
==== Front
Ann Med Surg (Lond)
Ann Med Surg (Lond)
MS9
Annals of Medicine and Surgery
2049-0801
Lippincott Williams & Wilkins Hagerstown, MD

10.1097/MS9.0000000000000244
00031
3
Case Reports
Partial Sheehan’s syndrome with abdominal tuberculosis presented with pancytopenia and fluctuating thyroid profile: a case report
http://orcid.org/0000-0001-6902-1262
Yadav Prashant MBBS aydvprashant26@gmail.com

http://orcid.org/0000-0001-5997-2021
Bari Md Anwarul FCPS, MD aanwardmc@yahoo.com

http://orcid.org/0000-0003-0293-8898
Saha Akash akashsaha.ssmc@gmail.com
b
Yadav Sushmita MBBS cyadavsushmita11@gmail.com

Khan Amzad H. FCPS aefti1987@yahoo.com

a Department of Medicine
b Sir Salimullah Medical College & Mitford Hospital, Dhaka
c Jalalabad Ragib-Rabeya Medical College, Sylhet, Bangladesh
* Corresponding author. Address: Sir Salimullah Medical College & Mitford Hospital, Dhaka 1100, Bangladesh. Tel.: + 8801313725283. E-mail address: ydvprashant26@gmail.com (P. Yadav).
3 2023
13 2 2023
85 3 506513
12 10 2022
24 12 2022
Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc.
2023
https://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0/

Introduction:

Sheehan’s syndrome is a well-recognized cause of panhypopituitarism secondary to pituitary apoplexy, followed by postpartum hemorrhage. Depending upon the degree of ischemic injury, it can be either partial or complete.

Case presentation:

We report an interesting case of a 35-year-old woman admitted to our hospital with complaints of abdominal distension, which was later presumed to be due to disseminated tuberculosis (TB) after excluding the possible differentials. During the treatment course, she was going through repeated attacks of hypovolemic shock and hypoglycemia due to adrenocortical insufficiency. This, along with the history of prolonged amenorrhea 4 years back due to severe postpartum hemorrhage in her last pregnancy, has led us to our diagnosis of partial Sheehan’s syndrome. After 1 month of starting steroid and anti-TB therapy, it was quite surprising when she presented with features of pancytopenia and antitubercular drug-induced hepatitis.

Discussion:

Sheehan’s syndrome may have a varying degree of presentation depending upon the degree of damage to the pituitary gland, which includes amenorrhea, lactation failure, adrenocortical insufficiency, hyponatremia, hypoglycemia, as well as pancytopenia in some rare instances The hormone panel especially the thyroid profile should be monitored carefully. Such cases are often challenging to deal with because of their varying degrees of presentation and the delay in diagnosis due to a lack of clinical suspicion.

Conclusion:

Therefore, we believe that this rare presentation of pancytopenia in Sheehan’s syndrome with fluctuating thyroid profile and abdominal TB in the background will let clinicians approach such a rare disease differently.

Keywords

adrenocortical insufficiency
case report
disseminated TB
hypothyroidism
pancytopenia
partial Sheehan’s syndrome
OPEN-ACCESSTRUE
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pmcHighlights

Sheehan’s syndrome shows a varying degree of anterior pituitary hormone deficiency followed by postpartum hemorrhage.

A 34-year-old woman presented with abdominal distension, later presumed to be due to disseminated tuberculosis (TB).

She was going through repeated attacks of hypovolemic shock and hypoglycemia due to adrenocortical insufficiency.

She had a significant past history of prolonged amenorrhea and lactational failure followed by severe postpartum hemorrhage in her last pregnancy 4 years back.

After 1 month of steroid and anti-TB therapy, she presented pancytopenia and anti-TB drug-induced hepatitis.

