, Warin EM. Depression and sickle cell anemia. South Med J. 1981;74:766–768. [PubMed]
• Iloeje SO. Psychiatric morbidity among children with sickle cell disease. Dev Med Child Neurol. 1991;33:1087–94. [PubMed]
• Yang YM, Cepeda M, Price C, Shah A, Mankad V. Depression in children and adolescents with sickle cell disease. Arch Pediatr Adolesc Med. 1994;148:457–60. [PubMed]
• Udofia O, Oseikhuemen AE. Psychiatric morbidity in patients with sickle cell anemia. West Afr J Med. 1996;15:196–200. [PubMed]
• Pegelow CH, Wang W, Granger S, Hsu LL, et al. Silent infarcts in children with sickle cell anemia and abnormal cerebral artery velocity. Arch Neurol. 2001;58:2017–21. doi: 10.1001/archneur.58.12.2017. [PubMed] [Cross Ref]
• Statius van Eps LW, van der Sande JJ, Valk J. Acute Psychosis in a patient with a combination of sickle cell disease and hemoglobin C disease. Ned Tijdschr Geneeskd. 137:302–4. 1993 Feb 6.[PubMed]
• Norman RMG, Malla AK. Stressful life events and schizophrenia. Br J Psychiatry. 1993;162:161.[PubMed]

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Teresa Gallo, Parent, West Coast PANDAS/PANS Symposium April 2014

Published on May 15, 2014

Teresa Gallo tells her story of hope about her daughter Tessa.

Click here to read more

Iron overload among a psychiatric outpatient population.

J Clin Psychiatry. 1997 Feb;58(2):74-8.

Feifel D¹, Young CW.

Author information

Abstract

BACKGROUND:

Iron overload has been suggested to be an unrecognized cause of psychiatric morbidity. This study sought to estimate the prevalence of iron overload in a large outpatient psychiatric clinic.

METHOD:

A retrospective review of screening blood chemistries was conducted on 661 active outpatients at a large, university outpatient psychiatric clinic to identify elevated iron status results (plasma iron, percentage of iron saturation) suggestive of iron overload. Patients with positive profiles were asked to undergo a subsequent blood chemistry to confirm positive results (plasma iron, percentage of iron saturation, plus plasma ferritin). Patients with positive repeated iron chemistry results were considered likely candidates for iron overload.

RESULTS:

Twenty-one patients (3.2%) were identified as meeting one of the criteria suggestive of iron overload on initial screening reports. Thirty-one percent of those who underwent subsequent, confirmatory testing (5/16) continued to meet one of the criteria. On the basis of these results, we estimated a 1% (3.2 x 0.31) prevalence rate of likely candidates for iron overload. A review of these patients’ charts indicated that they carried an unexpectedly high rate of bipolar affective disorder (80%) as a diagnosis and were, without exception, atypical in that they were resistant to conventional psychiatric treatment and lacked a family history for this disorder. The prevalence of positive iron overload profiles on a routine blood chemistry was similar to the prevalence of positive thyroid abnormalities based on TSH results in this population.

CONCLUSION:

Blood chemistry profiles suggestive of iron overload may be associated with a small portion of treatment-resistant psychiatric patients. Routine screening for iron abnormalities, especially in treatment-resistant patients, should be considered. Further studies are required to determine the causal association, if any, between iron excess and primary psychiatric illnesses.