Introduction

Sheehan’s syndrome, first described by Sheehan in 1937, is a well-known cause of panhypopituitarism secondary to pituitary apoplexy, followed by postpartum hemorrhage (PPH)1. Depending upon the degree of ischemic injury, it can be either partial or complete. It is a rare complication that affects 1 in 100 000 births worldwide and is the most common cause of hypopituitarism in low-income or middle-income countries. As per the study, 0.5% of all known cases of female hypopituitarism are caused by Sheehan’s syndrome2. The disease is often called empty sella syndrome. Except for some scar tissue caused by ischemic necrosis of the pituitary gland, the sella turcica is empty. The mechanism of ischemia in such situations is unknown. Hypotension, and hypophysial artery vasospasm, are hypothesized to decrease arterial perfusion of the anterior pituitary. The pituitary gland may be more susceptible to hypoxemia during pregnancy due to its hyperestrogenic state. Some degree of hypopituitarism has been identified in 32% of women with severe postpartum bleeding3.

Sheehan’s syndrome is characterized by varying degrees of anterior pituitary hormone deficiency. Hypovolemic shock, hypoglycemia, and hyponatremia could be etiologically attributed to hypocortisolism, amenorrhea to low gonadotropin levels, agalactia to low prolactin levels, and other nonspecific symptoms (headache, fatigue, anorexia) to growth hormone (GH) deficiency and they could be intricated consequences of hypocortisolism and hypothyroidism. The number of hormonal axes affected by pituitary gland damage determines the severity. Sheehan’s syndrome develops when 70–90% of the gland is destroyed; anterior pituitary is most commonly involved4. The primary involvement is in the secretion of GH and prolactin (90–100%), whereas deficiencies in cortisol, gonadotropin, and thyroid-stimulating hormone (TSH) secretion range from 50 to 100%5. The case of Sheehan’s syndrome is often challenging to deal with because of the varying degree of presentation and the delay in diagnosis due to a lack of clinical suspicion.

We report an interesting as well as a rare scenario of a 35-year-old woman who was admitted to our hospital with complaints of abdominal distension, which was later presumed to be due to disseminated tuberculosis (TB) after excluding the possible differentials. During the treatment course, she was going through repeated attacks of hypovolemic shock and hypoglycemia, which was refractory to fluid resuscitation and glucose administration due to adrenocortical insufficiency. This, along with the history of prolonged amenorrhea 4 years back due to severe PPH in her last pregnancy, has led us to our diagnosis of partial Sheehan’s syndrome. After 1 month of starting steroid and anti-TB therapy, it was quite surprising when she presented with features of pancytopenia and antitubercular drug-induced hepatitis. Moreover, her fluctuating thyroid profile has taught us the important relation between TSH and thyroid hormone level, which we think will be important learning points for clinicians. This work has been reported in line with CAse REports (CARE) 2020 criteria.

Case presentation

A 36-year-old female patient presented to our hospital with abdominal distension for 10 days which was gradual in onset and generalized in nature, sparing the face and lower limbs. This abdominal distension was associated with diffuse, dull and nonradiating abdominal pain, discomfort, and a sense of heaviness but was not associated with respiratory distress and reduced urine volume. There was no history of vomiting of blood or passage of black tarry stool and no history of yellowish discoloration of skin and sclera. She also had complaints of generalized fatigue and malaise for the last 1 and a half years which was gradually progressive and associated with generalized body aches. The pain and fatigue worsened over the years to such an extent that it stopped her from performing household activities. In the past few months, she also experienced occasional constipation, loss of hair, and decreased libido.

On further query, she gave a history of PPH 4 years back, while giving birth to a healthy female baby by caesarian section under the supervision of a specialized gynecologist, which was complicated by prolonged profuse bleeding and could not be managed conservatively due to which she had to undergo a hysterectomy. She was transfused with seven units of fresh whole blood during this event. Since then, she has been unable to breastfeed her baby and has failed to resume her regular menstruation. She did not give any history of fever, cough, night sweats, and no any history of contact with TB patients. There is no history of headache, visual disturbance, and convulsion. She did not complain of joint pain, rash, oral ulcer, photosensitivity, or active bleeding from any sites. She has been married for 20 years and mother of five children. The age of her last child was 5 years. She was immunized according to the EPI (Expanded Programme on Immunization) schedule. She also completed the schedule of the tetanus vaccine before her conception. She had a significant past history of taking steroids and vitamin supplements. She could not mention any documentation regarding the prescription which was stopped abruptly 3 months back. Before admitting to our hospital, she was treated by a physician in a private clinic for subacute intestinal obstruction who diagnosed her with a case of hypothyroid with normal TSH and low fT4 (free T4; thyroxine) and referred her to our hospital for further management. He had prescribed the patient levothyroxine 50 mg, which she had been taking since last week.

On general examination, she was ill-looking with a dull face, mildly anemic, pulse 92/min, blood pressure 85/65 mmHg, respiratory rate 18/min, and postural hypotension was absent. On systemic examination, the abdomen was distended, the umbilicus was centrally placed, and the flank was full. The liver and spleen were not palpable. The shifting dullness was present, but a fluid thrill was absent. Bowel sound was present. There was no palpable para-aortic lymph node. On nervous system examination, her higher psychic function was altered; speech was slurred, and cranial nervous system examination revealed no abnormality. Glasgow Coma Scale was 11/15. On examination of the motor system, delayed relaxation of ankle jerk was not present. There were no abnormalities with sensory or cerebellar function and no sign of meningeal irritation. All other systemic examinations (cardiovascular and respiratory) revealed no abnormalities.

During the course of treatment in our ward, she was undergoing recurrent episodes of hypovolemic shock and hypoglycemia due to acute adrenal crisis, which was conservatively managed with dextrose, intravenous (i.v.) fluid, and i.v. hydrocortisone, respectively. From the detailed history and clinical examination, we made a provisional diagnosis of Sheehan’s syndrome with adrenocortical insufficiency. Therefore, to confirm our diagnosis, we have gone through a series of laboratory investigations, as shown in Table 1 1. The CBC (complete blood count) report showed a high rise in erythrocyte sedimentation rate and mildly decreased hemoglobin concentration. Her serum electrolyte revealed hyponatremia. On chest X-ray, the findings were unremarkable, as shown in Figure 1. Abdominal X-ray showed dilated bowel loops and air-fluid levels, as shown in Figure 2.

Table 1 Initial investigations

CBC report	
Parameters	Test value	Reference value	
Hb (g/dl)	11	11.5–15.5	
ESR (mm in the first hour)	38	20	
RBC (million/μl)	3.72	3.8–5.5	
WBC (/cumm)	8580	4000–11 000	
Platelet (/cumm)	450 000	150 000–400 000	
Differential count	
 Polymorphs	61%	40–75%	
 Lymphocyte	32%	20–45%	
 Monocytes	5%	2–10%	
 PCV	32%	36–50%	
 MCV (fl)	86.8	83–96	
 MCH (pg)	29.6	27–32	
 MCHC (g/dl)	34.1	31.5–34.5	
CBC, complete blood count; ESR, erythrocyte sedimentation rate; Hb, hemoglobin; MCH, mean corpuscular hemoglobin; MCHC, mean corpuscular hemoglobin concentration; MCV, mean corpuscular volume; PCV, packed-cell volume; RBC, red blood cells; WBC, white blood cells.

Figure 1 Plain X-ray chest posteroanterior views showing normal findings.

Figure 2 Plain X-ray abdomen in erect posture showing dilated bowel loops with air-fluid level.

On the ultrasonography of the abdomen (Fig. 3) ascites were present. The liver, gallbladder, pancreas, kidney, and urinary bladder appeared normal. The uterus could not be visualized. Both tubo-ovarian regions appeared normal. Ascitic fluid was aspirated and sent for examination. The findings are shown in Table 2. On microscopic examination of ascitic fluid, we found the lymphocyte count to be 90% with no presence of any malignant cells. Smears were cellular, containing many lymphocytes, histiocytes, and mesothelial cells in the proteinaceous fluid background. A biochemical study of the ascitic fluid showed exudative fluid with serum ascites albumin gradient (SAAG)=0.3 g/dl with low sugar, increased protein, and high adenosine deaminase (ADA) level, which was suggestive of TB. The Gene Xpert for the detection of Mycobacterium tuberculosis from ascitic fluid was negative. Her ANA (antinuclear antibody) screening test was negative. We also had a plan for a colonoscopy and biopsy, but as the patient was already hemodynamically unstable, we could not perform it.

Table 2 Ascitic fluid study

Physical examination	
 Quantity	2 ml	
 Color	Straw	
Microscopic examination	
 RBC	8–10/HPF	
 WBC (total)	670/cumm	
 Lymphocyte	90%	
 Polymorphs	10%	
 Malignant cells	Nil	
Biochemical	
 Sugar	4.09 mmol/l	
 Protein	5 g/dl	
 ADA	32.6 U/l	
 Albumin	3 g/dl	
Others	
 SAAG	0.3 g/dl (exudative)	
 Gene Xpert	Negative	
 ANA	Negative	
ADA, adenosine deaminase; ANA, antinuclear antibody; RBC, red blood cells; SAAG, serum ascites albumin gradient; WBC, white blood cells.

Figure 3 Ultrasonography of the abdomen.

MRI of the brain revealed a smaller-sized pituitary gland with normal signal intensity on T1W1, T2W, and FLAIR (fluid-attenuated inversion recovery). MRI feature was consistent with a small-sized pituitary gland with partial empty sella as shown in Figure 4. Thus, this case was confirmed to be partial Sheehan’s syndrome.

Figure 4 MRI of the brain consistent with small-sized pituitary gland with partial empty sella.

Her real-time reverse transcription-PCR for coronavirus disease 2019 was negative. After performing a thyroid profile multiple times in 15 days apart from renowned centers, we could not establish hypothyroidism. However, her antithyroid peroxidase was on the higher side, which is tabulated in Table 3. Levothyroxine was stopped initially due to a dilemma in the thyroid profile. Therefore, we concluded that the first report showing hypothyroidism was probably erroneous, which might mislead us to a catastrophe if we had continued levothyroxine without first correcting the adrenal crisis. Then the hormone panel was evaluated, which showed reduced anterior pituitary hormones like luteinizing hormone and follicle-stimulating hormone. Her serum adrenocorticotropic hormone (ACTH) and morning cortisol were low. The causes of ascites were evaluated and excluded. As ascitic fluid studies showed exudative ascites with lymphocytosis, the patient was kept on anti-TB trial therapy for 14 days, along with oral prednisolone 20 mg. The patient was discharged and advised to follow up after 14 days.

Table 3 Thyroid function test

Parameters	Test values	Reference value	
	21/11/2021	7/12/2021	16/12/2021	4/9/2022		
TSH (μU/ml)	0.78	0.95	0.43	1.07	0.35–5.01	
FT4 (ng/dl)	0.22	0.964	0.963	0.40	0.71–1.48	
FT3 (fmol/ml)		5.61				
TSHI	−0.08	0.11	−0.24	0.08		
Antithyroid peroxidase antibody	
	Test value (IU/ml)	Reference value (IU/ml)				
Initial	182.65	<5.61				
Follow-up	71.27	<5.61				
FT3, free T3 (FT3; tri-iodothyronine); FT4, free T4 (FT4; thyroxine); TSH, thyroid-stimulating hormone; TSHI, thyroid-stimulating hormone index.

After 1 month, the patient came with complaints of anorexia, nausea, vomiting, and generalized weakness for 4 days, along with yellowish discoloration of skin and sclera. An investigation is shown in Table 4. Serum bilirubin (serum bilirubin), SGPT (serum glutamic pyruvic transaminase), GGT (gamma-glutamyl transferase), and PT (prothrombin time) of the liver function test were on the higher side, suggestive of anti-TB drug-induced hepatotoxicity. She had electrolyte imbalance with hyponatremia which was managed conservatively. CBC report showed pancytopenia. Her iron profile was normal. Peripheral blood film revealed normocytic anemia with leucopenia and thrombocytopenia. Then we performed bone marrow aspiration; bone marrow study showed features of hypocellular marrow with normal megakaryocytes as shown in Figure 5. Prednisolone 30 mg/day was started in two separate doses (20 mg in the morning and 10 mg in the afternoon). We increased the dose of the steroid, keeping in consideration that rifampicin is a cytochrome P-450 inducer. As we increased the dose of steroid, her blood components started rising to the normal level progressively. Although this time, all her anterior pituitary hormone levels were low, her thyroid profile was still normal.

Table 4 Follow-up after 1-month anti-TB therapy

Parameters	Test values	Reference values	
Liver function test			
 Serum bilirubin (total) (mg/dl)	6.2	0.2–1.0	
 SGPT (U/l)	139	Up to 40	
 GGT (U/l)	76	5–40	
Complete blood count	
 Hb (g/dl)	6.9	11.5–15.5	
 ESR (mm in the first hour)	23	20	
 RBC (million/μl)	2.35	3.8–5.5	
 WBC (/cumm)	2910	4000–11 000	
 Platelet (/cumm)	72 000	150 000–400 000	
 Reticulocyte	1%	0.5–2.5%	
ESR, erythrocyte sedimentation rate; GGT, gamma-glutamyl transferase; Hb, hemoglobin; RBC, red blood cells; SGPT, serum glutamic pyruvic transaminase; WBC, white blood cells.

Figure 5 Bone marrow showing hypocellular marrow.

In the last follow-up after 6 months, she had completed anti-TB medications; ascites were resolved, which was confirmed by the CT-abdomen, which is shown in Figure 6, and she could perform her household activities, but this time the patient had gained weight. We performed routine investigations, including thyroid profile. Surprisingly, her thyroid profile revealed thyroid hormones way below the normal range, and also, TSH was below its lower limit, which was expected to be presented earlier. Her antithyroid peroxidase was also high, which let us presume that her hypothyroidism might be associated with an autoimmune condition which already existed during the first presentation or might be associated with Sheehan’s syndrome but presented later in our case6. After tapering the doses of steroids, she was advised to take oral prednisolone (10 mg) and levothyroxine 50 mg.

Figure 6 Follow-up computed tomography abdomen showing normal findings.

Discussion

Disseminated TB is a life-threatening disease caused by the hematogenous spread of M. tuberculosis. The diagnosis is challenging because of the subtle nonspecific clinical presentation, which generally affects the underlying organ, particularly the lung, liver, spleen, bone marrow, kidney, adrenals, thyroid, and eyes7. Tuberculous peritonitis is a rare presentation of extrapulmonary TB. As its symptoms overlap with those of various disorders, it is difficult to diagnose it. Delays in diagnosis lead to delays in therapy, which worsens the outcome. Ascites, abdominal pain, and fever are all clinical features of peritoneal TB8. In our case, the patient came with moderate ascites and abdominal pain, which was gradually worsening day by day. To confirm our diagnosis, we did ascitic fluid studies, which showed absolute lymphocytosis. Biochemical tests revealed low glucose and a high amount of protein which suggests a bacterial infection. The ADA and SAAG test was also indicative of abdominal TB8. Though the gene Xpert was negative, we had gone for anti-TB trial therapy for 14 days according to our national guideline, and the patient responded well to ascites with which she presented previously. The diagnosis of Sheehan’s syndrome was an eventual diagnosis in our case. The patient had come with abdominal distension and some subtle symptoms, like malaise, weakness, and electrolyte imbalance, especially hyponatremia9. In addition to this, the patient was going through repeated attacks of hypovolemic shock and hypoglycemia during the course of treatment which led us to evaluate the cause of the adrenal crisis. We presumed that the adrenocortical insufficiency during the initial presentation might be associated with starting levothyroxine abruptly by the physician without properly evaluating the consequences. In our ward, the first target was to tackle her adrenal crisis which was managed by intravenous steroids (hydrocortisone) and i.v. fluids. And hypoglycemia was managed by i.v. dextrose 200 ml. However, on taking a detailed history from the patient, we came to know that she had a previous history of PPH 4 years back, for which a hysterectomy was done. And following that period, she failed to lactate and resumed her regular mensuration. This, along with her adrenal crisis, was the key to our diagnosis. Therefore, we immediately performed an MRI of the brain, which revealed partial empty sella.

Sheehan syndrome is often called empty sella syndrome. Ischemic necrosis of the pituitary gland followed by PPH is the main feature of its pathogenicity3. GH and prolactin deficiency are seen in 90–100% of cases, and cortisol, gonadotrophin, and TSH are decreased in 50–100% of cases10. On further evaluation, all anterior pituitary hormones were low except TSH. In this approach, we could confirm our diagnosis as partial Sheehan syndrome with adrenocortical insufficiency and disseminated TB in the background. A woman with Sheehan’s syndrome with undiagnosed hypopituitarism might be asymptomatic until her body is exposed to stressful situations like surgery or infection many years after her delivery, and then she presents with adrenal crisis5,11. Sheehan’s syndrome may have a varying degree of presentation which includes amenorrhea, lactation failure, adrenocortical insufficiency, hyponatremia, hypoglycemia, as well as pancytopenia in some rare instances depending upon the degree of damage to the pituitary gland5,12.

Sheehan’s syndrome also presents with electrolyte imbalance in most cases which needs to be conservatively managed. Hyponatremia is the most common electrolyte imbalance, occurring in 33–69% of cases5,13. Hyponatremia can be caused by inappropriate ADH secretion. A study shows a significant correlation between serum sodium levels with thyroid and thyroid-stimulating hormones, as well as cortisol and corticotropin. GH directly increases sodium reabsorption in renal tubules and is involved in sodium uptake via the renin–angiotensin–aldosterone system14,15.

Hypoglycemia caused by a deficiency of ACTH is a noteworthy manifestation of Sheehan’s syndrome. The ability of the human body to tolerate fasting is dependent on glycogen stores and gluconeogenesis. Cortisol deficiency causes anorexia and weight loss, which depletes the body’s glycogen stores. This increases the body’s reliance on the gluconeogenesis pathway for glucose synthesis. Due to cortisol deficiency and glycogen depletion, the low level of gluconeogenesis precursors (like gluconeogenic amino acids and fatty acids) results in an impaired ability to tolerate fasting. Furthermore, a lack of GH contributes to hypoglycemia16. Low cortisol and GH levels were reported in this patient, which contributed to reduced fasting tolerance and recurrent episodes of hypoglycemia17.

Normally, in Sheehan syndrome, hypothyroidism is reported before the adrenal crisis. Maccagnan et al. assessed pituitary functioned in patients with pituitary apoplexy and treated them conservatively. Two weeks following apoplexy, gonadotropin, thyrotropin, and corticotropin deficiency were observed in 80%, 50%, and 33%, respectively3. Considering thyroid hormone replacement can exacerbate the adrenal crisis by increasing the rate of glucocorticoid metabolism, glucocorticoids are replaced first in individuals with secondary hypothyroidism with adrenal insufficiency17. So attending physicians must keep this important point while dealing with the case of Sheehan’s syndrome in the ward. Similarly, some other obstacles need to be clear regarding the normal TSH level in hypopituitarism. There are some theories to explain this condition. One possible cause is that TSH in patients with the pituitary disease is not well processed and biologically not as active as in normal individuals18. Another cause is associated with the pulsatile secretion of TSH, which is hampered by pituitary failure. Moreover, the TSH assay does not demonstrate 24-h TSH secretion in the body, so patients with normal TSH may have less thyroid-stimulating action19,20. So to overcome this hormonal challenge, we need a better parameter to monitor thyroid status in a patient with hypopituitarism. To exclude confusion, we should calculate the TSH index by the following formula:

TSH index = Log (TSH) + 0.1345 × fT4,

where the reference range is between −2 to +2 [SD]. The TSH Index, based on simple thyroid function tests, gives a reliable indication of the severity of pituitary dysfunction in hypopituitary individuals. It estimates the probability of pituitary stimulation test failure and extends the diagnosis of TSH deficiency into areas of the normal thyroid function test reference ranges21.

What made this case more challenging was her follow-up visit after 1 month. She came back with complaints of jaundice and bone marrow features suggestive of marrow aplasia. This presentation was unique to us as all the blood cells were drastically decreased. Anemia is a well-recognized feature of hypopituitarism11,13. Several studies have been published indicating somatotrophin, prolactin, ACTH, cortisone, androgens, and thyroid hormone levels stimulate erythropoiesis indirectly, either by increasing the synthesis of erythropoietin or by increasing the biological effect of endogenous erythropoietin22,23. There has been very little literature showing pancytopenia with hypocellular bone marrow associated with Sheehan’s syndrome. However, pancytopenia as a result of anterior hormone deficiency has not been investigated. It is a consequence of the loss of effect of the pituitary hormone on metabolic reactions to hematopoiesis, which is related to hypopituitarism. How anterior pituitary insufficiency can lead to complete marrow aplasia is still unclear11,22. Simple replacement therapy with thyroid and cortisol hormones results in complete recovery, so clinicians need to be aware of this rare presentation of Sheehan’s syndrome as a treatable etiology of pancytopenia in women5,22. However, anti-TB therapy has its own spectrum of hematologic toxicity and blood cell abnormalities. The levels of hemoglobin, hematocrit, and platelet count of the TB patients were significantly lowered after completion of the intensive phase of TB treatment and, therefore, should be monitored regularly24–26. Therefore, the management of Sheehan’s syndrome is a multidisciplinary approach that needs strict follow-up with endocrinology and hematology specialists.

Conclusion

Though Sheehan syndrome has an increased prevalence in developing countries, physicians often miss the diagnosis due to a lack of proper obstetric history and clinical examination as well as relevant investigations. They treat the patient rationally, which delays the diagnosis. Similarly, Sheehan’s syndrome may rarely present with pancytopenia, which can be managed by hormone replacement. The hormone panel, especially the thyroid profile, should be monitored carefully. Early diagnosis may improve the lifestyle of the patient in the long run, and the patient needs to be regularly followed up. Therefore, we believe that this rare presentation of pancytopenia in Sheehan’s syndrome with fluctuating thyroid profile and abdominal TB in the background will let clinicians approach such a rare disease differently.

Ethical approval

None to declare.

Patient consent

Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

Source of funding

This research did not receive any grant from funding agencies in the public, commercial, or non-profit organizations.

Author contribution

P.Y. conceived, designed, and took entire responsibility for publishing this study under the supervision of M.A.B. M.A.B. and A.H.K. were the physicians under whom the patient was treated. P.Y., A.S., and S.Y. helped in drafting and editing the manuscript. M.A.B. and A.H.K. reviewed the manuscript. All the authors provided intellectual input to the study and approved the final version of the manuscript.

Conflicts of interest disclosure

There are no conflicts of interest.

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Guarantor

Prashant Yadav and Anwarul Bari accept full responsibility for the work and/or the conduct of the study, had access to data, and controlled the decision to publish.

Provenance and peer review

Not commissioned, externally peer-reviewed.

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

Published online 10 February 2023
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